Cholesterol hdl. Medical search

The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.

Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.

Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.

A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)

A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.

Cholesterol present in food, especially in animal products.

Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.

Low-density subclass of the high-density lipoproteins, with particle sizes between 8 to 13 nm.

An enzyme that catalyzes the oxidation of cholesterol in the presence of molecular oxygen to 4-cholesten-3-one and hydrogen peroxide. The enzyme is not specific for cholesterol, but will also oxidize other 3-hydroxysteroids. EC 1.1.3.6.

A membrane-bound cytochrome P450 enzyme that catalyzes the 7-alpha-hydroxylation of CHOLESTEROL in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP7, converts cholesterol to 7-alpha-hydroxycholesterol which is the first and rate-limiting step in the synthesis of BILE ACIDS.

The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.

Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.

Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.

Substances used to lower plasma CHOLESTEROL levels.

A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.

An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC 2.3.1.26.

A superfamily of large integral ATP-binding cassette membrane proteins whose expression pattern is consistent with a role in lipid (cholesterol) efflux. It is implicated in TANGIER DISEASE characterized by accumulation of cholesteryl ester in various tissues.

A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.

Steroids with a hydroxyl group at C-3 and most of the skeleton of cholestane. Additional carbon atoms may be present in the side chain. (IUPAC Steroid Nomenclature, 1987)

Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.

Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.

An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC 2.3.1.43.

Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones.

A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.

Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.

Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.

Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.

An emulsifying agent produced in the LIVER and secreted into the DUODENUM. Its composition includes BILE ACIDS AND SALTS; CHOLESTEROL; and ELECTROLYTES. It aids DIGESTION of fats in the duodenum.

A family of sterols commonly found in plants and plant oils. Alpha-, beta-, and gamma-isomers have been characterized.

Cyclic GLUCANS consisting of seven (7) glucopyranose units linked by 1,4-glycosidic bonds.

A family of MEMBRANE TRANSPORT PROTEINS that require ATP hydrolysis for the transport of substrates across membranes. The protein family derives its name from the ATP-binding domain found on the protein.

The process of converting an acid into an alkyl or aryl derivative. Most frequently the process consists of the reaction of an acid with an alcohol in the presence of a trace of mineral acid as catalyst or the reaction of an acyl chloride with an alcohol. Esterification can also be accomplished by enzymatic processes.

Conditions with excess LIPIDS in the blood.

Cholesterol which is substituted by a hydroxy group in any position.

A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.

Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.

A class of organic compounds known as STEROLS or STEROIDS derived from plants.

Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.

A homologous group of cyclic GLUCANS consisting of alpha-1,4 bound glucose units obtained by the action of cyclodextrin glucanotransferase on starch or similar substrates. The enzyme is produced by certain species of Bacillus. Cyclodextrins form inclusion complexes with a wide variety of substances.

The second most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. It has a high lipid affinity and is known to displace APOLIPOPROTEIN A-I from HDL particles and generates a stable HDL complex. ApoA-II can modulate the activation of LECITHIN CHOLESTEROL ACYLTRANSFERASE in the presence of APOLIPOPROTEIN A-I, thus affecting HDL metabolism.

A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.

Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a choline moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and choline and 2 moles of fatty acids.

A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.

The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.

Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.

Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.

A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.

A strongly basic anion exchange resin whose main constituent is polystyrene trimethylbenzylammonium Cl(-) anion.

An intermediate in the synthesis of cholesterol.

Cell surface proteins that bind lipoproteins with high affinity. Lipoprotein receptors in the liver and peripheral tissues mediate the regulation of plasma and cellular cholesterol metabolism and concentration. The receptors generally recognize the apolipoproteins of the lipoprotein complex, and binding is often a trigger for endocytosis.

Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.

Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.

Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.

A complex of polyene antibiotics obtained from Streptomyces filipinensis. Filipin III alters membrane function by interfering with membrane sterols, inhibits mitochondrial respiration, and is proposed as an antifungal agent. Filipins I, II, and IV are less important.

A diet that contributes to the development and acceleration of ATHEROGENESIS.

An enzyme that catalyzes the hydrolysis of CHOLESTEROL ESTERS and some other sterol esters, to liberate cholesterol plus a fatty acid anion.

Uptake of substances through the lining of the INTESTINES.

A class of sphingolipids found largely in the brain and other nervous tissue. They contain phosphocholine or phosphoethanolamine as their polar head group so therefore are the only sphingolipids classified as PHOSPHOLIPIDS.

Detergent-insoluble CELL MEMBRANE components. They are enriched in SPHINGOLIPIDS and CHOLESTEROL and clustered with glycosyl-phosphatidylinositol (GPI)-anchored proteins.

A highly dense subclass of the high-density lipoproteins, with particle sizes below 7 nm. They are also known as nascent HDL, composed of a few APOLIPOPROTEIN A-I molecules which are complexed with PHOSPHOLIPIDS. The lipid-poor pre-beta-HDL particles serve as progenitors of HDL3 and then HDL2 after absorption of free cholesterol from cell membranes, cholesterol esterification, and acquisition of apolipoproteins A-II, Cs, and E. Pre-beta-HDL initiate the reverse cholesterol transport process from cells to liver.

A cholesterol derivative found in human feces, gallstones, eggs, and other biological matter.

A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.

Presence or formation of GALLSTONES in the BILIARY TRACT, usually in the gallbladder (CHOLECYSTOLITHIASIS) or the common bile duct (CHOLEDOCHOLITHIASIS).

An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.

A broad category of receptor-like proteins that may play a role in transcriptional-regulation in the CELL NUCLEUS. Many of these proteins are similar in structure to known NUCLEAR RECEPTORS but appear to lack a functional ligand-binding domain, while in other cases the specific ligands have yet to be identified.

Unsaturated derivatives of the steroid androstane containing at least one double bond at any site in any of the rings.

A triterpene that derives from the chair-boat-chair-boat folding of 2,3-oxidosqualene. It is metabolized to CHOLESTEROL and CUCURBITACINS.

An autosomal recessively inherited disorder caused by mutation of ATP-BINDING CASSETTE TRANSPORTERS involved in cellular cholesterol removal (reverse-cholesterol transport). It is characterized by near absence of ALPHA-LIPOPROTEINS (high-density lipoproteins) in blood. The massive tissue deposition of cholesterol esters results in HEPATOMEGALY; SPLENOMEGALY; RETINITIS PIGMENTOSA; large orange tonsils; and often sensory POLYNEUROPATHY. The disorder was first found among inhabitants of Tangier Island in the Chesapeake Bay, MD.

Lipid-laden macrophages originating from monocytes or from smooth muscle cells.

Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)

A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.

A large group of structurally diverse cell surface receptors that mediate endocytic uptake of modified LIPOPROTEINS. Scavenger receptors are expressed by MYELOID CELLS and some ENDOTHELIAL CELLS, and were originally characterized based on their ability to bind acetylated LOW-DENSITY LIPOPROTEINS. They can also bind a variety of other polyanionic ligand. Certain scavenger receptors can internalize micro-organisms as well as apoptotic cells.

Leukocyte differentiation antigens and major platelet membrane glycoproteins present on MONOCYTES; ENDOTHELIAL CELLS; PLATELETS; and mammary EPITHELIAL CELLS. They play major roles in CELL ADHESION; SIGNAL TRANSDUCTION; and regulation of angiogenesis. CD36 is a receptor for THROMBOSPONDINS and can act as a scavenger receptor that recognizes and transports oxidized LIPOPROTEINS and FATTY ACIDS.

Cholesterol derivatives having an additional double bond in any position. 24-Dehydrocholesterol is DESMOSTEROL. The other most prevalent dehydrocholesterol is the 7-isomer. This compound is a precursor of cholesterol and of vitamin D3.

Blocking of a blood vessel by CHOLESTEROL-rich atheromatous deposits, generally occurring in the flow from a large artery to small arterial branches. It is also called arterial-arterial embolization or atheroembolism which may be spontaneous or iatrogenic. Patients with spontaneous atheroembolism often have painful, cyanotic digits of acute onset.

Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.

Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation.

An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.

An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3.

Regular course of eating and drinking adopted by a person or animal.

A group of autosomal recessive disorders in which harmful quantities of lipids accumulate in the viscera and the central nervous system. They can be caused by deficiencies of enzyme activities (SPHINGOMYELIN PHOSPHODIESTERASE) or defects in intracellular transport, resulting in the accumulation of SPHINGOMYELINS and CHOLESTEROL. There are various subtypes based on their clinical and genetic differences.

The rate dynamics in chemical or physical systems.

Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.

A mitochondrial cytochrome P450 enzyme that catalyzes the side-chain cleavage of C27 cholesterol to C21 pregnenolone in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP11A1 gene, catalyzes the breakage between C20 and C22 which is the initial and rate-limiting step in the biosynthesis of various gonadal and adrenal steroid hormones.

Transport proteins that carry specific substances in the blood or across cell membranes.

Artificial, single or multilaminar vesicles (made from lecithins or other lipids) that are used for the delivery of a variety of biological molecules or molecular complexes to cells, for example, drug delivery and gene transfer. They are also used to study membranes and membrane proteins.

Relating to the size of solids.

A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins).

The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.

The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)

A sterol regulatory element binding protein that regulates GENES involved in CHOLESTEROL synthesis and uptake.

An autosomal recessively inherited disorder caused by mutation of LECITHIN CHOLESTEROL ACYLTRANSFERASE that facilitates the esterification of lipoprotein cholesterol and subsequent removal from peripheral tissues to the liver. This defect results in low HDL-cholesterol level in blood and accumulation of free cholesterol in tissue leading to a triad of CORNEAL OPACITY, hemolytic anemia (ANEMIA, HEMOLYTIC), and PROTEINURIA.

The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.

Elements of limited time intervals, contributing to particular results or situations.

An NAPH-dependent cytochrome P450 enzyme that catalyzes the oxidation of the side chain of sterol intermediates such as the 27-hydroxylation of 5-beta-cholestane-3-alpha,7-alpha,12-alpha-triol.

A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.

Layers of lipid molecules which are two molecules thick. Bilayer systems are frequently studied as models of biological membranes.

A condition of elevated levels of TRIGLYCERIDES in the blood.

An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).

Cytochrome P-450 monooxygenases (MIXED FUNCTION OXYGENASES) that are important in steroid biosynthesis and metabolism.

Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.

7-carbon saturated monocarboxylic acids.

Derivatives of the saturated steroid cholestane with methyl groups at C-18 and C-19 and an iso-octyl side chain at C-17.

A ubiquitous family of proteins that transport PHOSPHOLIPIDS such as PHOSPHATIDYLINOSITOL and PHOSPHATIDYLCHOLINE between membranes. They play an important role in phospholipid metabolism during vesicular transport and SIGNAL TRANSDUCTION.

Excrement from the INTESTINES, containing unabsorbed solids, waste products, secretions, and BACTERIA of the DIGESTIVE SYSTEM.

A storage reservoir for BILE secretion. Gallbladder allows the delivery of bile acids at a high concentration and in a controlled manner, via the CYSTIC DUCT to the DUODENUM, for degradation of dietary lipid.

Conditions with abnormally low levels of LIPOPROTEINS in the blood. This may involve any of the lipoprotein subclasses, including ALPHA-LIPOPROTEINS (high-density lipoproteins); BETA-LIPOPROTEINS (low-density lipoproteins); and PREBETA-LIPOPROTEINS (very-low-density lipoproteins).

An autosomal recessive disorder of CHOLESTEROL metabolism. It is caused by a deficiency of 7-dehydrocholesterol reductase, the enzyme that converts 7-dehydrocholesterol to cholesterol, leading to an abnormally low plasma cholesterol. This syndrome is characterized by multiple CONGENITAL ABNORMALITIES, growth deficiency, and INTELLECTUAL DISABILITY.

Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.

An enzyme which catalyzes the hydrolysis of an aryl-dialkyl phosphate to form dialkyl phosphate and an aryl alcohol. It can hydrolyze a broad spectrum of organophosphate substrates and a number of aromatic carboxylic acid esters. It may also mediate an enzymatic protection of LOW DENSITY LIPOPROTEINS against oxidative modification and the consequent series of events leading to ATHEROMA formation. The enzyme was previously regarded to be identical with Arylesterase (EC 3.1.1.2).

Cholesterol substituted in any position by a keto moiety. The 7-keto isomer inhibits 3-hydroxy-3-methylglutaryl-CoA reductase activity and inhibits cholesterol uptake in the coronary arteries and aorta in vitro.

Fatty acids which are unsaturated in only one position.

Organic compounds that contain silicon as an integral part of the molecule.

The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.

Centrifugation with a centrifuge that develops centrifugal fields of more than 100,000 times gravity. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

Glucose in blood.

Intermediate-density subclass of the high-density lipoproteins, with particle sizes between 7 to 8 nm. As the larger lighter HDL2 lipoprotein, HDL3 lipoprotein is lipid-rich.

Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.

The motion of phospholipid molecules within the lipid bilayer, dependent on the classes of phospholipids present, their fatty acid composition and degree of unsaturation of the acyl chains, the cholesterol concentration, and temperature.

A class of lipoproteins that carry dietary CHOLESTEROL and TRIGLYCERIDES from the SMALL INTESTINE to the tissues. Their density (0.93-1.006 g/ml) is the same as that of VERY-LOW-DENSITY LIPOPROTEINS.

The processes whereby the internal environment of an organism tends to remain balanced and stable.

An indicator of body density as determined by the relationship of BODY WEIGHT to BODY HEIGHT. BMI=weight (kg)/height squared (m2). BMI correlates with body fat (ADIPOSE TISSUE). Their relationship varies with age and gender. For adults, BMI falls into these categories: below 18.5 (underweight); 18.5-24.9 (normal); 25.0-29.9 (overweight); 30.0 and above (obese). (National Center for Health Statistics, Centers for Disease Control and Prevention)

Established cell cultures that have the potential to propagate indefinitely.

A condition marked by the development of widespread xanthomas, yellow tumor-like structures filled with lipid deposits. Xanthomas can be found in a variety of tissues including the SKIN; TENDONS; joints of KNEES and ELBOWS. Xanthomatosis is associated with disturbance of LIPID METABOLISM and formation of FOAM CELLS.

The main trunk of the systemic arteries.

A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.

RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.

A cluster of metabolic risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components of metabolic syndrome X include excess ABDOMINAL FAT; atherogenic DYSLIPIDEMIA; HYPERTENSION; HYPERGLYCEMIA; INSULIN RESISTANCE; a proinflammatory state; and a prothrombotic (THROMBOSIS) state. (from AHA/NHLBI/ADA Conference Proceedings, Circulation 2004; 109:551-556)

Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.

A genus of the family Muridae having three species. The present domesticated strains were developed from individuals brought from Syria. They are widely used in biomedical research.

An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.

A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).

A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993).

A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.

Oils derived from plants or plant products.

The BILE DUCTS and the GALLBLADDER.

Fats containing one or more double bonds, as from oleic acid, an unsaturated fatty acid.

Animal reproductive bodies, or the contents thereof, used as food. The concept is differentiated from OVUM, the anatomic or physiologic entity.

A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)

Antilipemic agent with high ophthalmic toxicity. According to Merck Index, 11th ed, the compound was withdrawn from the market in 1962 because of its association with the formation of irreversible cataracts.

A major primary bile acid produced in the liver and usually conjugated with glycine or taurine. It facilitates fat absorption and cholesterol excretion.

The interstitial fluid that is in the LYMPHATIC SYSTEM.

FATTY ACIDS in which the carbon chain contains one or more double or triple carbon-carbon bonds.

An anticholesteremic agent that inhibits sterol biosynthesis in animals.

Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.

The 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholanic acid family of bile acids in man, usually conjugated with glycine or taurine. They act as detergents to solubilize fats for intestinal absorption, are reabsorbed by the small intestine, and are used as cholagogues and choleretics.

A group of fatty acids that contain 18 carbon atoms and a double bond at the omega 9 carbon.

The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.

Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.

CHOLESTENES with one or more double bonds and substituted by any number of keto groups.

A 21-carbon steroid, derived from CHOLESTEROL and found in steroid hormone-producing tissues. Pregnenolone is the precursor to GONADAL STEROID HORMONES and the adrenal CORTICOSTEROIDS.

Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.

Derivatives of ACETIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the carboxymethane structure.

A tyrosine phosphoprotein that plays an essential role in CAVEOLAE formation. It binds CHOLESTEROL and is involved in LIPIDS transport, membrane traffic, and SIGNAL TRANSDUCTION.

Chromatography on thin layers of adsorbents rather than in columns. The adsorbent can be alumina, silica gel, silicates, charcoals, or cellulose. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

Intracellular receptors that can be found in the cytoplasm or in the nucleus. They bind to extracellular signaling molecules that migrate through or are transported across the CELL MEMBRANE. Many members of this class of receptors occur in the cytoplasm and are transported to the CELL NUCLEUS upon ligand-binding where they signal via DNA-binding and transcription regulation. Also included in this category are receptors found on INTRACELLULAR MEMBRANES that act via mechanisms similar to CELL SURFACE RECEPTORS.

Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.

A diet that contains limited amounts of fat with less than 30% of calories from all fats and less than 10% from saturated fat. Such a diet is used in control of HYPERLIPIDEMIAS. (From Bondy et al, Metabolic Control and Disease, 8th ed, pp468-70; Dorland, 27th ed)

Abstaining from all food.

Particles consisting of aggregates of molecules held loosely together by secondary bonds. The surface of micelles are usually comprised of amphiphatic compounds that are oriented in a way that minimizes the energy of interaction between the micelle and its environment. Liquids that contain large numbers of suspended micelles are referred to as EMULSIONS.

Unsaturated fats or oils used in foods or as a food.

Closed vesicles of fragmented endoplasmic reticulum created when liver cells or tissue are disrupted by homogenization. They may be smooth or rough.

The remnants of plant cell walls that are resistant to digestion by the alimentary enzymes of man. It comprises various polysaccharides and lignins.

An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed)

The relationship between the dose of an administered drug and the response of the organism to the drug.

A synthetic phospholipid used in liposomes and lipid bilayers for the study of biological membranes.

(Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.

Cytoplasm stored in an egg that contains nutritional reserves for the developing embryo. It is rich in polysaccharides, lipids, and proteins.

A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.

Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.

The first committed enzyme of the biosynthesis pathway that leads to the production of STEROLS. it catalyzes the synthesis of SQUALENE from farnesyl pyrophosphate via the intermediate PRESQUALENE PYROPHOSPHATE. This enzyme is also a critical branch point enzyme in the biosynthesis of ISOPRENOIDS that is thought to regulate the flux of isoprene intermediates through the sterol pathway.

CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.

The physical or physiological processes by which substances, tissue, cells, etc. take up or take in other substances or energy.

A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS and CHYLOMICRON REMNANTS. Apo C-III, synthesized in the liver, is an inhibitor of LIPOPROTEIN LIPASE. Apo C-III modulates the binding of chylomicron remnants and VLDL to receptors (RECEPTORS, LDL) thus decreases the uptake of triglyceride-rich particles by the liver cells and subsequent degradation. The normal Apo C-III is glycosylated. There are several polymorphic forms with varying amounts of SIALIC ACID (Apo C-III-0, Apo C-III-1, and Apo C-III-2).

PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.

A lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol.

Unstable isotopes of carbon that decay or disintegrate emitting radiation. C atoms with atomic weights 10, 11, and 14-16 are radioactive carbon isotopes.

An autosomal recessive lipid storage disorder that is characterized by accumulation of CHOLESTEROL and SPHINGOMYELINS in cells of the VISCERA and the CENTRAL NERVOUS SYSTEM. Type C (or C1) and type D are allelic disorders caused by mutation of gene (NPC1) encoding a protein that mediate intracellular cholesterol transport from lysosomes. Clinical signs include hepatosplenomegaly and chronic neurological symptoms. Type D is a variant in people with a Nova Scotia ancestry.

Proteins which are present in or isolated from SOYBEANS.

The product of conjugation of cholic acid with taurine. Its sodium salt is the chief ingredient of the bile of carnivorous animals. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as a cholagogue and cholerectic.

The main structural proteins of CAVEOLAE. Several distinct genes for caveolins have been identified.

Studies comparing two or more treatments or interventions in which the subjects or patients, upon completion of the course of one treatment, are switched to another. In the case of two treatments, A and B, half the subjects are randomly allocated to receive these in the order A, B and half to receive them in the order B, A. A criticism of this design is that effects of the first treatment may carry over into the period when the second is given. (Last, A Dictionary of Epidemiology, 2d ed)

Steroids with methyl groups at C-10 and C-13 and a branched 8-carbon chain at C-17. Members include compounds with any degree of unsaturation; however, CHOLESTADIENES is available for derivatives containing two double bonds.

Maleness or femaleness as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or effect of a circumstance. It is used with human or animal concepts but should be differentiated from SEX CHARACTERISTICS, anatomical or physiological manifestations of sex, and from SEX DISTRIBUTION, the number of males and females in given circumstances.

Procedures for finding the mathematical function which best describes the relationship between a dependent variable and one or more independent variables. In linear regression (see LINEAR MODELS) the relationship is constrained to be a straight line and LEAST-SQUARES ANALYSIS is used to determine the best fit. In logistic regression (see LOGISTIC MODELS) the dependent variable is qualitative rather than continuously variable and LIKELIHOOD FUNCTIONS are used to find the best relationship. In multiple regression, the dependent variable is considered to depend on more than a single independent variable.

The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.

A spirostan found in DIOSCOREA and other plants. The 25S isomer is called yamogenin. Solasodine is a natural derivative formed by replacing the spiro-ring with a nitrogen, which can rearrange to SOLANINE.

Oil from ZEA MAYS or corn plant.

A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).

A sterol regulatory element binding protein that regulates expression of GENES involved in FATTY ACIDS metabolism and LIPOGENESIS. Two major isoforms of the protein exist due to ALTERNATIVE SPLICING.

A butterlike product made of refined vegetable oils, sometimes blended with animal fats, and emulsified usually with water or milk. It is used as a butter substitute. (From Random House Unabridged Dictionary, 2d ed)

A bile acid, usually conjugated with either glycine or taurine. It acts as a detergent to solubilize fats for intestinal absorption and is reabsorbed by the small intestine. It is used as cholagogue, a choleretic laxative, and to prevent or dissolve gallstones.

Endocytic/exocytic CELL MEMBRANE STRUCTURES rich in glycosphingolipids, cholesterol, and lipid-anchored membrane proteins that function in ENDOCYTOSIS (potocytosis), transcytosis, and SIGNAL TRANSDUCTION. Caveolae assume various shapes from open pits to closed vesicles. Caveolar coats are composed of CAVEOLINS.

Serum triglyceride: a possible risk factor for ruptured abdominal aortic aneurysm. (1/5144)

BACKGROUND: We aimed to determine the relationship between ruptured abdominal aortic aneurysm (AAA) and serum concentrations of lipids and apolipoproteins. METHODS: A cohort of 21 520 men, aged 35-64 years, was recruited from men attending the British United Provident Association (BUPA) clinic in London for a routine medical examination in 1975-1982. Smoking habits, weight, height and blood pressure were recorded at entry. Lipids and apolipoproteins were measured in stored serum samples from the 30 men who subsequently died of ruptured AAA and 150 matched controls. RESULTS: Triglyceride was strongly related to risk of ruptured AAA. In univariate analyses the risk in men on the 90th centile of the distribution relative to the risk in men on the 10th (RO10-90) was 12 (95% confidence interval [CI] : 3.8-37) for triglyceride, 5.5 (95% CI: 1.8-17) for apolipoprotein B (apoB) (the protein component of low density lipoprotein [LDL]), 0.15 (95% CI : 0.04-0.56) for apo A1 (the protein component of high density lipoprotein [HDL]), 3.7 (95% CI: 1.4-9.4) for body mass index and 3.0 (95% CI: 1.1-8.5) for systolic blood pressure. Lipoprotein (a) (Lp(a)) was not a significant risk factor (RO10-90 = 1.6, 95% CI: 0.6-3.0). In multivariate analysis triglyceride retained its strong association. CONCLUSION: Triglyceride appears to be a strong risk factor for ruptured AAA, although further studies are required to clarify this. If this and other associations are cause and effect, then changing the distribution of risk factors in the population (by many people stopping smoking and adopting a lower saturated fat diet and by lowering blood pressure) could achieve an important reduction in mortality from ruptured AAA. (+info)

Association of the inflammatory state in active juvenile rheumatoid arthritis with hypo-high-density lipoproteinemia and reduced lipoprotein-associated platelet-activating factor acetylhydrolase activity. (2/5144)

OBJECTIVE: To investigate the relationship between the quantitative and qualitative abnormalities of apolipoprotein B (Apo B)- and Apo A-I-containing lipoproteins and between lipoprotein-associated platelet-activating factor acetylhydrolase (PAF-AH) activity in patients with juvenile rheumatoid arthritis (JRA) as a function of the inflammatory state. METHODS: Twenty-six JRA patients and 22 age- and sex-matched control subjects with normal lipid levels participated in the study. Fourteen patients had active disease, and 12 had inactive disease. Plasma lipoproteins were fractionated by gradient ultracentrifugation into 9 subfractions, and their chemical composition and mass were determined. The PAF-AH activity associated with lipoprotein subfractions and the activity in plasma were also measured. RESULTS: Patients with active JRA had significantly lower plasma total cholesterol and high-density lipoprotein (HDL) cholesterol levels as compared with controls, due to the decrease in the mass of both the HDL2 and HDL3 subfractions. Patients with active JRA also had higher plasma triglyceride levels, mainly due to the higher triglyceride content of the very low-density lipoprotein plus the intermediate-density lipoprotein subfraction. The plasma PAF-AH activity in patients with active JRA was lower than that in controls, mainly due to the decrease in PAF-AH activity associated with the intermediate and dense low-density lipoprotein subclasses. The lipid abnormalities and the reduction in plasma PAF-AH activity were significantly correlated with plasma C-reactive protein levels and were not observed in patients with inactive JRA. CONCLUSION: This is the first study to show that patients with active JRA exhibit low levels of HDL2 and HDL3 and are deficient in plasma PAF-AH activity. These alterations suggest that active JRA is associated with partial loss of the antiinflammatory activity of plasma Apo B- and Apo A-I-containing lipoproteins. (+info)

Chlamydia pneumoniae antibodies are associated with an atherogenic lipid profile. (3/5144)

OBJECTIVE: To determine, within a representative population group of men and women, whether alteration of the lipid profile might underlie the reported association between Chlamydia pneumoniae and ischaemic heart disease. DESIGN AND SETTING: Cross sectional survey in an area with a high incidence of ischaemic heart disease. SUBJECTS: 400 randomly selected participants in the World Health Organisation MONICA project's third population survey in Northern Ireland. MAIN OUTCOME MEASURES: Stored sera were examined by microimmunofluorescence for IgG antibodies to C pneumoniae at a dilution of 1 in 64. Mean total and high density lipoprotein (HDL) cholesterol were compared between seropositive and seronegative individuals with adjustment for age, measures of socioeconomic status, smoking habit, alcohol consumption, body mass index, and the season during which blood had been taken. RESULTS: In seropositive men, adjusted mean serum total cholesterol and HDL cholesterol were 0.5 mmol/l (9.2%) higher and 0.11 mmol/l (9.3%) lower, respectively, than in seronegative men. Differences in women did not achieve statistical significance, but both total cholesterol and HDL cholesterol were higher (3.6% and 5.8%, respectively) in seropositive than in seronegative individuals. CONCLUSIONS: There is serological evidence that C pneumoniae infection is associated with an atherogenic lipid profile in men. Altered lipid levels may underlie the association between C pneumoniae and ischaemic heart disease. (+info)

Effect of fasting on temporal variation in the nephrotoxicity of amphotericin B in rats. (4/5144)

Evidence for temporal variation in the nephrotoxicity of amphotericin B was recently reported in experimental animals. The role of food in these variations was determined by studying the effect of a short fasting period on the temporal variation in the renal toxicity of amphotericin B. Twenty-eight normally fed and 28 fasted female Sprague-Dawley rats were used. Food was available ad libitum to the fed rats, while the fasted animals were fasted 12 h before and 24 h after amphotericin B injection to minimize stress for the animals. Water was available ad libitum to both groups of rats, which were maintained on a 14-h light, 10-h dark regimen (light on at 0600 h). Renal toxicity was determined by comparing the levels of excretion of renal enzyme and the serum creatinine and blood urea nitrogen (BUN) levels at the time of the maximal (0700 h) or the minimal (1900 h) nephrotoxicity after the intraperitoneal administration of a single dose of dextrose (5%; control group) or amphotericin B (50 mg/kg of body weight; treated group) to the rats. The nephrotoxicities obtained after amphotericin B administration at both times of day were compared to the nephrotoxicities observed for time-matched controls. In fed animals, the 24-h urinary excretion of N-acetyl-beta-D-glucosaminidase and beta-galactosidase was significantly higher when amphotericin B was injected at 0700 and 1900 h. The excretion of these two enzymes was reduced significantly (P < 0.05) in fasting rats, and this effect was larger at 0700 h (P < 0.05) than at 1900 h. The serum creatinine level was also significantly higher (P < 0.05) in fed animals treated at 0700 h than in fed animals treated at 1900 h. Fasting reduced significantly (P < 0.05) the increase in the serum creatinine level, and this effect was larger in the animals treated at 0700 h. Similar data were obtained for BUN levels. Amphotericin B accumulation was significantly higher (P < 0.05) in the renal cortexes of fed rats than in those of fasted animals, but there was no difference according to the time of injection. These results demonstrated that fasting reduces the nephrotoxicity of amphotericin B and that food availability is of crucial importance in the temporal variation in the renal toxicity of amphotericin B in rats. (+info)

The impact of an amino acid-based peritoneal dialysis fluid on plasma total homocysteine levels, lipid profile and body fat mass. (5/5144)

BACKGROUND: The caloric load from glucose-based peritoneal dialysis (PD) fluids contributes to hypertriglyceridaemia, adiposity and, as result of anorexia, protein malnutrition in PD patients. It has been suggested that replacement of a glucose-based by an amino acids-based PD fluid (AA-PDF) for one exchange per day might improve the nutritional status and lipid profile. Due to the uptake of methionine from the dialysate, however, exposure to AA-PDF might aggravate hyperhomocysteinaemia, a frequently occurring risk factor for atherosclerosis in uraemic patients. METHODS: We studied the impact of a once daily exchange with 1.1% AA-PDF instead of glucose-based PD fluid for 2 months on plasma methionine and total homocysteine (tHcy) levels, lipid profile, butyrylcholinesterase (BChE) and body fat mass of seven stable PD patients. Results are expressed as mean+/-SEM. RESULTS: Methionine levels did not increase significantly during therapy, but tHcy levels increased substantially from 60+/-12 to 84+/-19 micromol/l after 1 month (P=0.039), and to 85+/-22 micromol/l after 2 months of AA-PDF treatment. Serum triglyceride concentration decreased from 3.0+/-0.4 mmol/l at entry to 2.6+/-0.5 mmol/l (at 1 month, P=0.041 vs baseline). Serum BChE also decreased from 6.9+/-0.4 U/ml at entry to 6.3+/-0.4 U/ml after 2 months (P=0.014). Total cholesterol concentration and cholesterol fractions did not change. The reduced exposure to glucose-based PD fluid for 2 months resulted in a 0.5 kg reduction in fat mass which was due mainly to a reduction in fat mass of the trunk region (0.3 kg, P=0.031). CONCLUSIONS: It is concluded that methionine-containing AA-PDF induces an increase in the plasma tHcy level. This might, potentially, offset the beneficial effects of an improved serum lipid profile and reduced fat mass on the risk of cardiovascular disease in PD patients. Lowering the methionine content of the fluid, therefore, may be required to overcome this adverse effect. (+info)

Survey of total error of precipitation and homogeneous HDL-cholesterol methods and simultaneous evaluation of lyophilized saccharose-containing candidate reference materials for HDL-cholesterol. (6/5144)

BACKGROUND: Standardization of HDL-cholesterol is needed for risk assessment. We assessed for the first time the accuracy of HDL-cholesterol testing in The Netherlands and evaluated 11 candidate reference materials (CRMs). METHODS: The total error (TE) of HDL-cholesterol measurements was assessed in native human sera by 25 Dutch clinical chemistry laboratories. Concomitantly, the suitability of lyophilized, saccharose-containing CRMs (n = 11) for HDL-cholesterol was evaluated. RESULTS: In the precipitation method group, which included 25 laboratories and four methods, the mean (minimum-maximum) TE was 11.5% (2.7-25.2%), signifying that 18 of 25 laboratories satisfied the TE goal of +info)

Elevated hepatic lipase activity and low levels of high density lipoprotein in a normotriglyceridemic, nonobese Turkish population. (7/5144)

Low levels of high density lipoprotein cholesterol (HDL-C) are associated with increased risk of coronary heart disease and, in the United States, are often associated with hypertriglyceridemia and obesity. In Turkey, low HDL-C levels are highly prevalent, 53% of men and 26% of women having HDL-C levels <35 mg/dl, in the absence of hypertriglyceridemia and obesity. In this study to investigate the cause of low HDL-C levels in Turks, various factors affecting HDL metabolism were assessed in normotriglyceridemic Turkish men and women living in Istanbul and in non-Turkish men and women living in San Francisco. Turkish men and women had significantly lower HDL-C levels than the San Francisco men and women, as well as markedly lower apolipoprotein A-I levels (25 and 39 mg/dl lower, respectively). In both Turkish and non-Turkish subjects, the mean body mass index was <27 kg/m2, the mean triglyceride level was <120 mg/dl, and the mean total cholesterol was 170-180 mg/dl. The mean hepatic triglyceride lipase activity was 21% and 31% higher in Turkish men and women, respectively, than in non-Turkish men and women, and remained higher even after subjects with a body mass index >50th percentile for men and women in the United States were excluded from the analysis. As no dietary or behavioral factors have been identified in the Turkish population that account for increased hepatic triglyceride lipase activity, the elevation most likely has a genetic basis. high density lipoprotein in a normotriglyceridemic, nonobese Turkish population. (+info)

Comparison of synthetic saponin cholesterol absorption inhibitors in rabbits: evidence for a non-stoichiometric, intestinal mechanism of action. (8/5144)

The hypocholesterolemic activities of pamaqueside and tiqueside, two structurally similar saponins, were evaluated in cholesterol-fed rabbits. The pharmacological profiles of the saponins were virtually identical: both dose-dependently decreased the intestinal absorption of labeled cholesterol 25-75%, increased fecal neutral sterol excretion up to 2.5-fold, and decreased hepatic cholesterol content 10-55%. High doses of pamaqueside (>5 mg/kg) or tiqueside (>125 mg/kg) completely prevented hypercholesterolemia. Decreases in plasma and hepatic cholesterol levels were strongly correlated with increased neutral sterol excretion. Ratios of neutral sterol excreted to pamaqueside administered were greater than 1:1 at all doses, in opposition to the formation of a stoichiometric complex previously suggested for tiqueside and other saponins. Ratios in tiqueside-treated rabbits were less than unity, a reflection of its lower potency. Pamaqueside-treated rabbits exhibited a more rapid decline in plasma cholesterol concentrations than control animals fed a cholesterol-free diet, indicating that the compound also inhibited the absorption of biliary cholesterol. Intravenous administration of pamaqueside had no effect on plasma cholesterol levels despite plasma levels twice those observed in rabbits given pamaqueside orally. These data indicate that pamaqueside and tiqueside induce hypocholesterolemia by blocking lumenal cholesterol absorption via a mechanism that apparently differs from the stoichiometric complexation of cholesterol hypothesized for other saponins. (+info)

There are several types of hypercholesterolemia, including:

1. Familial hypercholesterolemia: This is an inherited condition that causes high levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, in the blood.
2. Non-familial hypercholesterolemia: This type of hypercholesterolemia is not inherited and can be caused by a variety of factors, such as a high-fat diet, lack of exercise, obesity, and certain medical conditions, such as hypothyroidism or polycystic ovary syndrome (PCOS).
3. Mixed hypercholesterolemia: This type of hypercholesterolemia is characterized by high levels of both LDL and high-density lipoprotein (HDL) cholesterol in the blood.

The diagnosis of hypercholesterolemia is typically made based on a physical examination, medical history, and laboratory tests, such as a lipid profile, which measures the levels of different types of cholesterol and triglycerides in the blood. Treatment for hypercholesterolemia usually involves lifestyle changes, such as a healthy diet and regular exercise, and may also include medication, such as statins, to lower cholesterol levels.

There are several types of hyperlipidemia, including:

1. High cholesterol: This is the most common type of hyperlipidemia and is characterized by elevated levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol.
2. High triglycerides: This type of hyperlipidemia is characterized by elevated levels of triglycerides in the blood. Triglycerides are a type of fat found in the blood that is used for energy.
3. Low high-density lipoprotein (HDL) cholesterol: HDL cholesterol is known as "good" cholesterol because it helps remove excess cholesterol from the bloodstream and transport it to the liver for excretion. Low levels of HDL cholesterol can contribute to hyperlipidemia.

Symptoms of hyperlipidemia may include xanthomas (fatty deposits on the skin), corneal arcus (a cloudy ring around the iris of the eye), and tendon xanthomas (tender lumps under the skin). However, many people with hyperlipidemia have no symptoms at all.

Hyperlipidemia can be diagnosed through a series of blood tests that measure the levels of different types of cholesterol and triglycerides in the blood. Treatment for hyperlipidemia typically involves dietary changes, such as reducing intake of saturated fats and cholesterol, and increasing physical activity. Medications such as statins, fibric acid derivatives, and bile acid sequestrants may also be prescribed to lower cholesterol levels.

In severe cases of hyperlipidemia, atherosclerosis (hardening of the arteries) can occur, which can lead to cardiovascular disease, including heart attacks and strokes. Therefore, it is important to diagnose and treat hyperlipidemia early on to prevent these complications.

Arteriosclerosis can affect any artery in the body, but it is most commonly seen in the arteries of the heart, brain, and legs. It is a common condition that affects millions of people worldwide and is often associated with aging and other factors such as high blood pressure, high cholesterol, diabetes, and smoking.

There are several types of arteriosclerosis, including:

1. Atherosclerosis: This is the most common type of arteriosclerosis and occurs when plaque builds up inside the arteries.
2. Arteriolosclerosis: This type affects the small arteries in the body and can cause decreased blood flow to organs such as the kidneys and brain.
3. Medial sclerosis: This type affects the middle layer of the artery wall and can cause stiffness and narrowing of the arteries.
4. Intimal sclerosis: This type occurs when plaque builds up inside the innermost layer of the artery wall, causing it to become thick and less flexible.

Symptoms of arteriosclerosis can include chest pain, shortness of breath, leg pain or cramping during exercise, and numbness or weakness in the limbs. Treatment for arteriosclerosis may include lifestyle changes such as a healthy diet and regular exercise, as well as medications to lower blood pressure and cholesterol levels. In severe cases, surgery may be necessary to open up or bypass blocked arteries.

The disease begins with endothelial dysfunction, which allows lipid accumulation in the artery wall. Macrophages take up oxidized lipids and become foam cells, which die and release their contents, including inflammatory cytokines, leading to further inflammation and recruitment of more immune cells.

The atherosclerotic plaque can rupture or ulcerate, leading to the formation of a thrombus that can occlude the blood vessel, causing ischemia or infarction of downstream tissues. This can lead to various cardiovascular diseases such as myocardial infarction (heart attack), stroke, and peripheral artery disease.

Atherosclerosis is a multifactorial disease that is influenced by genetic and environmental factors such as smoking, hypertension, diabetes, high cholesterol levels, and obesity. It is diagnosed by imaging techniques such as angiography, ultrasound, or computed tomography (CT) scans.

Treatment options for atherosclerosis include lifestyle modifications such as smoking cessation, dietary changes, and exercise, as well as medications such as statins, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors. In severe cases, surgical interventions such as bypass surgery or angioplasty may be necessary.

In conclusion, atherosclerosis is a complex and multifactorial disease that affects the arteries and can lead to various cardiovascular diseases. Early detection and treatment can help prevent or slow down its progression, reducing the risk of complications and improving patient outcomes.

Cholelithiasis is a common condition that affects millions of people worldwide. It can occur at any age but is more common in adults over 40 years old. Women are more likely to develop cholelithiasis than men, especially during pregnancy or after childbirth.

The symptoms of cholelithiasis can vary depending on the size and location of the gallstones. Some people may not experience any symptoms at all, while others may have:

* Abdominal pain, especially in the upper right side of the abdomen
* Nausea and vomiting
* Fever
* Shaking or chills
* Loss of appetite
* Yellowing of the skin and eyes (jaundice)

If left untreated, cholelithiasis can lead to complications such as inflammation of the gallbladder (cholangitis), infection of the bile ducts (biliary sepsis), or blockage of the common bile duct. These complications can be life-threatening and require immediate medical attention.

The diagnosis of cholelithiasis is usually made through a combination of imaging tests such as ultrasound, CT scan, or MRI, and blood tests to check for signs of inflammation and liver function. Treatment options for cholelithiasis include:

* Watchful waiting: If the gallstones are small and not causing any symptoms, doctors may recommend monitoring the condition without immediate treatment.
* Medications: Oral medications such as bile salts or ursodiol can dissolve small gallstones and relieve symptoms.
* Laparoscopic cholecystectomy: A minimally invasive surgical procedure to remove the gallbladder through small incisions.
* Open cholecystectomy: An open surgery to remove the gallbladder, usually performed when the gallstones are large or there are other complications.

It is important to seek medical attention if you experience any symptoms of cholelithiasis, as early diagnosis and treatment can help prevent complications and improve outcomes.

People with Tangier disease often have extremely high levels of low-density lipoprotein (LDL) cholesterol, which can lead to the development of cardiovascular disease at an early age. The disorder is caused by mutations in the gene that codes for a protein called ATP-binding cassette transporter 1 (ABC1), which plays a critical role in the transport of cholesterol and other lipids in the body.

The symptoms of Tangier disease can vary depending on the severity of the disorder, but may include:

* High levels of LDL cholesterol
* Low levels of HDL cholesterol
* Abnormal liver function tests
* Yellowing of the skin and eyes (jaundice)
* Fatigue
* Weakness
* Muscle cramps
* Heart disease
* Stroke

Tangier disease is usually diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment for the disorder typically involves a combination of dietary modifications, medications, and lipid-lowering therapy to reduce the levels of LDL cholesterol and increase the levels of HDL cholesterol. In some cases, a liver transplant may be necessary to treat the liver damage that can occur as a result of the disorder.

There are several types of dyslipidemias, including:

1. Hyperlipidemia: Elevated levels of lipids and lipoproteins in the blood, which can increase the risk of CVD.
2. Hypolipidemia: Low levels of lipids and lipoproteins in the blood, which can also increase the risk of CVD.
3. Mixed dyslipidemia: A combination of hyperlipidemia and hypolipidemia.
4. Familial dyslipidemia: An inherited condition that affects the levels of lipids and lipoproteins in the blood.
5. Acquired dyslipidemia: A condition caused by other factors, such as poor diet or medication side effects.

Dyslipidemias can be diagnosed through a variety of tests, including fasting blood sugar (FBS), lipid profile, and apolipoprotein testing. Treatment for dyslipidemias often involves lifestyle changes, such as dietary modifications and increased physical activity, as well as medications to lower cholesterol and triglycerides.

In conclusion, dyslipidemias are abnormalities in the levels or composition of lipids and lipoproteins in the blood that can increase the risk of CVD. They can be caused by a variety of factors and diagnosed through several tests. Treatment often involves lifestyle changes and medications to lower cholesterol and triglycerides.

Coronary disease is often caused by a combination of genetic and lifestyle factors, such as high blood pressure, high cholesterol levels, smoking, obesity, and a lack of physical activity. It can also be triggered by other medical conditions, such as diabetes and kidney disease.

The symptoms of coronary disease can vary depending on the severity of the condition, but may include:

* Chest pain or discomfort (angina)
* Shortness of breath
* Fatigue
* Swelling of the legs and feet
* Pain in the arms and back

Coronary disease is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electrocardiograms (ECGs), stress tests, and cardiac imaging. Treatment for coronary disease may include lifestyle changes, medications to control symptoms, and surgical procedures such as angioplasty or bypass surgery to improve blood flow to the heart.

Preventative measures for coronary disease include:

* Maintaining a healthy diet and exercise routine
* Quitting smoking and limiting alcohol consumption
* Managing high blood pressure, high cholesterol levels, and other underlying medical conditions
* Reducing stress through relaxation techniques or therapy.

There are three main types of Niemann-Pick diseases:

1. Type A: This is the most common and severe form of the disease, and it typically affects infants before the age of one. It is characterized by progressive loss of motor skills, seizures, and death before the age of two.
2. Type B: This form of the disease usually presents in adulthood and is characterized by gradually worsening neurological symptoms, including muscle weakness, ataxia (loss of coordination), and dementia. Life expectancy for individuals with type B Niemann-Pick disease is typically between 20 and 40 years.
3. Type C: This form of the disease is less severe than types A and B and is often diagnosed in childhood or adolescence. It is characterized by a range of symptoms, including developmental delays, learning disabilities, and mild neurological problems.

Niemann-Pick diseases are caused by mutations in the genes that code for proteins involved in lipid metabolism. These proteins play a crucial role in the transport of lipids within cells, particularly in the brain and other organs. Without these proteins, lipids accumulate in cells and cause damage to their membranes and organelles.

There is currently no cure for Niemann-Pick diseases, but researchers are working on developing new treatments that may help alleviate some of the symptoms and slow the progression of the disease. These treatments include enzyme replacement therapy, gene therapy, and small molecule therapies. In addition, clinical trials are underway to evaluate the safety and effectiveness of these new treatments in humans.

In summary, Niemann-Pick diseases are a group of rare and severe genetic disorders that affect the transport of lipids within cells. There is currently no cure for these diseases, but researchers are working on developing new treatments that may help alleviate some of the symptoms and slow the progression of the disease.

Answer: Type A, B, and C Niemann-Pick disease are three forms of a group of rare genetic disorders that affect lipid metabolism, with types A and B being more severe and type C being less severe.

1. Coronary artery disease: The narrowing or blockage of the coronary arteries, which supply blood to the heart.
2. Heart failure: A condition in which the heart is unable to pump enough blood to meet the body's needs.
3. Arrhythmias: Abnormal heart rhythms that can be too fast, too slow, or irregular.
4. Heart valve disease: Problems with the heart valves that control blood flow through the heart.
5. Heart muscle disease (cardiomyopathy): Disease of the heart muscle that can lead to heart failure.
6. Congenital heart disease: Defects in the heart's structure and function that are present at birth.
7. Peripheral artery disease: The narrowing or blockage of blood vessels that supply oxygen and nutrients to the arms, legs, and other organs.
8. Deep vein thrombosis (DVT): A blood clot that forms in a deep vein, usually in the leg.
9. Pulmonary embolism: A blockage in one of the arteries in the lungs, which can be caused by a blood clot or other debris.
10. Stroke: A condition in which there is a lack of oxygen to the brain due to a blockage or rupture of blood vessels.

The condition is caused by mutations in the genes that code for proteins involved in cholesterol transport and metabolism, such as the low-density lipoprotein receptor gene (LDLR) or the PCSK9 gene. These mutations lead to a decrease in the ability of the liver to remove excess cholesterol from the bloodstream, resulting in high levels of LDL cholesterol and low levels of HDL cholesterol.

Hyperlipoproteinemia type II is usually inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases can be caused by spontaneous mutations or incomplete penetrance, where not all individuals with the mutated gene develop the condition.

Symptoms of hyperlipoproteinemia type II can include xanthomas (yellowish deposits of cholesterol in the skin), corneal arcus (a white, waxy deposit on the iris of the eye), and tendon xanthomas (small, soft deposits of cholesterol under the skin). Treatment typically involves a combination of dietary changes and medication to lower LDL cholesterol levels and increase HDL cholesterol levels. In severe cases, liver transplantation may be necessary.

Hyperlipoproteinemia type II is a serious condition that can lead to cardiovascular disease, including heart attacks, strokes, and peripheral artery disease. Early diagnosis and treatment are important to prevent or delay the progression of the disease and reduce the risk of complications.

The primary symptom of LCAT deficiency is a high level of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, in the blood. This can lead to the development of cholesterol deposits in the skin, eyes, and other tissues, which can cause a range of health problems including xanthomas (yellowish patches on the skin), corneal arcus (a cloudy ring around the cornea of the eye), and xanthelasma (yellowish patches on the eyelids).

Treatment for LCAT deficiency typically involves a combination of dietary changes, such as reducing intake of saturated fats and cholesterol, and medication to lower cholesterol levels. In some cases, liver transplantation may be necessary.

Prevention of LCAT deficiency is not possible, as it is a genetic disorder that is inherited in an autosomal recessive pattern. This means that a child must inherit two copies of the mutated LCAT gene, one from each parent, to develop the condition. However, early detection and treatment can help manage the symptoms and prevent complications.

The diagnosis of LCAT deficiency is based on a combination of clinical features, laboratory tests, and genetic analysis. Laboratory tests may include measurements of lipid levels in the blood, as well as assays for LCAT enzyme activity. Genetic testing can identify the presence of mutations in the LCAT gene that cause the condition.

Overall, LCAT deficiency is a rare and potentially serious genetic disorder that affects the body's ability to metabolize cholesterol and other fats. Early diagnosis and treatment can help manage the symptoms and prevent complications, but there is currently no cure for the condition.

Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.

There are several ways to measure body weight, including:

1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.

It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.

There are several causes of hypertriglyceridemia, including:

* Genetics: Some people may inherit a tendency to have high triglyceride levels due to genetic mutations that affect the genes involved in triglyceride metabolism.
* Obesity: Excess body weight is associated with higher triglyceride levels, as there is more fat available for energy.
* Diabetes: Both type 1 and type 2 diabetes can lead to high triglyceride levels due to insulin resistance and altered glucose metabolism.
* High-carbohydrate diet: Consuming high amounts of carbohydrates, particularly refined or simple carbohydrates, can cause a spike in blood triglycerides.
* Alcohol consumption: Drinking too much alcohol can increase triglyceride levels in the blood.
* Certain medications: Some drugs, such as anabolic steroids and some antidepressants, can raise triglyceride levels.
* Underlying medical conditions: Certain medical conditions, such as hypothyroidism, kidney disease, and polycystic ovary syndrome (PCOS), can also contribute to high triglyceride levels.

Hypertriglyceridemia is typically diagnosed with a blood test that measures the level of triglycerides in the blood. Treatment options for hypertriglyceridemia depend on the underlying cause of the condition, but may include lifestyle modifications such as weight loss, dietary changes, and medications to lower triglyceride levels.

The most common form of hypolipoproteinemia is familial hypobetalipoproteinemia (FHBL), which is caused by mutations in the gene encoding apoB, a protein component of low-density lipoproteins (LDL). People with FHBL have extremely low levels of LDL cholesterol and often develop symptoms such as fatty liver disease, liver cirrhosis, and cardiovascular disease.

Another form of hypolipoproteinemia is familial hypoalphalipoproteinemia (FHAL), which is caused by mutations in the gene encoding apoA-I, a protein component of high-density lipoproteins (HDL). People with FHAL have low levels of HDL cholesterol and often develop symptoms such as cardiovascular disease and premature coronary artery disease.

Hypolipoproteinemia can be diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment for the disorder typically involves managing associated symptoms and reducing lipid levels through diet, exercise, and medication. In some cases, liver transplantation may be necessary.

Prevention of hypolipoproteinemia is challenging, as it is often inherited in an autosomal recessive pattern, meaning that both parents must be carriers of the mutated gene to pass it on to their children. However, genetic counseling and testing can help identify carriers and allow for informed family planning.

Overall, hypolipoproteinemia is a rare and complex group of disorders that affect lipid metabolism and transport. While treatment and management options are available, prevention and early diagnosis are key to reducing the risk of complications associated with these disorders.

The symptoms of SLOS can vary in severity and may include:

1. Developmental delays and intellectual disability
2. Distinctive facial features, such as a prominent forehead, narrow eyes, and a short nose
3. Skeletal abnormalities, including short stature, joint deformities, and scoliosis
4. Heart defects, such as atrial septal defects or ventricular septal defects
5. Kidney problems, such as kidney stones or chronic kidney disease
6. Vision problems, such as cataracts or glaucoma
7. Hearing loss or deafness
8. Increased risk of infections
9. Poor muscle tone and coordination
10. Delayed motor milestones

SLOS is usually diagnosed by a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment is focused on managing the symptoms and preventing complications. This may include medications to control seizures, physical therapy to improve muscle tone and coordination, and speech and language therapy to address communication difficulties.

The prognosis for individuals with SLOS varies depending on the severity of the mutation and the presence of other health problems. Some individuals with mild forms of the disorder may have a relatively normal life expectancy, while others with more severe forms may have a shorter life span. Early diagnosis and intervention are critical to improving outcomes for individuals with SLOS.

There are several types of hyperlipoproteinemias, each with distinct clinical features and laboratory findings. The most common forms include:

1. Familial hypercholesterolemia (FH): This is the most common type of hyperlipoproteinemia, caused by mutations in the LDLR gene that codes for the low-density lipoprotein receptor. FH is characterized by extremely high levels of low-density lipoprotein (LDL) cholesterol in the blood, which can lead to premature cardiovascular disease, including heart attacks and strokes.
2. Familial hypobetalipoproteinemia (FHBL): This rare disorder is caused by mutations in the APOB100 gene that codes for a protein involved in lipid metabolism. FHBL is characterized by very low levels of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol, as well as a deficiency of Apolipoprotein B-100, a protein that helps transport lipids in the blood.
3. Hypertriglyceridemia: This condition is caused by mutations in genes that regulate triglyceride metabolism, leading to extremely high levels of triglycerides in the blood. Hypertriglyceridemia can increase the risk of pancreatitis and other health problems.
4. Lipoprotein lipase deficiency: This rare disorder is caused by mutations in the LPL gene that codes for the enzyme lipoprotein lipase, which helps break down triglycerides in the blood. Lipoprotein lipase deficiency can lead to very high levels of triglycerides and cholesterol in the blood, increasing the risk of pancreatitis and other health problems.
5. Familial dyslipidemia: This is a group of rare inherited disorders that affect lipid metabolism and can cause extremely high or low levels of various types of cholesterol and triglycerides in the blood. Some forms of familial dyslipidemia are caused by mutations in genes that code for enzymes involved in lipid metabolism, while others may be caused by unknown factors.
6. Chylomicronemia: This rare disorder is characterized by extremely high levels of chylomicrons (type of triglyceride-rich lipoprotein) in the blood, which can increase the risk of pancreatitis and other health problems. The exact cause of chylomicronemia is not fully understood, but it may be related to genetic mutations or other factors that affect lipid metabolism.
7. Hyperchylomicronemia: This rare disorder is similar to chylomicronemia, but it is characterized by extremely high levels of chylomicrons in the blood, as well as very low levels of HDL (good) cholesterol. Hyperchylomicronemia can increase the risk of pancreatitis and other health problems.
8. Hypoalphalipoproteinemia: This rare disorder is characterized by extremely low levels of apolipoprotein A-I (ApoA-I), a protein that plays a key role in lipid metabolism and helps to regulate the levels of various types of cholesterol and triglycerides in the blood. Hypoalphalipoproteinemia can increase the risk of pancreatitis and other health problems.
9. Hypobetalipoproteinemia: This rare disorder is characterized by extremely low levels of apolipoprotein B (ApoB), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. Hypobetalipoproteinemia can increase the risk of pancreatitis and other health problems.
10. Sitosterolemia: This rare genetic disorder is caused by mutations in the gene that codes for sterol-CoA-desmethylase (SCD), an enzyme involved in the metabolism of plant sterols. Sitosterolemia can cause elevated levels of plant sterols and sitosterol in the blood, which can increase the risk of pancreatitis and other health problems.
11. Familial hyperchylomicronemia type 1 (FHMC1): This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. FHMC1 can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
12. Familial hyperchylomicronemia type 2 (FHMC2): This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein A-IV (APOA4), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. FHMC2 can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
13. Lipoprotein (a) deficiency: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein (a), a protein that helps to regulate the levels of lipoproteins in the blood. Lipoprotein (a) deficiency can cause low levels of lipoprotein (a) and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
14. Chylomicron retention disease: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of chylomicrons in the blood. Chylomicron retention disease can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
15. Hypertriglyceridemia-apolipoprotein C-II deficiency: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of triglycerides in the blood. Hypertriglyceridemia-apolipoprotein C-II deficiency can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
16. Familial partial lipodystrophy (FPLD): This rare genetic disorder is characterized by the loss of fat tissue in certain areas of the body, such as the arms, legs, and buttocks. FPLD can cause elevated levels of lipids in the blood, which can increase the risk of pancreatitis and other health problems.
17. Lipodystrophy: This rare genetic disorder is characterized by the loss of fat tissue in certain areas of the body, such as the face, arms, and legs. Lipodystrophy can cause elevated levels of lipids in the blood, which can increase the risk of pancreatitis and other health problems.
18. Abetalipoproteinemia: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein B, a protein that helps to regulate the levels of lipids in the blood. Abetalipoproteinemia can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
19. Chylomicronemia: This rare genetic disorder is characterized by the presence of excessively large amounts of chylomicrons (type of lipid particles) in the blood. Chylomicronemia can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
20. Hyperlipidemia due to medications: Certain medications, such as corticosteroids and some anticonvulsants, can cause elevated levels of lipids in the blood.

It's important to note that many of these disorders are rare and may not be common causes of high triglycerides. Additionally, there may be other causes of high triglycerides that are not listed here. It's important to talk to a healthcare provider for proper evaluation and diagnosis if you have concerns about your triglyceride levels.

The most common form of xanthomatosis is called familial hypercholesterolemia, which is caused by a deficiency of low-density lipoprotein (LDL) receptors in the body. This results in high levels of LDL cholesterol in the blood, which can lead to the accumulation of cholesterol and other lipids in the skin, eyes, and other tissues.

Other forms of xanthomatosis include:

* Familial apo A-1 deficiency: This is a rare disorder caused by a deficiency of apolipoprotein A-1 (apoA-1), a protein that plays a critical role in the transportation of triglycerides and cholesterol in the blood.
* familial hyperlipidemia: This is a group of rare genetic disorders that are characterized by high levels of lipids in the blood, including cholesterol and triglycerides.
* Chylomicronemia: This is a rare disorder caused by a deficiency of lipoprotein lipase, an enzyme that breaks down triglycerides in the blood.

The symptoms of xanthomatosis vary depending on the specific form of the condition and the organs affected. They may include:

* Yellowish deposits (xanthomas) on the skin, particularly on the elbows, knees, and buttocks
* Deposits in the eyes (corneal arcus)
* Fatty liver disease
* High levels of cholesterol and triglycerides in the blood
* Abdominal pain
* Weight loss

Treatment for xanthomatosis typically involves managing the underlying genetic disorder, which may involve dietary changes, medication, or other therapies. In some cases, surgery may be necessary to remove affected tissue.

In summary, xanthomatosis is a group of rare genetic disorders that are characterized by deposits of lipids in the skin and other organs. The symptoms and treatment vary depending on the specific form of the condition.

1. Abdominal obesity (excess fat around the waistline)
2. High blood pressure (hypertension)
3. Elevated fasting glucose (high blood sugar)
4. High serum triglycerides (elevated levels of triglycerides in the blood)
5. Low HDL cholesterol (low levels of "good" cholesterol)

Having three or more of these conditions is considered a diagnosis of metabolic syndrome X. It is estimated that approximately 34% of adults in the United States have this syndrome, and it is more common in women than men. Risk factors for developing metabolic syndrome include obesity, lack of physical activity, poor diet, and a family history of type 2 diabetes or CVD.

The term "metabolic syndrome" was first introduced in the medical literature in the late 1980s, and since then, it has been the subject of extensive research. The exact causes of metabolic syndrome are not yet fully understood, but it is believed to be related to insulin resistance, inflammation, and changes in body fat distribution.

Treatment for metabolic syndrome typically involves lifestyle modifications such as weight loss, regular physical activity, and a healthy diet. Medications such as blood pressure-lowering drugs, cholesterol-lowering drugs, and anti-diabetic medications may also be prescribed if necessary. It is important to note that not everyone with metabolic syndrome will develop type 2 diabetes or CVD, but the risk is increased. Therefore, early detection and treatment are crucial in preventing these complications.

There are several different types of obesity, including:

1. Central obesity: This type of obesity is characterized by excess fat around the waistline, which can increase the risk of health problems such as type 2 diabetes and cardiovascular disease.
2. Peripheral obesity: This type of obesity is characterized by excess fat in the hips, thighs, and arms.
3. Visceral obesity: This type of obesity is characterized by excess fat around the internal organs in the abdominal cavity.
4. Mixed obesity: This type of obesity is characterized by both central and peripheral obesity.

Obesity can be caused by a variety of factors, including genetics, lack of physical activity, poor diet, sleep deprivation, and certain medications. Treatment for obesity typically involves a combination of lifestyle changes, such as increased physical activity and a healthy diet, and in some cases, medication or surgery may be necessary to achieve weight loss.

Preventing obesity is important for overall health and well-being, and can be achieved through a variety of strategies, including:

1. Eating a healthy, balanced diet that is low in added sugars, saturated fats, and refined carbohydrates.
2. Engaging in regular physical activity, such as walking, jogging, or swimming.
3. Getting enough sleep each night.
4. Managing stress levels through relaxation techniques, such as meditation or deep breathing.
5. Avoiding excessive alcohol consumption and quitting smoking.
6. Monitoring weight and body mass index (BMI) on a regular basis to identify any changes or potential health risks.
7. Seeking professional help from a healthcare provider or registered dietitian for personalized guidance on weight management and healthy lifestyle choices.

Type 2 diabetes can be managed through a combination of diet, exercise, and medication. In some cases, lifestyle changes may be enough to control blood sugar levels, while in other cases, medication or insulin therapy may be necessary. Regular monitoring of blood sugar levels and follow-up with a healthcare provider are important for managing the condition and preventing complications.

Common symptoms of type 2 diabetes include:

* Increased thirst and urination
* Fatigue
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet
* Recurring skin, gum, or bladder infections

If left untreated, type 2 diabetes can lead to a range of complications, including:

* Heart disease and stroke
* Kidney damage and failure
* Nerve damage and pain
* Eye damage and blindness
* Foot damage and amputation

The exact cause of type 2 diabetes is not known, but it is believed to be linked to a combination of genetic and lifestyle factors, such as:

* Obesity and excess body weight
* Lack of physical activity
* Poor diet and nutrition
* Age and family history
* Certain ethnicities (e.g., African American, Hispanic/Latino, Native American)
* History of gestational diabetes or delivering a baby over 9 lbs.

There is no cure for type 2 diabetes, but it can be managed and controlled through a combination of lifestyle changes and medication. With proper treatment and self-care, people with type 2 diabetes can lead long, healthy lives.

Symptoms of NPC typically appear in infancy or childhood and can include:

* Delayed development and intellectual disability
* Seizures
* Loss of motor skills
* Vision loss and blindness
* Hearing loss and deafness
* Increased risk of infections
* Enlargement of the liver and spleen

There is currently no cure for NPC, but various treatments can help manage the symptoms. These may include:

* Medications to control seizures and muscle stiffness
* Physical therapy to maintain muscle strength and mobility
* Occupational therapy to improve daily functioning
* Speech therapy to address communication difficulties
* Liver transplantation in some cases

NPC is usually diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. It can be challenging to diagnose NPC because the symptoms are similar to those of other disorders, and the genetic mutations responsible for the disease can be difficult to identify.

There is ongoing research into the causes and treatment of NPC, including gene therapy and small molecule therapies. However, more work needs to be done to understand the underlying mechanisms of the disease and to develop effective treatments.

The buildup of plaque in the coronary arteries is often caused by high levels of low-density lipoprotein (LDL) cholesterol, smoking, high blood pressure, diabetes, and a family history of heart disease. The plaque can also rupture, causing a blood clot to form, which can completely block the flow of blood to the heart muscle, leading to a heart attack.

CAD is the most common type of heart disease and is often asymptomatic until a serious event occurs. Risk factors for CAD include:

* Age (men over 45 and women over 55)
* Gender (men are at greater risk than women, but women are more likely to die from CAD)
* Family history of heart disease
* High blood pressure
* High cholesterol
* Diabetes
* Smoking
* Obesity
* Lack of exercise

Diagnosis of CAD typically involves a physical exam, medical history, and results of diagnostic tests such as:

* Electrocardiogram (ECG or EKG)
* Stress test
* Echocardiogram
* Coronary angiography

Treatment for CAD may include lifestyle changes such as a healthy diet, regular exercise, stress management, and quitting smoking. Medications such as beta blockers, ACE inhibitors, and statins may also be prescribed to manage symptoms and slow the progression of the disease. In severe cases, surgical intervention such as coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) may be necessary.

Prevention of CAD includes managing risk factors such as high blood pressure, high cholesterol, and diabetes, quitting smoking, maintaining a healthy weight, and getting regular exercise. Early detection and treatment of CAD can help to reduce the risk of complications and improve quality of life for those affected by the disease.

There are several factors that can contribute to the development of insulin resistance, including:

1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.

There are several ways to diagnose insulin resistance, including:

1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.

There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:

1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.

Medications that may be used to treat insulin resistance include:

1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.

It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.

The condition is caused by mutations in genes that code for proteins involved in lipid metabolism, such as the low-density lipoprotein receptor gene (LDLR), apolipoprotein A-1 gene (APOA1), and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. These mutations can lead to the overproduction or underexpression of certain lipids, leading to the characteristic lipid abnormalities seen in HeFH.

HeFH is usually inherited in an autosomal dominant manner, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases may be caused by recessive inheritance or de novo mutations. The condition can affect both children and adults, and it is important for individuals with HeFH to be monitored closely by a healthcare provider to manage their lipid levels and reduce the risk of cardiovascular disease.

Treatment for HeFH typically involves a combination of dietary modifications, such as reducing saturated fat intake and increasing fiber and omega-3 fatty acid intake, and medications, such as statins, to lower cholesterol levels. In some cases, apheresis or liver transplantation may be necessary to reduce lipid levels. Early detection and management of HeFH can help prevent or delay the development of cardiovascular disease, which is the leading cause of death worldwide.

The most common types of biliary fistulas are:

1. Bile duct-enteric fistula: This type of fistula connects the bile ducts to the small intestine.
2. Bile duct-skin fistula: This type of fistula connects the bile ducts to the skin, which can lead to a bile leak and infection.
3. Bile duct-liver fistula: This type of fistula connects the bile ducts to the liver, which can cause bleeding and infection.

Symptoms of biliary fistula may include:

* Jaundice (yellowing of the skin and whites of the eyes)
* Pale or clay-colored stools
* Dark urine
* Fatigue
* Loss of appetite
* Weight loss

Diagnosis of biliary fistula is typically made through a combination of imaging tests such as endoscopy, CT scan, and MRI. Treatment options for biliary fistula include:

1. Endoscopic therapy: This may involve the use of an endoscope to repair or close off the fistula.
2. Surgery: In some cases, surgery may be necessary to repair or remove the damaged bile ducts.
3. Stent placement: A stent may be placed in the bile ducts to help keep them open and allow for proper drainage.

It is important to seek medical attention if you experience any symptoms of biliary fistula, as it can lead to serious complications such as infection or bleeding.

The main clinical features of hypoalphalipoproteinemias include:

1. Low levels of HDL-C (high-density lipoprotein cholesterol) and/or LDL-C (low-density lipoprotein cholesterol) in the blood, leading to a increased risk of cardiovascular disease.
2. Elevated levels of triglycerides in the blood.
3. Elevated levels of very low-density lipoproteins (VLDL) and intermediate-density lipoproteins (IDL) in the blood.
4. Decreased levels of apolipoprotein A-I and/or apolipoprotein E in the blood.
5. Abnormal fatty acid metabolism.
6. Increased risk of pancreatitis.
7. Increased risk of hemorrhagic stroke.
8. Cognitive impairment.
9. Neurological manifestations such as ataxia, seizures, and peripheral neuropathy.
10. Eye disorders such as retinal degeneration and cataracts.

The diagnosis of hypoalphalipoproteinemia is based on a combination of clinical features, laboratory tests, and genetic analysis. Treatment for these disorders is primarily focused on managing the symptoms and preventing complications, such as cardiovascular disease and pancreatitis. This may include dietary modifications, medications to lower triglycerides and raise HDL-C, and in some cases, liver transplantation.

Hypoalphalipoproteinemias are rare genetic disorders that affect the metabolism of lipids and can lead to a range of clinical manifestations including cardiovascular disease, pancreatitis, and cognitive impairment. Early diagnosis and management are critical to preventing complications and improving outcomes for individuals with these disorders.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

Gallstones can be made of cholesterol, bilirubin, or other substances found in bile. They can cause a variety of symptoms, including:

* Abdominal pain (often in the upper right abdomen)
* Nausea and vomiting
* Fever
* Yellowing of the skin and eyes (jaundice)
* Tea-colored urine
* Pale or clay-colored stools

Gallstones can be classified into several types based on their composition, size, and location. The most common types are:

* Cholesterol gallstones: These are the most common type of gallstone and are usually yellow or green in color. They are made of cholesterol and other substances found in bile.
* Pigment gallstones: These stones are made of bilirubin, a yellow pigment found in bile. They are often smaller than cholesterol gallstones and may be more difficult to detect.
* Mixed gallstones: These stones are a combination of cholesterol and pigment gallstones.

Gallstones can cause a variety of complications, including:

* Gallbladder inflammation (cholecystitis)
* Infection of the bile ducts (choledochalitis)
* Pancreatitis (inflammation of the pancreas)
* Blockage of the common bile duct, which can cause jaundice and infection.

Treatment for gallstones usually involves surgery to remove the gallbladder, although in some cases, medications may be used to dissolve small stones. In severe cases, emergency surgery may be necessary to treat complications such as inflammation or infection.

There are two types of hypertension:

1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.

Some common causes of secondary hypertension include:

* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use

There are also several risk factors for hypertension, including:

* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress

Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:

* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease

Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.

There are several types of diabetes mellitus, including:

1. Type 1 DM: This is an autoimmune condition in which the body's immune system attacks and destroys the cells in the pancreas that produce insulin, resulting in a complete deficiency of insulin production. It typically develops in childhood or adolescence, and patients with this condition require lifelong insulin therapy.
2. Type 2 DM: This is the most common form of diabetes, accounting for around 90% of all cases. It is caused by a combination of insulin resistance (where the body's cells do not respond properly to insulin) and impaired insulin secretion. It is often associated with obesity, physical inactivity, and a diet high in sugar and unhealthy fats.
3. Gestational DM: This type of diabetes develops during pregnancy, usually in the second or third trimester. Hormonal changes and insulin resistance can cause blood sugar levels to rise, putting both the mother and baby at risk.
4. LADA (Latent Autoimmune Diabetes in Adults): This is a form of type 1 DM that develops in adults, typically after the age of 30. It shares features with both type 1 and type 2 DM.
5. MODY (Maturity-Onset Diabetes of the Young): This is a rare form of diabetes caused by genetic mutations that affect insulin production. It typically develops in young adulthood and can be managed with lifestyle changes and/or medication.

The symptoms of diabetes mellitus can vary depending on the severity of the condition, but may include:

1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Cuts or bruises that are slow to heal
5. Tingling or numbness in hands and feet
6. Recurring skin, gum, or bladder infections
7. Flu-like symptoms such as weakness, dizziness, and stomach pain
8. Dark, velvety skin patches (acanthosis nigricans)
9. Yellowish color of the skin and eyes (jaundice)
10. Delayed healing of cuts and wounds

If left untreated, diabetes mellitus can lead to a range of complications, including:

1. Heart disease and stroke
2. Kidney damage and failure
3. Nerve damage (neuropathy)
4. Eye damage (retinopathy)
5. Foot damage (neuropathic ulcers)
6. Cognitive impairment and dementia
7. Increased risk of infections and other diseases, such as pneumonia, gum disease, and urinary tract infections.

It is important to note that not all individuals with diabetes will experience these complications, and that proper management of the condition can greatly reduce the risk of developing these complications.

The condition is caused by mutations in genes that code for enzymes involved in lipid metabolism, such as ACY1 and APOB100. These mutations lead to a deficiency in the breakdown and transport of lipids in the body, resulting in the accumulation of chylomicrons and other lipoproteins in the blood.

Symptoms of hyperlipoproteinemia Type IV can include abdominal pain, fatigue, and joint pain, as well as an increased risk of pancreatitis and cardiovascular disease. Treatment typically involves a combination of dietary modifications, such as reducing intake of saturated fats and cholesterol, and medications to lower lipid levels. In severe cases, liver transplantation may be necessary.

Hyperlipoproteinemia Type IV is a rare disorder, and the prevalence is not well-defined. However, it is estimated to affect approximately 1 in 100,000 individuals worldwide. The condition can be diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis.

In summary, hyperlipoproteinemia Type IV is a rare genetic disorder that affects the metabolism of lipids and lipoproteins in the body, leading to elevated levels of chylomicrons and other lipoproteins in the blood, as well as low levels of HDL. The condition can cause a range of symptoms and is typically treated with dietary modifications and medications.

There are several types of inborn errors of lipid metabolism, each with its own unique set of symptoms and characteristics. Some of the most common include:

* Familial hypercholesterolemia: A condition that causes high levels of low-density lipoprotein (LDL) cholesterol in the blood, which can lead to heart disease and other health problems.
* Fabry disease: A rare genetic disorder that affects the body's ability to break down certain fats, leading to a buildup of toxic substances in the body.
* Gaucher disease: Another rare genetic disorder that affects the body's ability to break down certain lipids, leading to a buildup of toxic substances in the body.
* Lipoid cerebral degeneration: A condition that causes fatty deposits to accumulate in the brain, leading to cognitive decline and other neurological problems.
* Tangier disease: A rare genetic disorder that affects the body's ability to break down certain lipids, leading to a buildup of toxic substances in the body.

Inborn errors of lipid metabolism can be diagnosed through a variety of tests, including blood tests and genetic analysis. Treatment options vary depending on the specific disorder and its severity, but may include dietary changes, medication, and other therapies. With proper treatment and management, many individuals with inborn errors of lipid metabolism can lead active and fulfilling lives.

Various cholesterol medications may be useful if LDL cholesterol, triglycerides, and/or HDL cholesterol is abnormal.[citation ... Other signs of metabolic syndrome include high blood pressure, decreased fasting serum HDL cholesterol, elevated fasting serum ... reduced HDL cholesterol; and a trend toward increased triglycerides, blood pressure, and glucose in the genetically susceptible ... or specific treatment for this lipid abnormality Reduced HDL cholesterol: < 40 mg/dL (1.03 mmol/L) in males, < 50 mg/dL (1.29 ...

https://en.wikipedia.org/wiki/Metabolic_syndrome

hdl:21.11116/0000-0000-2F49-B. PMID 29301957. v t e (All articles with dead external links, Articles with dead external links ... Cholesterol phase transition from liquid to crystalline form is linked to inflammation. Cholesterol crystals are believed to ... A cholesterol crystal is a solid, crystalline form of cholesterol found in gallstones and atherosclerosis. Gallstones occurring ... Cholesterol crystals are a hallmark of atherosclerosis, which is believed to be an early cause of atherosclerotic inflammation ...

https://en.wikipedia.org/wiki/Cholesterol_crystal

Decrease non-HDL cholesterol. Statin treatment reduces cardiovascular mortality by about 31%. Stopping smoking and avoidance of ... Niacin, fibrates and CETP Inhibitors, while they may increase HDL cholesterol do not affect the risk of cardiovascular disease ... metabolism toward a more atherogenic form by decreasing the HDL cholesterol level while increasing LDL and total cholesterol ... One of them relates to serum cholesterol level. In most populations, the serum total cholesterol level increases as age ...

https://en.wikipedia.org/wiki/Cardiovascular_disease

... and high-density lipoprotein cholesterol (HDL-C, in mg/dL) along with body-mass index (BMI). The index can be estimated using ... "The Triglyceride-to-HDL Cholesterol Ratio". Diabetes Care. 34 (8): 1869-1874. doi:10.2337/dc10-2234. ISSN 0149-5992. PMC ... Calculator to estimate METS-IR, the TyG index and TG/HDL-C ratio (CS1 location test, All articles with unsourced statements, ... suggested that the TyG and TG/HDL-C indexes had superior performance in their population owing to ethnic-specific variations in ...

https://en.wikipedia.org/wiki/Metabolic_Score_for_Insulin_Resistance

Drugs in this class substantially increase HDL cholesterol, lower LDL cholesterol, and enhance reverse cholesterol transport. ... CETP inhibitors inhibit cholesterylester transfer protein (CETP), which normally transfers cholesterol from HDL cholesterol to ... "CETP inhibitors to increase HDL cholesterol levels". N. Engl. J. Med. 356 (13): 1364-6. doi:10.1056/NEJMe078029. PMID 17387130 ... Barkowski RS, Frishman WH (May 2018). "HDL metabolism and CETP inhibition". Cardiol Rev. 16 (3): 154-62. doi:10.1097/CRD. ...

https://en.wikipedia.org/wiki/CETP_inhibitor

The drug was aimed at raising the blood levels of HDL cholesterol. Prevailing observations indicate that high HDL levels ... hdl:2297/15762. PMID 12444911. S2CID 22400248. Simeon Bennett & Naomi Kresge. "Roche Drops After Halting Cholesterol Drug ... Plaque reduction is an anticipated observation following an increase in HDL.[citation needed] As of 2010[update] five phase II ... A 24-week clinical trial showed that dalcetrapib did increase HDL-C levels, supporting the agent's desired effect. Further, the ...

https://en.wikipedia.org/wiki/Dalcetrapib

hdl:1885/102663. PMID 26068693. S2CID 29808041. Retrieved 17 February 2016. "ABC Catalyst Gets It Right on Cholesterol". ... which questioned the link between cholesterol, cholesterol-reducing medication and ill-health. A large number of individuals ... cite web}}: ,author= has generic name (help) "Sections of the medical community question Catalyst program about cholesterol and ... "PM - Backlash against ABC's Catalyst program questioning heart disease-cholesterol links 31/10/2013". Abc.net.au. 4 May 2013. ...

https://en.wikipedia.org/wiki/Maryanne_Demasi

Vrielink, Alice; University of London (1989). The crystal structure determination of cholesterol oxidase. hdl:10044/1/47699. ... She received a PhD in 1989 from the University of London where she worked on the structure of cholesterol oxidase. She also has ... Vrielink, Alice; Lloyd, Lesley F; Blow, David M (5 June 1991). "Crystal structure of cholesterol oxidase from Brevibacterium ... Vrielink, Alice; Lloyd, Lesley F; Blow, David M (5 June 1991). "Crystal structure of cholesterol oxidase from Brevibacterium ...

https://en.wikipedia.org/wiki/Alice_Vrielink

... total cholesterol, b) HDL cholesterol, c) LDL cholesterol, and d) triglycerides. Results may be expressed as "calculated", ... Total cholesterol is defined as the sum of HDL, LDL, and VLDL. Usually, only the total, HDL, and triglycerides are measured. ... More current testing methods determine LDL ("bad") and HDL ("good") cholesterol separately, allowing cholesterol analysis to be ... cholesterol. HDL particles are thought to transport cholesterol back to the liver, either for excretion or for other tissues ...

https://en.wikipedia.org/wiki/Cholesterol

When the HDL molecule is cholesterol rich, its shape is changed into more spherical and it becomes less dense (HDL 2). This is ... Discoidal (Nascent) HDL: Initially, HDL is discoidal in shape because it lacks esterified cholesterol but as it keeps ... and the phospholipid component of HDL acts as a sink for the mobilised cholesterol. The cholesterol is converted to cholesteryl ... Cholesterol from non-hepatic peripheral tissues is transferred to HDL by the ABCA1 (ATP-binding cassette transporter). ...

https://en.wikipedia.org/wiki/Reverse_cholesterol_transport

Mani P, Rohatgi A (August 2015). "Niacin Therapy, HDL Cholesterol, and Cardiovascular Disease: Is the HDL Hypothesis Defunct ... and raise blood high density lipoprotein cholesterol (HDL-C, often referred to as "good" cholesterol). There are two forms: ... "Merck begins overseas recall of HDL cholesterol drug". Reuters. 11 January 2013. Aguilar F, Charrondiere UR, Dusemund B, ... Niacin reduces synthesis of low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), ...

https://en.wikipedia.org/wiki/Niacin

The study showed the value of HDL cholesterol. Medical College of Georgia established the Curtis G. Hames Chair in Family ...

https://en.wikipedia.org/wiki/Curtis_G._Hames

It reduces triglyceride levels and increases HDL cholesterol. It may have less marked adverse effects than niacin, although it ... which leads indirectly to a reduction in LDL and increase in HDL cholesterol. Acipimox is completely absorbed from the gut. It ... Consequently, VLDL cholesterol production in the liver is reduced, ...

https://en.wikipedia.org/wiki/Acipimox

hdl:2115/45489. ISSN 1347-6947. PMID 21071871. S2CID 12182924. "Salkowski test for cholesterol - Its principle and procedure". ... If a sample does not contain any cholesterol or other sterols the tested solution remains unchanged and retains its original ... in a case of cholesterol. Red colour of a solution is a consequence of bi-sulfonic acid of a bi-cholestadien, which is a ... besides cholesterol and other sterols also for creatinine, carbon monoxide, glucose and indoles). A solution that has tested ...

https://en.wikipedia.org/wiki/Salkowski's_test

... cholesterol and triglyceride concentrations. High density lipoprotein (HDL) cholesterol did not change. Although there is only ... Using these and other soy foods to replace foods high in animal protein that contain saturated fat and cholesterol may confer ... Extension may result in diminished flavor, but fat and cholesterol are reduced. Vitamin and mineral fortification can be used ... In 2006, an American Heart Association review of soy protein benefits indicated only weak confirmation for the cholesterol- ...

https://en.wikipedia.org/wiki/Soy_protein

Cholesterol effluxes from cells as free cholesterol and is transported in HDL as esterified cholesterol. LCAT is the enzyme ... high plasma unesterified cholesterol in HDL particles, and low cholesterol ester in HDL particles but normal levels in low- ... that esterifies the free cholesterol on HDL to cholesterol ester and allows the maturation of HDL. LCAT deficiency does not ... HDL) metabolism, but in fish-eye disease the enzyme cannot esterify, or make the acid into an alkyl, cholesterol in HDL ...

https://en.wikipedia.org/wiki/Lecithin_cholesterol_acyltransferase_deficiency

The antibody does not bind the good forms of cholesterol such as HDL. In the gastrointestinal tract, the antibody acts as a ... Anti-cholesterol is a naturally occurring antibody to cholesterol produced by mammals. This antibody serves a 'housekeeping' or ... January 1996). "Immunization with cholesterol-rich liposomes induces anti-cholesterol antibodies and reduces diet-induced ... An immunoglobulin protein, anti-cholesterol may be found both in circulation as well as in the digestive tract. In circulation ...

https://en.wikipedia.org/wiki/Anti-cholesterol

... partly through increasing HDL cholesterol whilst reducing LDL cholesterol. In 1999, Malcolm Law and Nicholas Wald published a ... Consumption of animal fat and serum cholesterol concentrations increased only recently in France but did so decades ago in ... from CHD is more likely to be linked to past levels of serum cholesterol and fat consumption than to current serum cholesterol ... Cholesterol and The French Paradox (Frank Cooper, 2009); The French Women Don't Get Fat Cookbook (Mireille Guiliano, 2010). ...

https://en.wikipedia.org/wiki/French_paradox

... cholesterol)". GPnotebook. Royal College of Pathologists of Australasia; Cholesterol (HDL and LDL) - plasma or serum Last ... Retrieved on September 12, 2009 "HDL Cholesterol: The Test". September 3, 2001. Archived from the original on 2001-09-03. GP ... hdl:2434/51239. PMID 12456231. Kline JA, Williams GW, Hernandez-Nino J (May 2005). "D-dimer concentrations in normal pregnancy ... Cholesterol? Last Update July 21, 2009. Retrieved on July 21, 2009 Derived from values in mg/dL to mmol/L, using molar mass of ...

https://en.wikipedia.org/wiki/Reference_ranges_for_blood_tests

"The role of HDL-cholesterol in preventing atherosclerotic disease". European Heart Journal Supplements. 7: F4-F8. doi:10.1093/ ... Other studies have associated hardiness with cholesterol and hormonal variations. Bartone and associates examined hardiness ... levels against a full lipid profile including high-density lipoprotein, usually considered a beneficial type of cholesterol. ...

https://en.wikipedia.org/wiki/Hardiness_(psychology)

HDL). All the lipoproteins carry cholesterol, but elevated levels of the lipoproteins other than HDL (termed non-HDL ... "Meta-regression analysis of the effects of dietary cholesterol intake on LDL and HDL cholesterol". The American Journal of ... A diet high in sugar or saturated fats increases total cholesterol and LDL. Trans fats have been shown to reduce levels of HDL ... Levels of LDL or non-HDL cholesterol both predict future coronary heart disease; which is the better predictor is disputed. ...

https://en.wikipedia.org/wiki/Hypercholesterolemia

... cholesterol) or low levels of high-density lipoprotein (HDL, "good" cholesterol). These parameters in turn are believed to be ... it also decreases levels of HDL ("good cholesterol"). The net increase in LDL/HDL ratio with trans fat, a widely accepted ... "bad cholesterol"), lowering levels of high-density lipoprotein (HDL, often termed "good cholesterol"), increasing triglycerides ... high cholesterol may be caused by many factors. Other indicators, such as high LDL/HDL ratio, have proved to be more predictive ...

https://en.wikipedia.org/wiki/Fat

Statins should be considered to lower elevated non-HDL-Cholesterol. Additional measures are avoidance of agents known to ...

https://en.wikipedia.org/wiki/Lipoprotein_lipase_deficiency

... a decrease in HDL cholesterol has been observed.: 253 At high doses (5 to 60 mg/day), for instance those used in the treatment ... hdl:10665/345533. WHO/MHP/HPS/EML/2021.02. Kim JJ, Kurita T, Bulun SE (February 2013). "Progesterone action in endometrial ... and does not affect cholesterol side-chain cleavage enzyme (P450scc), 17α-hydroxylase/17,20-lyase, 21-hydroxylase, or 11β- ...

https://en.wikipedia.org/wiki/Norethisterone

The first Framingham Risk Score included age, sex, LDL cholesterol, HDL cholesterol, blood pressure (and also whether the ... HDL cholesterol, mg/dL: 60 or higher: Minus 1 point. 50-59: 0 points. 40-49: 1 point. Under 40: 2 points. Systolic blood ... HDL cholesterol, mg/dL: 60 or higher: Minus 1 point. 50-59: 0 points. 40-49: 1 point. Under 40: 2 points. Systolic blood ... The National Cholesterol Education Program NCEP's ATP III guidelines also list diabetes as a CHD risk equivalent since it also ...

https://en.wikipedia.org/wiki/Framingham_Risk_Score

However, the high density lipoprotein (HDL) can remove cholesterol again. If, however, a certain amount of LDL accumulates ... According to Bhakdi's hypothesis, LDL is generally not oxidized, but cholesterol is also absorbed by monocytes and foam cells ... Terminal C5b-9 complement deposition coincides with cholesterol accumulation in the aortic intima of hypercholesterolemic ... especially cholesterol. This is transported in the blood via LDL and absorbed by the cells that need it via cellular receptors ...

https://en.wikipedia.org/wiki/Sucharit_Bhakdi

Members of this family promote cholesterol efflux from macrophage cells. They are present in various lipoprotein complexes, ... including HDL, LDL and VLDL. GRCh38: Ensembl release 89: ENSG00000184831 - Ensembl, May 2017 GRCm38: Ensembl release 89: ... probably as a VLDL-associated protein that is subsequently transferred to HDL. Apolipoprotein O is the first chondroitine ...

https://en.wikipedia.org/wiki/Apolipoprotein_O

Fibrates effectively lower serum triglycerides and raises serum HDL-cholesterol levels. Although clinical benefits of fibrate ... In macrophages, PPAR-α inhibits the uptake of glycated low-density lipoprotein (LDL cholesterol), inhibits foam cell ( ...

https://en.wikipedia.org/wiki/Peroxisome_proliferator-activated_receptor_alpha

... together these actions decrease serum VLDL levels and increase HDL-cholesterol; the mechanism behind HDL elevation is currently ... Chylomicrons are degraded, VLDLs are converted to LDLs, and LDLs are converted to HDL. This is accompanied by a slight increase ... HDL) levels GI distress Musculoskeletal pain Increased incidence of gallstone Hypokalemia (low blood potassium) Increased risk ...

https://en.wikipedia.org/wiki/Gemfibrozil

"Multiple rare alleles contribute to low plasma levels of HDL cholesterol". Science. 305 (5685): 869-872. Bibcode:2004Sci...305 ...

https://en.wikipedia.org/wiki/Medical_genetics

M. tuberculosis can also grow on the lipid cholesterol as a sole source of carbon, and genes involved in the cholesterol-use ... hdl:10400.14/3388. PMID 16095939. Krämer M, Bongaerts J, Bovenberg R, Kremer S, Müller U, Orf S, et al. (October 2003). " ... Lanosterol can then be converted into other sterols such as cholesterol and ergosterol. Organisms vary in their ability to ... Wipperman MF, Sampson NS, Thomas ST (2014). "Pathogen roid rage: cholesterol utilization by Mycobacterium tuberculosis". ...

https://en.wikipedia.org/wiki/Metabolism

Women were 60% more likely to have mammograms and recipients overall were 20% more likely to have their cholesterol checked; In ... hdl:10419/215175. S2CID 198255625. {{cite journal}}: Cite journal requires ,journal= (help) Miller, Sarah; Altekruse, Sean; ...

https://en.wikipedia.org/wiki/Medicaid

Amlodipine Atorvastatin (lowers cholesterol) Fenofibrate (lowers triglycerides, raises HDL) Losartan Adrenocorticotropic ... hdl:2263/13907. PMID 18727958. Spaia S, Magoula I, Tsapas G, Vayonas G (2000). "Effect of pyrazinamide and probenecid on ...

https://en.wikipedia.org/wiki/Uricosuric

hdl:2262/36848. PMID 20122998. Shen RF, Tai HH (1998). "Thromboxanes: synthase and receptors". J. Biomed. Sci. 5 (3): 153-172. ... P450 proteins are monooxygenases that catalyze many reactions involved in drug metabolism and synthesis of cholesterol, ...

https://en.wikipedia.org/wiki/Thromboxane-A_synthase

Doses of levothyroxine that normalize serum TSH may not normalize abnormal levels of LDL cholesterol and total cholesterol. ... hdl:10665/325771. WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO. "The Top 300 of 2020". ClinCalc. Retrieved 7 October ... elevated cholesterol levels), but was withdrawn due to cardiac side effects.[citation needed] Once weekly thyroxine (OWT) ...

https://en.wikipedia.org/wiki/Levothyroxine

hdl:1874/329744. PMID 26160969. S2CID 19123557. Linsky A, Meterko M, Stolzmann K, Simon SR (June 2017). "Supporting medication ... and drugs for high cholesterol. For people with a life limiting condition such as a dementia, it is important to consider when ...

https://en.wikipedia.org/wiki/Medication_discontinuation

hdl:10284/3294. ISSN 0022-3263. PMID 19053615. Media related to Phenyl group at Wikimedia Commons (Articles with short ... It is used to lower cholesterol in people with hypercholesterolaemia. Fexofenadine (Allegra, Telfast), another blockbuster drug ...

https://en.wikipedia.org/wiki/Phenyl_group

hdl:1959.17/66356. PMID 16594881. S2CID 20500743. Archived from the original on 2008-04-11. Krawitz R (2004). "Borderline ... although they also experienced weight gain and raised cholesterol. Another small study found that patients who had undergone ...

https://en.wikipedia.org/wiki/Management_of_borderline_personality_disorder

The functional loss of aSMase activity may also be due to altered trafficking (causing accumulation of cholesterol) or by ... Lipid deposits are encouraged by high levels of circulating LDL, often caused by inadequate removal by HDL particles. Acid ... Atherosclerosis occurs from the thickening of the artery walls through depositing of cholesterol and triglyceride on the cell ...

https://en.wikipedia.org/wiki/Acid_sphingomyelinase

hdl:1805/22476. ISSN 1365-2648. PMID 29943401. S2CID 49415051. Matarese, Maria; Clari, Marco; De Marinis, Maria Grazia; ... cholesterol measurements, eye and foot examinations, diabetes education, and aspirin use. Research has found that people in ...

https://en.wikipedia.org/wiki/Self-care

In the one paper, they reported that they had measured the levels of Coenzyme Q10 and cholesterol in the plasma of young and ... hdl:10261/230490. PMID 32639220. S2CID 220412289. Trevisson E, DiMauro S, Navas P, Salviati L. (2011). "Coenzyme Q deficiency ... They found that individuals with higher levels of functional capacity also had lower levels of cholesterol and lipid ... higher activity was associated with higher plasma Q10 levels and higher Coenzyme Q10/Cholesterol ratios. The higher Coenzyme ...

https://en.wikipedia.org/wiki/Plácido_Navas_Lloret

... low high density cholesterol (HDL) levels, high blood pressure, and abdominal obesity. Metabolic syndrome has been associated ...

https://en.wikipedia.org/wiki/Obesity_and_fertility

HDL) cholesterol and low-density lipoprotein (LDL) cholesterol. Although lauric acid consumption may create a more favorable ... "Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and ... "Lower your cholesterol". National Health Service. Retrieved 2011-03-16. Foster R, Williamson CS, Lunn J (2009). "Culinary oils ... "Heart Healthy Eating: Cholesterol". Dietitians of Canada. 2010-09-01. Archived from the original on 2013-09-21. Retrieved 2013- ...

https://en.wikipedia.org/wiki/Coconut_oil

Torcetrapib was originally hyped as a drug that could block a protein that converts HDL cholesterol into LDL with the potential ... to "redefine cardiovascular treatment". One clinical trial showed that the drug could increase HDL and decrease LDL. Two days ...

https://en.wikipedia.org/wiki/Invalid_science

A 2018 review found evidence that ginger could decrease body weight in obese subjects and increase HDL-cholesterol. Although ...

https://en.wikipedia.org/wiki/Ginger

hdl:11336/94743. PMID 29573319. S2CID 4228374. Bolton, Judy L.; Dunlap, Tareisha L.; Dietz, Birgit M. (2018). "Formation and ... Naturally occurring catechols 3,4-dihydroxy-9,10-secoandrosta-1,3,5(10)-triene-9,17-dione, a metabolite of cholesterol Catechin ... "Studies of a ring-cleaving dioxygenase illuminate the role of cholesterol metabolism in the pathogenesis of Mycobacterium ...

https://en.wikipedia.org/wiki/Catechol

"Effects of the CETP inhibitor evacetrapib administered as monotherapy or in combination with statins on HDL and LDL cholesterol ... and selective inhibitor of cholesteryl ester transfer protein that elevates HDL cholesterol without inducing aldosterone or ... When studied in a small clinical trial in people with elevated LDL and low HDL, significant improvements were noted in their ... "Study of Evacetrapib (LY2484595) in Participants With High Cholesterol (ACCENTUATE)". Kolata, Gina (3 April 2016). "Dashing ...

https://en.wikipedia.org/wiki/Evacetrapib

doi:10.1007/s40618-014-0186-2. hdl:11368/2831597. PMID 25403429. S2CID 207503049. Moore E, Wisniewski A, Dobs A (August 2003 ... and cholesterol. Taking more medication than directed may lead to health problems such as increased risk of cancer, heart ... attack from thickening of the blood, blood clots, and elevated cholesterol. The Standards of Care published by the World ...

https://en.wikipedia.org/wiki/Transgender_hormone_therapy

HDL) levels on overweight and obese people. The MSM group demonstrated higher HDL levels after 16 weeks (51.8 ± 2.8 mg/dL) when ... Consumption on High-Density Lipoprotein Cholesterol in Healthy Overweight and Obese Adults: A Randomized Controlled Trial". ... The authors also state more and larger studies are required to establish the relationship between MSM and HDL. The LD50 of MSM ...

https://en.wikipedia.org/wiki/Methylsulfonylmethane

hdl:2115/38856. S2CID 23981384. Varshney, Anshu D.; Sinha, Ravindra K. (2009). "Ultrahigh birefringent photonic crystal fiber: ... "Electroactive Prussian Blue Encapsulated Iron Oxide Nanostructures for Mediator-Free Cholesterol Estimation". Electroanalysis. ... synthesis and deposition of gold nanostructures was developed for fabrication of a highly sensitive and selective cholesterol ...

https://en.wikipedia.org/wiki/Ravindra_Kumar_Sinha_(physicist)

... elevated total cholesterol and LDL cholesterol, highlighting significantly reduced PPAR expression and alluding to PPAR ... hdl:20.500.11850/495857. S2CID 236284279. Archived from the original on July 22, 2021. Retrieved July 11, 2021. "Toxic 'Forever ... Another mechanism refers to agonism of PPARs contributing to alterations in cholesterol, triglyceride and uric acid levels ... Olsen GW, Burris JM, Burlew MM, Mandel JH (November 2000). "Plasma cholecystokinin and hepatic enzymes, cholesterol and ...

https://en.wikipedia.org/wiki/Per-_and_polyfluoroalkyl_substances

hdl:10292/2827. Heathcote, Damien; Carrol, Tim; Wang, Jui-Jen; Flower, Robert; Rodionov, Igor; Tuzikov, Alexander; Bovin, ... Lipids in FSL Kode constructs include: Diacyl/diakyl e.g. DOPE Sterols e.g. cholesterol Ceramides One of the important ... hdl:10292/2241. {{cite journal}}: Cite journal requires ,journal= (help) Henry, Stephen; Barr, Katie; Oliver, Caroline (2012 ... doi:10.1111/j.1537-2995.2008.01891.x. hdl:10292/4136. PMID 18783347. S2CID 222199165. Harrison, A L; Henry, S; Mahfoud, R; ...

https://en.wikipedia.org/wiki/Function-spacer-lipid_Kode_construct

Hafiane A, Gasbarrino K, Daskalopoulou SS (November 2019). "The role of adiponectin in cholesterol efflux and HDL biogenesis ... Oram JF, Vaughan AM (June 2000). "ABCA1-mediated transport of cellular cholesterol and phospholipids to HDL apolipoproteins". ... With cholesterol as its substrate, this protein functions as a cholesterol efflux pump in the cellular lipid removal pathway. ... ABCA1 mediates the efflux of cholesterol and phospholipids to lipid-poor apolipoproteins (apoA1 and apoE) (reverse cholesterol ...

https://en.wikipedia.org/wiki/ABCA1

hdl:11858/00-001M-0000-0019-1122-4. PMC 4109059. PMID 23417068. Plaschka, C.; Larivière, L.; Wenzeck, L.; Seizl, M.; Hemann, M ... "An ARC/Mediator subunit required for SREBP control of cholesterol and lipid homeostasis". Nature. 442 (7103): 700-4. Bibcode: ...

https://en.wikipedia.org/wiki/Mediator_(coactivator)

doi:10.1038/s41564-018-0305-5. hdl:1854/LU-8587985. PMID 30478288. S2CID 53726187. Favre B, Ryder NS (Feb 1996). " ... butenafine naftifine terbinafine Since squalene epoxidase is on the biosynthetic pathway leading to cholesterol, inhibitors of ... "Multiple genetic variants along candidate pathways influence plasma high-density lipoprotein cholesterol concentrations". ...

https://en.wikipedia.org/wiki/Squalene_monooxygenase

hdl:1874/9833. PMID 16009135. S2CID 18837009. Schrader M, Costello JL, Godinho LF, Azadi AS, Islinger M (May 2016). " ... It is vigorously debated whether peroxisomes are involved in isoprenoid and cholesterol synthesis in animals. Other known ... doi:10.1007/s00418-018-1724-3. hdl:20.500.11850/302080. PMID 30238155. S2CID 52307878. Shai N, Schuldiner M, Zalckvar E (May ... doi:10.1007/s00418-012-0941-4. hdl:10871/33969. ISSN 0948-6143. PMC 6182659. PMID 22415027. S2CID 14853309. Effelsberg D, Cruz- ...

https://en.wikipedia.org/wiki/Peroxisome

hdl:10315/38072. PMID 29101934. S2CID 40193168. Chowdhury M, Heald FA, Sanchez-Delgado JC, Pakosh M, Jacome-Hortua AM, Grace SL ... Nurses support patients in reducing medical risk factors such as high blood pressure, high cholesterol and diabetes. ... hdl:10315/38987. PMID 33836441. S2CID 233201693. Santiago de Araújo Pio C, Beckie TM, Varnfield M, Sarrafzadegan N, Babu AS, ... doi:10.1007/s11886-021-01543-x. hdl:10315/38989. PMID 34269894. S2CID 235916856. Turk-Adawi K, Supervia M, Lopez-Jimenez F, ...

https://en.wikipedia.org/wiki/Cardiac_rehabilitation

"Predominance of a proinflammatory phenotype in monocyte-derived macrophages from subjects with low plasma HDL-cholesterol". ... "Enhanced atheroprotection and lesion remodelling by targeting the foam cell and increasing plasma cholesterol acceptors". ...

https://en.wikipedia.org/wiki/Perilipin-2

In 1985, both drugs were also reported to increase serum levels of high density lipoprotein (HDL) cholesterol, total ... doi:10.1111/j.1528-1157.1995.tb05996.x. hdl:2027.42/65277. PMID 8784210. S2CID 22628709. Calzetti, S.; L. J. Findley; F. Pisani ... cholesterol, and apolipoproteins A and B. It was first reported to exacerbate hepatic porphyria in 1975. In 1981, it was shown ...

https://en.wikipedia.org/wiki/Primidone

HDL-cholesterol esters are converted to HDL-cholesterol by PEG-cholesterol esterase. The HDL-cholesterol is acted upon by PEG- ... Direct HDL-Cholesterol (mg/dL). Variable Name: LBDHDD. SAS Label: Direct HDL-Cholesterol (mg/dL). English Text: Direct HDL- ... Direct HDL-Cholesterol (mmol/L). Variable Name: LBDHDDSI. SAS Label: Direct HDL-Cholesterol (mmol/L). English Text: Direct HDL- ... Cholesterol - HDL (HDL_H) Data File: HDL_H.xpt First Published: October 2015. Last Revised: March 2016. ...

https://wwwn.cdc.gov/Nchs/Nhanes/2013-2014/HDL_H.htm

... cholesterol. It helps to remove bad cholesterol from your arteries, so a higher HDL level is better. ... HDL, or high-density lipoprotein, is the good ... What should my HDL level be?. With HDL cholesterol, higher ... How do I know what my HDL level is?. A blood test can measure your cholesterol levels, including HDL. When and how often you ... HDL and LDL have different purposes:. *HDL stands for high-density lipoproteins. It is sometimes called the "good" cholesterol ...

https://medlineplus.gov/hdlthegoodcholesterol.html

Low HDL cholesterol defined as serum HDL cholesterol ,40 mg/dL. † Overall estimates for men and women are age-adjusted by the ... "good cholesterol"). In all age groups, a higher percentage of men had low levels of HDL cholesterol than women. A higher ... "good cholesterol"). In all age groups, a higher percentage of men had low levels of HDL cholesterol than women. A higher ... During 2011-2012, an estimated 26.4% of U.S. adult males and 9.0% of females aged ≥20 years had low levels of HDL cholesterol ( ...

https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6306a6.htm?s_cid=mm6306a6_w

Cholesterol efflux capacity inversely correlates with HDL cholesterol fractional catabolic rate. *. W. Hancock-Cerutti. W. ... of HDL-C had impaired cholesterol transport through HDL. ... Aim: High density lipoprotein cholesterol (HDL-C) levels are ... Despite this association, a small proportion of subjects with elevated HDL-C develop coronary artery disease (CAD). We ... Next ArticleIdentification of populations with high vascular risk associated to HDL-c levels ...

https://www.atherosclerosis-journal.com/article/S0021-9150

Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational ... Only recently, the treat stroke to target trial has demonstrated the benefit of aggressive LDL-cholesterol lowering for ... However, in young and otherwise healthy people, cholesterol levels are rarely determined. If increased, would this be worth ... A comparison of two ldl cholesterol targets after ischemic stroke. N Engl J Med. 2019 ...

https://eso-stroke.org/non-hdl-cholesterol-in-the-young-is-it-worth-worrying/

... adjustment for treatment group and on-study HDL-cholesterol, LDL-cholesterol, and triglyceride concentrations. The associations ... changes in coronary artery stenosis and cardiovascular events in patients with coronary artery disease and low HDL-cholesterol ... Methods Gradient gel electrophoresis of on-study LDL-subclass cholesterol concentrations were measured in 32 placebo, 33 ... Conclusions Plasma LDL-IIIb cholesterol concentrations were related to ...

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0056782

Get the cost of HDL Cholesterol in Yerawada (Pune) city diagnostic centers. like NM Medical, Rane Laboratory (Yerawada), New ... Diagnostic Centers offering HDL Cholesterol at Yerawada in Pune:. NM Medical. Rs. 250.00 ...

https://www.medifee.com/tests/hdl-cholesterol-cost-in-pune/yerawada

HDL cholesterol performance using an ultracentrifugation reference measurement procedure and the designated comparison method. ... HDL cholesterol performance using an ultracentrifugation reference measurement procedure and the designated comparison method. ... HDL cholesterol performance using an ultracentrifugation reference measurement procedure and the designated comparison method. ... HDL cholesterol performance using an ultracentrifugation reference measurement procedure and the designated comparison method. ...

https://keio.pure.elsevier.com/en/publications/hdl-cholesterol-performance-using-an-ultracentrifugation-referenc

Click here to discover what an HDL 119 measurement means for your cholesterol levels! ... Are you wondering what the normal amount of HDL cholesterol is? ... HDL Cholesterol Level Chart: Symptoms and Causes HDL 119: Can ... Can HDL cholesterol be too high? HDL levels can be too high, which makes it lose its protective benefits. An HDL level of 119mg ... How to Reduce HDL Cholesterol to Optimal Levels. If you have high HDL cholesterol, you will need to make some changes to reduce ...

https://healthreporter.com/biomarkers/hdl-cholesterol-level-chart/hdl-cholesterol-119/

My total cholesterol level is way below the recommended 5 mmol/L (193 mg/DL) at 3.1 but total/HDL ratio is 2.95. Transcends ... Increasing HDL cholesterol level without increasing body fat percentage. Health tips arent a one size fits all solution ... Heres a summary of how I plan to increase HDL cholesterol levels at the same time as reducing body fat percentage.. 1. ... So I want to attack both low HDL and high body fat at the same time, therefore increasing good oils isnt an option - but Ill ...

https://liveforever.club/blog/increasing-hdl-cholesterol-level-without-increasing-body-fat-percentage

... serum cholesterol level." As I focus on in my video Coconut Oil and the Boost in HDL "Good" Cholesterol, research showing ... the hypothesis that HDL cholesterol is a causal risk factor." In easy phrases: "High HDL may not protect the heart." We ought ... But, its "time to face facts." The "lack of benefit of raising the HDL cholesterol level with the use of niacin…seriously ... Saturated fat could make HDL, the so-called good ldl cholesterol, go up, so whats the drawback? The drawback is that it ...

https://healthyfountain.com/coconut-oil-and-the-boost-in-hdl-good-cholesterol/

Being physically active is an important part of treating cholesterol thats higher than it should be. Discover which exercises ... What Is HDL Cholesterol?. Maintaining good HDL levels can help protect you against heart disease. ... Physical activity can lower bad cholesterol (LDL), raise good cholesterol (HDL), and lower the risk for heart disease in adults ... Like HDL and LDL cholesterol, triglycerides are a type of fat found in your blood and are the most common form of body fat. ...

https://www.everydayhealth.com/hs/healthy-living-high-cholesterol/effective-exercises-high-cholesterol-pictures/

... dc.creator. Klisić, ... Older age and HDL-cholesterol as independent predictors of liver fibrosis assessed by BARD score. en. ... Serum high density lipoprotein cholesterol (HDL-c), glucose and glycated hemoglobin were higher (P=0.028, P lt 0.001 and P= ... CONCLUSIONS: In conclusion, we found that older age and higher HDL-c, are independent predictors for advanced liver fibrosis ...

https://farfar.pharmacy.bg.ac.rs/handle/123456789/3302?show=full

HDL cholesterol efflux normalised to apoA-I is associated with future development of type 2 diabetes. Title HDL cholesterol ... Cholesterol efflux was quantified by incubation of cholesterol-loaded THP-1 cells with the participants apoB-depleted plasma. ... HDL-cholesterol efflux normalised to apoA-I was inversely associated with T2DM development in cardiovascular patients. This ... We measured cholesterol efflux in all CORDIOPREV study (NCT00924937) participants free of T2DM at baseline (n = 462) and ...

https://repository.tno.nl/islandora/object/uuid%3Ad9cb0a05-5b2b-40ba-9308-408d0677758c

Red Beet fiber significantly reduces LDL cholesterol and increases HDL.Jun 01, 2000. ...

https://greenmedinfo.com/substance/beet

HDL (mg/dL). LDL (mg/dL). BUN (mg/dL). Crea (mg/dL). UA (mg/dL). TP (mg/dL). CPK (U/L). Glu (mg/dL). ... GOT, glutamate-oxaloacetate transaminase; GPT, glutamate-pyruvate transferase; ALB, albumin; TC, total cholesterol; TG, ... total cholesterol (TC) levels, and low-density lipoprotein (LDL) levels in mice with obesity induced by a high-fat diet (HFD) [ ... cholesterol (MP Biomedicals, Santa Ana, CA, United States). The high-fat diet induced obesity animal model followed a previous ...

https://www.mdpi.com/2072-6643/14/6/1270

But high cholesterol can increase your risk of heart disease. Lifestyle changes can help. ... You need some cholesterol in your blood to build healthy cells. ... Eggs and cholesterol * HDL cholesterol: How to boost your good ... High-density lipoprotein (HDL). HDL, the "good" cholesterol, picks up excess cholesterol and takes it back to your liver. ... Cholesterol is a waxy substance found in your blood. Your body needs cholesterol to build healthy cells, but high levels of ...

https://www.mayoclinic.org/diseases-conditions/high-blood-cholesterol/symptoms-causes/syc-20350800?mc_id=us&utm_source=newsnetwork&utm_medium=l&utm_content=content&utm_campaign=mayoclinic&geo=national&placementsite=enterprise&cauid=100721

Understanding Cholesterol - LDL vs. HDL and Everything In Between. Thursday, April 3rd, 2008 Since I am operating a healthy ... Does Exercise Lower Cholesterol?. Thursday, September 22nd, 2022 Cholesterol and its role in our body is not something most ... Lastly comes the "good" cholesterol, high-density lipoproteins (HDL), which are the smallest and densest of the lipid-carriers ... In other words, they dispose of the cholesterol. How Do I Lower My Cholesterol?. There are several notable factors that can ...

https://www.projectswole.com/tag/cholesterol/

... the total cholesterol to HDL cholesterol ratio and postprandial lipemic responses compared with a low fat diet in normal weight ... An isoenergetic very low carbohydrate diet improves serum HDL cholesterol and triacylglycerol concentrations, ... LDL subclasses and HDL cholesterol (HDL-C) in men but the effects in women are unclear. We compared the effects of a very low ... the total cholesterol to HDL cholesterol ratio and postprandial lipemic responses compared with a low fat diet in normal weight ...

https://figshare.utas.edu.au/articles/journal_contribution/An_isoenergetic_very_low_carbohydrate_diet_improves_serum_HDL_cholesterol_and_triacylglycerol_concentrations_the_total_cholesterol_to_HDL_cholesterol_ratio_and_postprandial_lipemic_responses_compared_with_a_low_fat_diet_in_normal_weight_nor/22892393

High-dose of potent statins may not be sufficient to achieve therapeutic goals of ldlc and non-hdl cholesterol in patients at ... HDL cholesterol (NHDLc) risk patients using the initial treatment recommended by the brazilian guideline that achieved the LDL- ... Average LDL-c was 83.1mg/dL (SD 29.5) and NHDLc was 113.5mg/dL (SD 35). The mean TC was 152 mg/dL (SD 29.5), HDL-c was 39.5 (SD ... Inibidores de Hidroximetilglutaril-CoA Redutases; Dislipidemias; Fatores de Risco de Doenças Cardíacas; HDL-Colesterol; ...

https://pesquisa.bvsalud.org/portal/resource/pt/biblio-1397313

... cholesterol levels. Light to moderate drinking can raise good HDL cholesterol. Red wine is thought to be particularly ... The results found that daily moderate alcohol intake increased HDL cholesterol by an average of 18%, compared to when the ... One of the ways low to moderate wine drinking heart health is by boosting HDL ("good") ... beneficial as it can boost HDL while its polyphenols have been linked in some studies to help lower harmful, small dense LDL (" ...

https://www.eatthis.com/surprising-side-effects-wine-on-heart/

... or good cholesterol - Below 40 mg/dL in men, below 50 mg/dL in women, or taking medication for low HDL cholesterol level ... Measurement of HDL cholesterol should be used as part of the initial cardiovascular risk assessment but should not be used as a ... HDL cholesterol and residual risk of first cardiovascular events after treatment with potent statin therapy: an analysis from ... Fast Five Quiz: Lipids Management: High HDL Cholesterol Levels (Hyperalphalipoproteinemia) * Fast Five Quiz: Non-Statin Lipid- ...

https://emedicine.medscape.com/article/164163-overview

Circulating HN levels were positively correlated to cholesterol (p,0.017), LDL (p,0.001) and HDL (p,0.001). Linear regression ... Circulating HN levels were positively correlated to cholesterol (p , 0.017), LDL (p , 0.001), and HDL (p , 0.001). Linear ... total cholesterol (p,0.0001) and LDL (p,0.001) and negatively correlated with age (p,0.002), HbA1c (p,0.001) and glucose (p, ... and positively correlated with HDL (p,0.0001) and HN (p,0.003). Linear regression analysis showed that HbA1c and weight were ...

https://www.frontiersin.org/articles/10.3389/fendo.2019.00331/full

It decreases levels of HDL -- the good cholesterol. If you smoke a pack a day, you have more than twice the risk of a heart ... Maintain healthy cholesterol levels. If you need to lose weight, its going to take a little more effort. "For weight ... You may find, for example, that you have high cholesterol and it needs to be managed with medication. On the flip side, you may ... Limit how much saturated fat, trans fat, and cholesterol you eat. Only 30% of your daily calories should come from fat, with ...

https://www.medicinenet.com/script/main/art.asp?articlekey=86837

Wake Up World on Social ...

https://wakeup-world.com/tag/hdl/

Isolated Soy Protein Shown To Benefit Patients With Type 2 Diabetes; Enhances HDL Cholesterol Levels ...

https://www.naturalnews.com/protein_bars.html

HDL-Cholesterol (mg/dL) Baseline. 39.0. 40.5. 37.2. 39.0. 37.0. Mean % Change. at FINAL VISIT. 2%. -1%. 5%. 3%. 1%. ... total cholesterol, and LDL cholesterol levels and had no adverse effects on other lipid levels (see Table 4). ...

https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=28de9dcf-cc8c-4c06-9fcc-6a1279f2523f

High-density lipoprotein (HDL) cholesterol, often called "good" cholesterol. HDL helps the body get rid of extra cholesterol. ... Total cholesterol, which is the amount of the different types of cholesterol added together. The body needs some cholesterol. ... Low-density lipoprotein (LDL) cholesterol, often called "bad" cholesterol. LDL that builds up in the bloodstream can clog blood ...

https://kidshealth.org/HospitalSantJoandeDeu/en/parents/blood-test-lipid-panel.html

Higher good cholesterol linked to lower cancer risk ,,We already knew that higher HDL cholesterol is one of the strongest ... HDL metabolism and cardiovascular outcome may have made it difficult to detect any benefit of raising HDL cholesterol in this ... some interventions may raise HDL cholesterol by limiting its breakdown (harmful), while others raise it by increasing HDL ... Cholesterol Explained [video]. by Darya Rose , May 12, 2010 Enough people have asked me if the kind of cholesterol in egg yolks ...

https://summertomato.com/tag/hdl/page/2/

However, there was a change to the total cholesterol, HDL-cholesterol, and triglycerides lab equipment. (cdc.gov)
200mg/dl triglycerides involved 50-kDa dextran sulfate-MgCl 2 precipitation and cholesterol determination. (elsevier.com)
Furthermore, missense variants at two novel loci-PNPLA3 p.Ile148Met and PKD1L3 p.Thr429Ser-also influence levels of triglycerides and low-density lipoprotein cholesterol, respectively. (nih.gov)
Over time, this may cause your liver to pump out more cholesterol and blood fats called triglycerides. (medicinenet.com)

But having too much cholesterol in your blood raises your risk of coronary artery disease . (medlineplus.gov)
With HDL cholesterol, higher numbers are better, because a high HDL level can lower your risk for coronary artery disease and stroke . (medlineplus.gov)
Despite this association, a small proportion of subjects with elevated HDL-C develop coronary artery disease (CAD). (atherosclerosis-journal.com)
Plasma LDL-IIIb cholesterol concentrations were related to changes in coronary artery stenosis and cardiovascular events in patients with coronary artery disease and low HDL-cholesterol. (plos.org)
Red wine is thought to be particularly beneficial as it can boost HDL while its polyphenols have been linked in some studies to help lower harmful, small dense LDL ("bad") particles that are known to be drivers of coronary artery disease. (eatthis.com)

HDL and LDL are two types of lipoproteins.They are a combination of fat (lipid) and protein. (medlineplus.gov)
HDL stands for high-density lipoproteins. (medlineplus.gov)
Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol. (nih.gov)
In order for cholesterol to travel through blood, it must attach itself to small fat-carrying proteins called lipoproteins. (projectswole.com)
The least dense lipoproteins are the chylomicrons, which carry very little cholesterol. (projectswole.com)
Next, come the very low-density lipoproteins (VLDL), which roughly carry 15% of the circulating cholesterol. (projectswole.com)
Lastly comes the "good" cholesterol, high-density lipoproteins (HDL), which are the smallest and densest of the lipid-carriers. (projectswole.com)

Total and high-density lipoprotein cholesterol in adults: National Health and Nutrition Examination Survey, 2011-2012. (cdc.gov)
High density lipoprotein cholesterol (HDL-C) levels are negatively associated with cardiovascular disease in large epidemiological studies. (atherosclerosis-journal.com)
Background: Accurate high-density lipoprotein cholesterol (HDL-C) measurements are important for management of cardiovascular diseases. (elsevier.com)
Conclusions: Osaka UC and DCM were highly accurate, precise, and stable for many years, assisting manufacturers to calibrate products for clinical laboratories to accurately measure HDL-C for patients, calculate non-HDL-C, and estimate low-density lipoprotein cholesterol with the Friedewald equation. (elsevier.com)
High levels of high-density lipoprotein cholesterol can actually be a result of certain medications. (healthreporter.com)
RESULTS: Serum high density lipoprotein cholesterol (HDL-c), glucose and glycated hemoglobin were higher (P=0.028, P lt 0.001 and P=0.002, respectively), whereas serum transaminases and gamma glutamil transferase levels were lower in patients with advanced fibrosis than in those with no/ mild fibrosis (P=0.010, P lt 0.001 and P=0.005, respectively). (ac.rs)
Another novel gene, TEAD2, is found to be associated with high-density lipoprotein cholesterol through gene-based association analysis. (nih.gov)
In this group, however, there was an inverse linear trend between serum cotinine and high density lipoprotein cholesterol (p (cdc.gov)

According to "the experience and wisdom of 200 of the country's leading experts in cardiovascular diseases," in a report representing 29 nationwide medical organizations, together with the American Heart Association and the American College of Cardiology, we've recognized for practically half a century that "coconut oil is one of the most potent agents for elevating [blood] serum cholesterol level. (healthyfountain.com)

CONCLUSIONS: Among patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of less than 70 mg per deciliter (1.81 mmol per liter), there was no incremental clinical benefit from the addition of niacin to statin therapy during a 36-month follow-up period, despite significant improvements in HDL cholesterol and triglyceride levels. (nih.gov)
Factors you can control - such as inactivity, obesity and an unhealthy diet - contribute to harmful cholesterol and triglyceride levels. (mayoclinic.org)

1 Depending on the overall cardiovascular risk and LDL-cholesterol levels, Current European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) guidelines also recommend LDL-cholesterol lowering for primary prevention of cardiovascular disease. (eso-stroke.org)
A recent risk-evaluation and risk-modelling study from the Multinational Cardiovascular Risk Consortium sheds light on this important issue: Worrying about cholesterol is in fact worth it - even at young age. (eso-stroke.org)
Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium. (eso-stroke.org)
Targeting HDL-cholesterol to reduce residual cardiovascular risk. (ox.ac.uk)
BACKGROUND: In patients with established cardiovascular disease, residual cardiovascular risk persists despite the achievement of target low-density lipoprotein (LDL) cholesterol levels with statin therapy. (nih.gov)

With addition of reagent 2, HDL-cholesterol esters are converted to HDL-cholesterol by PEG-cholesterol esterase. (cdc.gov)

Test whether angiographically-documented changes in percent stenosis and clinical endpoints (coronary-related deaths, myocardial infarctions, stroke, revascularization for worsening ischemia) in the HDL-Atherosclerosis Treatment Study (HATS) were attributable to specific LDL-subclasses. (plos.org)
Williams PT, Zhao X-Q, Marcovina SM, Brown BG, Krauss RM (2013) Levels of Cholesterol in Small LDL Particles Predict Atherosclerosis Progression and Incident CHD in the HDL-Atherosclerosis Treatment Study (HATS). (plos.org)
The HDL-Atherosclerosis Treatment Study (HATS) was a double-blind randomized controlled clinical trial of simvastatin plus niacin and/or a mixture of antioxidants in 160 patients selected for clinical coronary disease with at least 3 stenoses of at least 30 percent of the luminal diameter or 1 stenosis of at least 50 percent, and low high-density lipoprotein (HDL)-cholesterol [1] . (plos.org)
Physical activity can lower bad cholesterol ( LDL ), raise good cholesterol (HDL), and lower the risk for heart disease in adults, according to a study published in the journal Atherosclerosis in December 2015. (everydayhealth.com)

Gradient gel electrophoresis of on-study LDL-subclass cholesterol concentrations were measured in 32 placebo, 33 simvastatin-niacin, 38 antioxidant, and 39 simvastatin-niacin & antioxidant treated participants. (plos.org)
That's why we used to offer individuals high-dose niacin-to lift their HDL. (healthyfountain.com)
The "lack of benefit of raising the HDL cholesterol level with the use of niacin…seriously undermine [ s ] the hypothesis that HDL cholesterol is a causal risk factor. (healthyfountain.com)
It is unclear whether extended-release niacin added to simvastatin to raise low levels of high-density lipoprotein (HDL) cholesterol is superior to simvastatin alone in reducing such residual risk. (nih.gov)

It is sometimes called the "good" cholesterol because it carries cholesterol from other parts of your body back to your liver. (medlineplus.gov)
To raise your HDL level, you need to eat good fats instead of bad fats. (medlineplus.gov)
Also called "good" cholesterol. (nih.gov)
The effect of "good" cholesterol on cardiovascular disease may be more complicated than previously thought, according to a new analysis. (nih.gov)
HDL, or high-density lipoprotein, is considered good cholesterol. (healthreporter.com)
The table below shows different HDL test results and whether they are good for your health. (healthreporter.com)
However I've had a look at the detailed results and the one that stands out to me is my HDL ratio - high-density lipoprotein is the good cholesterol that removes excessive LDL. (liveforever.club)
So I want to attack both low HDL and high body fat at the same time, therefore increasing good oils isn't an option - but I'll definitely be being more careful on bad oils and modify my diet to be lower in fat overall. (liveforever.club)
Even if virgin coconut oil and different saturated fat increase LDL "bad" ldl cholesterol, isn't that countered by the enhance in HDL "good" ldl cholesterol? (healthyfountain.com)
Saturated fat could make HDL, the so-called good ldl cholesterol, go up, so what's the drawback? (healthyfountain.com)
Swimming, which is also aerobic exercise, can be a good choice for your cholesterol-lowering fitness program. (everydayhealth.com)
In one study, men who strength-trained saw improvements related to high-density lipoprotein (HDL), the "good" cholesterol, compared with men who did not strength-train, regardless of their weight. (everydayhealth.com)
HDL , the "good" cholesterol, picks up excess cholesterol and takes it back to your liver. (mayoclinic.org)
It boosts your good HDL cholesterol levels. (eatthis.com)
One of the ways low to moderate wine drinking heart health is by boosting HDL ("good") cholesterol levels. (eatthis.com)
Light to moderate drinking can raise good HDL cholesterol. (eatthis.com)
Research shows that it raises your risk for high LDL ("bad") cholesterol and lowers levels of HDL ("good") cholesterol. (medicinenet.com)
HDL cholesterol is known as the good cholesterol because it transports or moves cholesterol from the artery walls back to the liver. (nih.gov)

My total cholesterol level is way below the recommended 5 mmol/L (193 mg/DL) at 3.1 but total/HDL ratio is 2.95. (liveforever.club)
Transcend's target is a ratio of less than 2.5, and as my total cholesterol is already pretty low, my only option is to try to increase my HDL. (liveforever.club)
And looking back over my blood test results spanning 5 years my HDL ratio has increased 2.55 to 2.95 - but even when I was really fit it still wasn't in the optimal range. (liveforever.club)
Effects of dietary cholesterol and saturated to polyunsaturated fatty-acid ratio on the hererogeneity of LDL and HDL particles in the 1.040-1.090 g/ml interval in the preruminant calf, Bos spp. (edpsciences.org)

It is sometimes called the "bad" cholesterol because a high LDL level leads to a buildup of cholesterol in your arteries. (medlineplus.gov)
LDL cholesterol builds up in the walls of your arteries, making them hard and narrow. (mayoclinic.org)
This means an unusually dangerous amount of cholesterol is present in your blood, and therefore arteries, at any given time. (projectswole.com)
Increasing LCAT should improve the body's ability to process cholesterol from arteries. (nih.gov)

Coconut oil elevated ldl cholesterol about 14 % over the management, which was in step with seven different interventional trials published thus far in a 2016 overview. (healthyfountain.com)

According to the National Heart, Lung, and Blood Institute (NHLBI), a person's first cholesterol screening should occur between the ages of 9 and 11, and then be repeated every five years after that. (mayoclinic.org)

What we do know is that too much alcohol can make you gain weight, and that lowers your HDL level. (medlineplus.gov)
Chronic kidney disease also lowers your HDL levels. (medicinenet.com)

Your liver makes cholesterol, and it is also in some foods, such as meat and dairy products. (medlineplus.gov)
Your liver then removes the cholesterol from your body. (medlineplus.gov)
In truth, a big enhance in blood ldl cholesterol was discovered inside hours of consuming a slice of cake made out of both coconut oil (or cod liver oil for that matter), however not from the similar cake made out of flaxseed oil. (healthyfountain.com)
CONCLUSIONS: In conclusion, we found that older age and higher HDL-c, are independent predictors for advanced liver fibrosis assessed with the BARD score. (ac.rs)
For example, your genetic makeup might make it more difficult for your body to remove LDL cholesterol from your blood or break it down in the liver. (mayoclinic.org)
These actually carry cholesterol from the cells to the liver so that they can be processed as bile acids, excreted in the bile as cholesterol, or returned to the plasma as a component of VLDL. (projectswole.com)
Your liver makes, processes, and breaks down cholesterol. (medicinenet.com)
When your liver doesn't work properly, it can affect your cholesterol levels. (medicinenet.com)
Along with processing cholesterol, your liver also breaks down alcohol. (medicinenet.com)
Bile acids are amphiphilic molecules synthesized from cholesterol in the liver. (diabetesjournals.org)
The liver processes the cholesterol so it can be removed from the body. (nih.gov)
An enzyme called LCAT helps make HDL in the blood which may enable HDL to transport it to the liver. (nih.gov)

Improving a person's HDL levels can decrease their risk of heart disease. (nih.gov)

The US Centers for Disease Control and Prevention (CDC) and Cholesterol Reference Method Laboratory Network (CRMLN) perform ultracentrifugation (UC) reference measurement procedure (RMP) to value assign HDL-C. Japanese CRMLN laboratory (Osaka) concurrently runs UC procedure and the designated comparison method (DCM). (elsevier.com)

Coconut oil can considerably raise levels of cholesterol inside hours of consumption. (healthyfountain.com)
Your body needs cholesterol to build healthy cells, but high levels of cholesterol can increase your risk of heart disease. (mayoclinic.org)

Diets that are high in saturated fats, refined carbs, and alcohol can raise your LDL and HDL cholesterol. (healthreporter.com)

You can boost your HDL level by losing weight, especially if you have lots of fat around your waist. (medlineplus.gov)

So, identical to having a excessive variety of trainers and gymnasium shorts may predict a decrease danger of coronary heart assault, having a excessive HDL additionally predicts a decrease danger of coronary heart assault. (healthyfountain.com)
And, should you intervene and actively decrease individuals's LDL by way of food regimen or medicine, their coronary heart illness danger drops-however not so with HDL. (healthyfountain.com)
People who dwell their entire lives with excessive HDL ranges don't appear to have a decrease danger of coronary heart assault, and should you give individuals a drug that will increase their HDL, it doesn't assist. (healthyfountain.com)
rhLCAT may be able to improve HDL levels and help decrease risk of worsening heart disease. (nih.gov)

Moderate alcohol may lower your HDL level, although more studies are needed to confirm that. (medlineplus.gov)
The results found that daily moderate alcohol intake increased HDL cholesterol by an average of 18%, compared to when the subjects abstained from alcohol. (eatthis.com)

Multivariate ordinal regression analysis showed independent associations and predictions of ages (OR=1.071, 95% CI 1.004-1.097, P lt 0.001), and HDL-c levels (OR= 2.549, 95% CI 1.087-5.989, P=0.032) on BARD score categories in patients with NAFLD. (ac.rs)

Cholesterol is a waxy substance found in your blood. (mayoclinic.org)

Hypothyroidism: People who have an underactive thyroid are more likely to have high levels of high-density lipoprotein (HDL). (healthreporter.com)
So, when you have an underactive thyroid, or hypothyroidism, your levels of total and LDL cholesterol go up. (medicinenet.com)

Menopause: Older women may experience an increase in HDL levels due to the changes they go through during menopause. (healthreporter.com)
When estrogen falls after menopause, your cholesterol goes up. (medicinenet.com)

When there's too much cholesterol in your blood, the cholesterol from LDL can increase your risk for developing cardiovascular diseases such as heart attack and stroke. (nih.gov)
Only recently, the treat stroke to target trial has demonstrated the benefit of aggressive LDL-cholesterol lowering for secondary stroke prevention. (eso-stroke.org)
A comparison of two ldl cholesterol targets after ischemic stroke. (eso-stroke.org)

In truth, HDL ranges " are among the most consistent and robust predictors of CVD [cardiovascular disease] risk. (healthyfountain.com)

LDL , the "bad" cholesterol, transports cholesterol particles throughout your body. (mayoclinic.org)

However, while treatment trials have shown that lowering LDL reduces the risk of heart disease, recent clinical trials haven't found that medicines aimed at raising HDL reduce the risk of heart attack. (nih.gov)
A team led by Dr. Sekar Kathiresan of Massachusetts General Hospital, Broad Institute and Harvard Medical School explored the relationship between HDL and heart disease using an approach called Mendelian randomization. (nih.gov)
If HDL is directly involved in heart disease, then inherited genetic variations that affect HDL levels should affect the risk of disease. (nih.gov)
Surprisingly, the researchers found that carriers of the HDL-boosting variant had the same risk for heart attack as non-carriers. (nih.gov)
The increase in HDL cholesterol linked to the genetic risk score wasn't associated with a lower risk of heart attack either. (nih.gov)
In contrast, the genetic score for LDL cholesterol accurately predicted heart attack risk. (nih.gov)
These results show that some ways of raising HDL cholesterol might not reduce risk of myocardial infarction [heart attack] in human beings. (nih.gov)
Future studies will be needed to understand both the role of HDL cholesterol and why its levels are associated with heart disease risk. (nih.gov)
It's possible that HDL itself may not directly lower the risk of heart disease but that blood HDL reflects another factor that does. (nih.gov)
An HDL cholesterol level of 119mg/dL is above optimal and can increase your risk of coronary heart disease and other cardiovascular diseases. (healthreporter.com)
You can monitor your cholesterol test results with a heart health app . (healthreporter.com)
It provides a space for users to monitor all aspects of their heart health, including blood pressure, LDL, and HDL levels. (healthreporter.com)
If your doctor suspects that your medications are causing your HDL levels to be above 119mg/dL, they may discuss dosage changes and other ways to reduce your HDL levels and your risk of heart disease while also keeping you on the medications you need. (healthreporter.com)
If you find you have high levels of HDL cholesterol and other family members have been diagnosed with heart disease before the age of 60 or died of a heart attack, your doctor may refer you to a specialist. (healthreporter.com)
Eating a whole, healthy, and balanced diet is one of the best ways that you can go about reducing your cholesterol level and, by extension, your risk of heart disease. (healthreporter.com)
The motive we know LDL ldl cholesterol actually is dangerous is as a result of individuals who had been simply born with genetically low LDL ldl cholesterol find yourself having a low danger of coronary heart illness. (healthyfountain.com)
In easy phrases: "High HDL may not protect the heart. (healthyfountain.com)
Physical activity is effective at lowering bad cholesterol levels because exercising muscles requires energy, explains Karol Watson, MD, PhD , a professor of medicine and cardiology, co-director of the UCLA Program in Preventive Cardiology, and director of the UCLA Barbra Streisand Women's Heart Health Program. (everydayhealth.com)
Brisk walking is great for lowering cholesterol, according to the American Heart Association, and most anyone can do it. (everydayhealth.com)
Running helps lower your cholesterol by increasing your heart rate. (everydayhealth.com)
You don't have to run a marathon or even a 5K to benefit your cholesterol levels - you simply have to get your heart pumping. (everydayhealth.com)
Your doctor might also suggest more-frequent tests if you have a family history of high cholesterol, heart disease or other risk factors, such as diabetes or high blood pressure. (mayoclinic.org)
It's linked with obesity, heart disease, and high cholesterol. (medicinenet.com)
To see if rhLCAT is a safe and effective method of improving HDL levels in people with heart disease. (nih.gov)

Illness and inflammation: Some infections and chronic inflammation could be the cause of an HDL level of 119mg/dL or more. (healthreporter.com)
Chronic stress causes a number of health problems, including high cholesterol. (medicinenet.com)

How can I raise my HDL level? (medlineplus.gov)
Getting regular exercise can raise your HDL level, as well as lower your LDL. (medlineplus.gov)
Some cholesterol medicines , including certain statins , can raise your HDL level, in addition to lowering your LDL level. (medlineplus.gov)
Health care providers don't usually prescribe medicines only to raise HDL. (medlineplus.gov)
Clinical trials are now underway to examine the cardiovascular benefits and risks of drug treatments that raise HDL levels. (nih.gov)
These oils can raise LDL cholesterol. (medicinenet.com)
Some medicines for high blood pressure, such as diuretics and older forms of beta-blockers, can also raise your cholesterol. (medicinenet.com)
Research shows that high cholesterol may harm kidney function and raise your risk of kidney disease. (medicinenet.com)

While circulating blood cholesterol is important to know about, you can also gauge increased cholesterol levels my examining the molecules that transport the cholesterol to the cells. (projectswole.com)
When there's too much sugar, it may attach to proteins, such as cholesterol molecules. (medicinenet.com)

Cholesterol is carried through your blood, attached to proteins. (mayoclinic.org)
This combination of proteins and cholesterol is called a lipoprotein. (mayoclinic.org)

The change in the percent stenosis of the most severe proximal lesions increased in association with higher concentrations of the small LDL subfractions LDL-IIIb (24.2-24.6 nm) and LDL-IVa (23.3-24.1 nm) before (both P = 0.002) and after (P = 0.01 and P = 0.03 respectively) adjustment for treatment group and on-study HDL-cholesterol, LDL-cholesterol, and triglyceride concentrations. (plos.org)

If you want to know how to lower your cholesterol with exercise, here are some great workouts that can help you start dropping those dangerous fats today! (projectswole.com)

There are several notable factors that can dramatically influence blood cholesterol levels. (projectswole.com)

Research shows that LDL and total cholesterol levels rise around and after your final period. (medicinenet.com)
Research shows that nephrotic syndrome, a type of kidney disorder, increases your LDL and total cholesterol levels. (medicinenet.com)
Obese women had a higher chance of being hypertensive and having high total TC, high TG, high LDL-C and low HDL-C levels than non-obese females. (who.int)

Here's a summary of how I plan to increase HDL cholesterol levels at the same time as reducing body fat percentage. (liveforever.club)
On the flip side, kidney problems may increase your cholesterol levels. (medicinenet.com)

High cholesterol can be inherited, but it's often the result of unhealthy lifestyle choices, which make it preventable and treatable. (mayoclinic.org)

Taking certain medicines can lower HDL levels in some people. (medlineplus.gov)
However, in young and otherwise healthy people, cholesterol levels are rarely determined. (eso-stroke.org)
For some people, high HDL levels are just a part of their genetic makeup. (healthreporter.com)
People over 65 should receive cholesterol tests annually. (mayoclinic.org)
Cholesterol and its role in our body is not something most people think about regularly, but it should be. (projectswole.com)
Second, you should try to lose weight since overweight individuals tend to exhibit higher cholesterol readings than thinner people due to the excess lipids floating around in their bodies. (projectswole.com)

Results: HDL-C regression equations obtained with CDC (x) and Osaka (y) were y=0.992x+0.542 (R 2 =0.996) for Osaka UC and y=1.004x-0.181 (R 2 =0.998) for DCM. (elsevier.com)

Higher levels of HDL, in contrast, have been associated with a lower risk of cardiovascular disease. (nih.gov)
The team confirmed that carriers of the LIPG 396Ser allele had higher HDL cholesterol than non-carriers but similar levels of other risk factors. (nih.gov)
In all age groups, a higher percentage of men had low levels of HDL cholesterol than women. (cdc.gov)
A higher percentage of men aged 40-59 years had low levels of HDL cholesterol than men aged ≥60 years. (cdc.gov)

There are a few ways your HDL levels can reach a point where they stop being protective and become dangerous. (healthreporter.com)
Having a excessive blood HDL stage is "no longer regarded as protective. (healthyfountain.com)
They also have lower amounts of protective HDL cholesterol. (medicinenet.com)

All patients received simvastatin, 40 to 80 mg per day, plus ezetimibe, 10 mg per day, if needed, to maintain an LDL cholesterol level of 40 to 80 mg per deciliter (1.03 to 2.07 mmol per liter). (nih.gov)

All exercises that expend energy will lower cholesterol ," Watson says. (everydayhealth.com)
Because aerobic exercises expend the most energy, they'll usually lower cholesterol most. (everydayhealth.com)
Does Exercise Lower Cholesterol? (projectswole.com)

It is a type of fat in your blood that helps remove extra cholesterol from your body. (nih.gov)
Your body uses thyroid hormones to help remove the extra cholesterol that it doesn't need. (medicinenet.com)

This makes cholesterol more harmful. (medicinenet.com)

If your doctor suspects that your 119mg/dL HDL levels are caused by your diet, they will likely suggest making lifestyle changes first. (healthreporter.com)
This is to find out whether your high HDL levels are caused by your diet or other factors. (healthreporter.com)
A healthy diet, regular exercise and sometimes medication can help reduce high cholesterol. (mayoclinic.org)
We reported previously that a very low carbohydrate diet favorably affected fasting and postprandial triacylglycerols, LDL subclasses and HDL cholesterol (HDL-C) in men but the effects in women are unclear. (edu.au)

Anatomy22

Organisms8

Diseases29

Chemicals and Drugs148

Analytical, Diagnostic and Therapeutic Techniques and Equipment22

Psychiatry and Psychology1

Phenomena and Processes29

Technology, Industry, Agriculture16

Health Care11

Geographicals1

Serum triglyceride: a possible risk factor for ruptured abdominal aortic aneurysm. (1/5144)

Association of the inflammatory state in active juvenile rheumatoid arthritis with hypo-high-density lipoproteinemia and reduced lipoprotein-associated platelet-activating factor acetylhydrolase activity. (2/5144)

Chlamydia pneumoniae antibodies are associated with an atherogenic lipid profile. (3/5144)

Effect of fasting on temporal variation in the nephrotoxicity of amphotericin B in rats. (4/5144)

The impact of an amino acid-based peritoneal dialysis fluid on plasma total homocysteine levels, lipid profile and body fat mass. (5/5144)

Survey of total error of precipitation and homogeneous HDL-cholesterol methods and simultaneous evaluation of lyophilized saccharose-containing candidate reference materials for HDL-cholesterol. (6/5144)

Elevated hepatic lipase activity and low levels of high density lipoprotein in a normotriglyceridemic, nonobese Turkish population. (7/5144)

Comparison of synthetic saponin cholesterol absorption inhibitors in rabbits: evidence for a non-stoichiometric, intestinal mechanism of action. (8/5144)

Cholesterol

Cholesterol, HDL

Cholesterol, LDL

Lipids

Lipoproteins, HDL

Cholesterol, Dietary

Cholesterol Esters

Lipoproteins, HDL2

Cholesterol Oxidase

Cholesterol 7-alpha-Hydroxylase

Apolipoprotein A-I

Lipoproteins

Triglycerides

Cholesterol, VLDL

Anticholesteremic Agents

Hypercholesterolemia

Sterol O-Acyltransferase

ATP Binding Cassette Transporter 1

Lipoproteins, LDL

Sterols

Apolipoproteins

Hydroxymethylglutaryl CoA Reductases

Phosphatidylcholine-Sterol O-Acyltransferase

Bile Acids and Salts

Liver

Cholesterol Ester Transfer Proteins

Lipid Metabolism

Phospholipids

Bile

Sitosterols

beta-Cyclodextrins

ATP-Binding Cassette Transporters

Esterification

Hyperlipidemias

Hydroxycholesterols

Scavenger Receptors, Class B

Dietary Fats

Phytosterols

Apolipoproteins B

Cyclodextrins

Apolipoprotein A-II

Apolipoproteins E

Phosphatidylcholines

Lipoproteins, VLDL

Biological Transport

Arteriosclerosis

Receptors, LDL

Lovastatin

Cholestyramine Resin

Desmosterol

Receptors, Lipoprotein

Hydroxymethylglutaryl-CoA Reductase Inhibitors

Apolipoproteins A

Mevalonic Acid

Hypolipidemic Agents

Filipin

Diet, Atherogenic

Sterol Esterase

Intestinal Absorption

Sphingomyelins

Membrane Microdomains

High-Density Lipoproteins, Pre-beta

Cholestanol

Atherosclerosis

Azetidines

Cholelithiasis

Risk Factors

Orphan Nuclear Receptors

Androstenes

Lanosterol

Tangier Disease

Foam Cells

Fatty Acids

Simvastatin

Receptors, Scavenger

Antigens, CD36

Dehydrocholesterols

Embolism, Cholesterol

Dyslipidemias

Membrane Lipids