The relation of serum very low density lipoproteins (VLDL) to hepatic steatosis was studied during protein malnutrition followed by refeeding of a balanced diet in growing rats. A control group was fed a balanced diet containing 15% casein for 42 days. Two depleted groups were fed low protein diets containing 2% casein (group C) or 5% gluten (group GI) (protein malnutrition phase) for 28 days and then were fed the balanced diet for 14 days (refeeding phase). The concentrations of phospholipids and proteins in both liver and serum VLDL were decreased during protein malnutrition, whereas triacylglycerols, unesterified cholesterol, and cholesteryl esters were higher in the liver and lower in the serum VLDL in the C and GI groups compared with the control group. There was a significant inverse relation between serum VLDL apolipoproteins and liver triacylglycerols on the one hand and between serum VLDL triacylglycerols and liver triacylglycerols on the other hand, in both depleted groups, although this
The effect of human plasma lipoproteins on lipogenesis from glucose has been studied in isolated rat adipocytes. The very-low-density lipoproteins increased lipogenesis specifically, whereas low-density lipoproteins and high-density lipoproteins were without effect. Such stimulation could be reproduced with partially delipidated very-low-density lipoproteins. Nod-esterified fatty acids and glycerol were also without effect. Pretreatment of the adipocytes with trypsin did not alter the effect of very-low-density lipoprotein. The presence of Ca2+ was required for the full activation of lipogenesis. The synthesis of acylglycerol fatty acids and of acylglycerol glycerol were equally increased. The effect of very-low-density lipoprotein was not additive to that of insulin. It is suggested that very-low-density lipoprotein may directly stimulate lipogenesis in fat-cells, particularly in states when the lipoproteins are present at high concentration in the circulation. ...
Macrophage receptor that binds to the apolipoprotein B48 (APOB) of dietary triglyceride (TG)-rich lipoproteins (TRL) or to a like domain of APOB in hypertriglyceridemic very low density lipoprotein (HTG-VLDL). Binds and internalizes TRL when out of the context of the macrophage. May provide essential lipids to reticuloendothelial cells. Could also be involved in foam cell formation with elevated TRL and remnant lipoprotein (RLP). Mediates the rapid high-affinity uptake of chylomicrons (CM), HTG-VLDL, and trypsinized (tryp) VLDL devoid of APOE in vitro in macrophages.
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Overproduction of VLDL-TG by the liver is a prominent sequel of insulin resistance, obesity, and diabetes1,2,32,33 and leads to dyslipidemia and cardiovascular disease.32,34 We here report, for the first time to our knowledge, that glycine lowers hepatic VLDL-TG secretion via the central nervous system (CNS). Glycine is the smallest nonessential amino acid and a coagonist of the NMDA receptor along with glutamate.29,30 NMDA receptors in the CNS are important for neurotransmission and have critical roles in mechanisms of synaptic plasticity and network synchronization.29 Our current study demonstrates that glycine-induced potentiation of NR1-containing NMDA receptors in the DVC is sufficient to trigger the hepatic vagus and lower VLDL-TG secretion in normal rats.. The NR1 subunit is an obligatory subunit that forms a functional NMDA receptor when combined with either NR2 or NR3 subunits.29 A typical NMDA receptor is a tetramer that most often consists of 2 glycine-binding NR1 subunits and 2 ...
Accelerated turnover of very low density lipoprotein triglycerides in chronic alcohol users. A possible mechanism for the up-regulation of high density lipoprotein by ethanol. doi: 10.1016/0021-9150(84)90194-1. The Reason: This one actually caught my attention not only because of the topic of the paper, but also because of its implications beyond the population studied. In short, frequent consumers of alcohol can present with an abnormally high HDL level, and this can eventually progress to high HDL along with high triglycerides. An unusual profile, for sure, and also one that can lead to thinking theyre healthier than they actually are, just by looking at their lipid profile. If you ask them to stop drinking for a while, their HDL goes back to reflecting their normal level. They found, in short, that this was likely due to rapid cycling of VLDL - both increased production, and increased clearance - resulting in higher HDL levels. I found this bit interesting, and perhaps especially relevant in ...
Hypertriglyceridemia is very common in diabetes and substantially increases the risk of cardiovascular diseases. Similarly, insulin resistance is associated with elevated plasma TGs and predisposes for cardiovascular complications. Although the regulation of circulating TG-rich lipoproteins is extremely complex in diabetes and insulin resistance, many studies consider increased hepatic VLDL secretion and impaired VLDL clearance mechanisms for dyslipidemia (5,6). It is postulated that the overall effect of insulin resistance and diabetes on VLDL production reflects raised fatty acid flux to the liver (6). Consequently, there is a stimulation of the assembly and output of apo B-100-containing lipoproteins (6,16). The aim of our investigation was to examine whether intestinal TG metabolism is also altered in Psammomys obesus animals that are characterized by insulin resistance and diabetes (17,18). We demonstrated that the development of the insulin-resistant/diabetic state is accompanied by 1) an ...
Hepatic steatosis is common in obesity and insulin resistance and results from a net retention of lipids in the liver. A key mechanism to prevent steatosis is to increase secretion of triglycerides (TG) packaged as very low-density lipoproteins (VLDL). Insulin controls nutrient partitioning via signaling through its cognate receptor in peripheral target organs such as liver, muscle and adipose tissue and via signaling in the CNS to orchestrate organ cross talk. While hepatic insulin signaling is known to suppress VLDL production from the liver, it is unknown whether brain insulin signaling independently regulates hepatic VLDL secretion. Here we show that in conscious, unrestrained male Sprague Dawley rats the infusion of insulin into the 3rd ventricle acutely increased hepatic TG secretion. Chronic infusion of insulin into the CNS via osmotic minipumps reduced the hepatic lipid content as assessed by non-invasive 1H-magnetic resonance spectroscopy and lipid profiling independent of changes in ...
ApoB-containing lipoproteins are assembled in at least 2 stages.11,13,17 The first of these, with the initiation step resulting in VLDL precursors, involves the folding of apoB into a precise secretion-competent conformation by interaction with the membrane lipids of the endoplasmic reticulum.17 In the present work, particles similar to the VLDL precursors were secreted in association with the HDL fraction of the medium (Figure 2), as has been shown previously.18,19 The second step, the maturation phase, depends on fusion of the VLDL precursor with a neutral, lipid-rich, apoB-free particle to produce full-size VLDL.17. Insulin inhibits the overall assembly of VLDL from apoB (see review1) by a mechanism that involves an increase in apoB degradation. Insulin injection directly into the portal vein in humans decreases VLDL output into the hepatic vein.4 A postprandial decrease in splanchnic VLDL output after an oral glucose load has also been reported,20 and increased portal insulin resulting from ...
Chronic inflammatory diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and psoriasis and infections, such as periodontal disease and HIV, are associated with an increased risk of cardiovascular disease. Patients with these disorders also have an increase in coronary artery calcium measured by CT and carotid intima media thickness measured by ultrasound. Inflammation and infections induce a variety of alterations in lipid metabolism that may initially dampen inflammation or fight infection, but if chronic could contribute to the increased risk of atherosclerosis. The most common changes are decreases in serum HDL and increases in triglycerides. The increase in serum triglycerides is due to both an increase in hepatic VLDL production and secretion and a decrease in the clearance of triglyceride rich lipoproteins. The mechanisms by which inflammation and infection decrease HDL levels are uncertain. There is also a consistent increase in lipoprotein (a) levels due to increased
Monoclonal antibody produced in mouse. Useful for ELISA. Binds to an epitope on the C-terminus of VLDL receptor ligand binding domain (amino acids 191-355, UniProtKB: locus VLDLR_HUMAN, accession P98155) and blocks apoE4 binding. Purified by immobilized Protein A. IgG1 class ...
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MRSA has a switch in its DNA which controls 4 genes that determine whether it sits on the skin surface as a virtual commensal or invades the tissues as a pathogen. One of these genes codes for a signalling peptide called AIP. In fact there is a choice of four different AIPs, AIP 1 being the one possessed by many particularly nasty clinical isolates of MRSA. AIP 1 is essential for the virulence of the bug and it is bound by the apoB100 protein. This binding is particularly effective when the protein is where it belongs, sitting on the surface of an LDL or VLDL particle. What seems to happen is that the AIP 1, which is lipid soluble, ends up in the lipid centre of the lipoprotein. In the mele of an acute infection the LDL particle becomes oxidised and so gets eaten, along with its AIP 1 burden, by a macrophage. Thus endeth the virulence factor of the MRSA, unless you have particularly low LDL or VLDL lipoprotein levels. In which case you are in big trouble ...
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When it comes to heart health, lipoproteins are commonly a topic of discussion. These crucial molecules transport fat-soluble substances through your bloodstream and play a vital role in your health. ...
TY - JOUR. T1 - The effect of a six-month exercise program on very low density lipoprotein apolipoprotein B secretion in type 2 diabetes. AU - Alam, S.. AU - Stolinski, M.. AU - Pentecost, C.. AU - Boroujerdi, Massoud. AU - Jones, R. H.. AU - Sonksen, P. H.. AU - Umpleby, A. M.. PY - 2004. Y1 - 2004. N2 - The dyslipidemia and insulin resistance of type 2 diabetes can be improved by aerobic exercise. The effect of 6 months supervised exercise on very low-density lipoprotein (VLDL) apolipoprotein B metabolism was investigated in patients with type 2 diabetes. Moderately obese patients (n = 18) were randomized into supervised (n = 9) and unsupervised (n = 9) exercise groups. All patients were given a training session and a personal exercise program and asked to exercise four times per week at 70% maximal oxygen uptake for 6 months. Patients in the supervised group had a weekly session with an exercise trainer. VLDL apolipoprotein (apo) B metabolism was measured with an infusion of 1-C-13 leucine ...
Exogenous estrogens (ethinyl estradiol, 1 µg/kg body weight per day), which stimulate triglyceride production in normal women and those with endogenous hypertriglyceridemia, were found to exert a paradoxical, hypolipidemic effect in six subjects (five women, one man) with type III hyperlipoproteinemia on diets both of normal and of fat-free, high-carbohydrate composition. Moreover, very low-density (VLD) lipoprotein lipid and apolipoprotein composition and electrophoretic mobility became normal during estrogen administration in these subjects. Levels of normal VLD lipoproteins remained mildly to moderately elevated in a type IV lipoprotein pattern. Estrogen withdrawal promptly restored the type III pattern with its abnormal enrichment of VLD lipoproteins with apolipoprotein E (the arginine-rich peptide). These findings suggest that estrogens facilitate the assimilation of chylomicron and VLD lipoprotein remnants, a defect that appears likely to represent the metabolic abnormality underlying ...
TY - JOUR. T1 - Hepatitis C virus. T2 - A new class of virus associated with particles derived from very low-density lipoproteins. AU - Ye, Jin. PY - 2012/5/1. Y1 - 2012/5/1. N2 - Hepatitis C virus (HCV) infects 3% of the world population and is the leading cause of liver failure in the United States. A unique feature of HCV is that the viral particles are integral to very low-density lipoprotein (VLDL)-derived lipoprotein particles. The virus is assembled into VLDL in hepatocytes and released out of the cells together with VLDL. The virus then infects more hepatocytes by entering the cells through the low-density lipoprotein receptor, which mediates uptake of majorities of VLDL-derived lipoprotein particles. These observations suggest that HCV may belong to a novel class of viruses that is associated with VLDL. Understanding the relationship between HCV and VLDL metabolism may reveal new strategies to treat HCV infection.. AB - Hepatitis C virus (HCV) infects 3% of the world population and is ...
The liver secretes triglyceride-rich VLDLs, and the triglycerides in these particles are taken up by peripheral tissues, mainly heart, skeletal muscle, and adipose tissue. Blocking hepatic VLDL secretion interferes with the delivery of liver-derived triglycerides to peripheral tissues and results in an accumulation of triglycerides in the liver. However, it is unclear how interfering with hepatic triglyceride secretion affects adiposity, muscle triglyceride stores, and insulin sensitivity. To explore these issues, we examined mice that cannot secrete VLDL [due to the absence of microsomal triglyceride transfer protein (Mttp) in the liver]. These mice exhibit markedly reduced levels of apolipoprotein B-100 in the plasma, along with reduced levels of triglycerides in the plasma. Despite the low plasma triglyceride levels, triglyceride levels in skeletal muscle were unaffected. Adiposity and adipose tissue triglyceride synthesis rates were also normal, and body weight curves were unaffected. Even ...
ApoC-II was the only apolipoprotein from human very low density lipoprotein that activated rat adipose tissue lipoprotein lipase. Activation was blocked by antiserum against apoC-II. Addition of increasing amounts of activator did not alter the apparent Km of lipoprotein lipase (0.32 mM triolein), but it did produce a progressive increase in the apparent Vmax from 0.8 to 2.2 µmoles free fatty acid/mg hour-1. Substrate concentrations above 1.27 mM triolein diminished activation by 0.25-5.0 µg/ml of apoC-II as much as 20%. Reversal of this apparent substrate inhibition was achieved by increasing the activator concentration to 50.0 µg/ml. Each of five nonactivating apolipoproteins-apoC-I, C-III-1, C-III-2, A-I, and A-II-inhibited lipoprotein lipase up to 85-100%. ApoC-II also produced less inhibition under appropriate conditions. Inhibition was dependent on apoprotein concentration, inversely related to substrate triglyceride concentration, and unobserved with nonlipoprotein proteins. The ...
Hypothesis 1: Ritonavir-based regimens increase triglycerides and VLDL by both increasing VLDL production and decreasing VLDL clearance.. Specific Aim 1A: To quantify the effect of ritonavir on VLDL production and clearance using stable isotope turnover and other clearance methods.. Specific Aim 1B: To determine the composition of the triglyceride rich particles.. Protocol 1: The effects of ritonavir-based regimens on VLDL production, VLDL clearance and triglyceride-rich lipoprotein composition in healthy normal volunteers. HIV-seronegative volunteers will be studied before and at the end of four weeks of taking ritonavir, lopinavir/ritonavir or atazanavir/ritonavir.. Hypothesis 2: NNRTI drugs do not increase HDL by increasing apo AI production, but rather by decreasing apo AI clearance, prolonging time in circulation.. Specific Aim 2A: To determine the composition of HDL before and after NNRTI and assess its function.. Specific Aim 2B: To quantify the effect of NNRTI on apo AI production and ...
Hypothesis 1: Ritonavir-based regimens increase triglycerides and VLDL by both increasing VLDL production and decreasing VLDL clearance.. Specific Aim 1A: To quantify the effect of ritonavir on VLDL production and clearance using stable isotope turnover and other clearance methods.. Specific Aim 1B: To determine the composition of the triglyceride rich particles.. Protocol 1: The effects of ritonavir-based regimens on VLDL production, VLDL clearance and triglyceride-rich lipoprotein composition in healthy normal volunteers. HIV-seronegative volunteers will be studied before and at the end of four weeks of taking ritonavir, lopinavir/ritonavir or atazanavir/ritonavir.. Hypothesis 2: NNRTI drugs do not increase HDL by increasing apo AI production, but rather by decreasing apo AI clearance, prolonging time in circulation.. Specific Aim 2A: To determine the composition of HDL before and after NNRTI and assess its function.. Specific Aim 2B: To quantify the effect of NNRTI on apo AI production and ...
Previously we showed that chemical inhibition of iPLA2β in rat hepatoma McA-RH7777 cells attenuated hepatic VLDL assembly/secretion. To gain an insight into the role that iPLA2β plays in vivo, we generated C57BL/6 mice with targeted disruption of iPLA2β gene. The iPLA2β−/− mice developed normally to their maturity. Under chow diet conditions, female iPLA2β−/− and wild-type littermate (10-week-old) displayed no discernable difference in plasma lipid concentration or apolipoprotein levels, nor was their plasma lipoprotein profiling changed as determined by rate floatation ultracentrifugation. However, iPLA2β−/− mice liver accumulated 20% less triacylglycerol (TG) than wt controls, whereas phosphatidylcholine (PC) and phosphatidylethanolamine (PE) levels were not significantly different. Determination of VLDL-TG production rate in vivo using mice injected with poloxamer 407 (to block the lipoprotein lipase activity) revealed that accumulation of plasma TG in iPLA2β−/− mice ...
a) Theres no connection whatsoever between cholesterol in food and cholesterol in blood and weve known that all along.. b) LDL stands for Low Density Lipoprotein. LDL is not cholesterol, let alone bad. LDL carries cholesterol and protein and triglycerides and phospholipids. How a carrier of four substances ends up being called one of them, I know not.. c) LDL is the residue of IDL (Intermediate Density Lipoprotein); IDL is the residue of VLDL (Very Low Density Lipoprotein). LDL, IDL and VLDL are all lipoproteins (think of lipoproteins as taxis that transport cholesterol, protein, triglycerides and phospholipids around the body to do their vital, life saving work). Another lipoprotein (the largest) is called a chylomicron and this transports dietary fat from the digestive system around the body to do its vital work. How any dietary fat, saturated or otherwise, leaps out of chylomicrons and finds its way into VLDL and then IDL and then LDL "to cause havoc in blood cells" is not only ...
Class of lipoproteins that transport triglycerides from the intestine and liver to adipose and muscle tissues. Synthesized by the liver, they contain primarily triglycerides in their lipid cores, with some cholesterol esters. As their triglycerides are cleaved by endothelial lipoprotein lipase and transferred to hepatic tissues, the VLDL (very-low-density lipoprotein) particles lose most of their apolipoprotein C and become intermediate-density lipoproteins. ...
Results A higher triglyceride/cholesterol ratio of LDL was found more in HCV-infected donors than in healthy volunteers, and the triglyceride/cholesterol ratio of LDL-LVP was much increased, suggesting that the LPL hydrolysis of triglyceride may be impaired. VLDL, VLDL-LVP, LDL-LVP, but not LDL, suppressed LPL lipolytic activity, which was restored by antibodies that recognised apoC-III/-IV and correlated with the steadily abundant apoC-III/-IV quantities in those particles. In a cell-based system, treatment with VLDL and LVPs reversed the LPL-mediated inhibition of HCV infection in apoC-III/-IV-dependent manners. A multivariate logistic regression revealed that plasma HCV viral loads correlated negatively with LPL lipolytic activity, but positively with the apoC-III content of VLDL. Additionally, apoC-III in VLDL was associated with a higher proportion of HCV-RNA than was IgG.. ...
TY - JOUR. T1 - Effect of dietary triacylglycerol structure on lipoprotein metabolism. T2 - A comparison of the effects of dioleoylpalmitoylglycerol in which palmitate is esterified to the 2-or 1(3)-position of the glycerol. AU - Pufal, Deborah A. AU - Quinlan, Paul T. AU - Salter, Andrew M. PY - 1995/8/24. Y1 - 1995/8/24. N2 - The effect on lipoprotein metabolism of diets enriched in different isomers of dioleoylpalmitoylglycerol was studied. One diet contained fat in which palmitate was esterified to the two outer positions of the glycerol (OOP) and the other in which it was esterified to the middle carbon (OPO). The lipid composition of chylomicrons was similar in rats fed either fat blend. However, triacylglycerol (TAG) in chylomicrons from OPO fed animals was relatively enriched in palmitic acid, at the expense of stearic, oleic and linoleic acids. Silver phase HPLC and 2-positional analysis clearly demonstrated that the identity of the fatty acid in the 2-position was similar in both ...
This gene encodes a member of the apolipoprotein C1 family. This gene is expressed primarily in the liver, and it is activated when monocytes differentiate into macrophages. The encoded protein plays a central role in high density lipoprotein (HDL) and very low density lipoprotein (VLDL) metabolism. This protein has also been shown to inhibit cholesteryl ester transfer protein in plasma. A pseudogene of this gene is located 4 kb downstream in the same orientation, on the same chromosome. This gene is mapped to chromosome 19, where it resides within a apolipoprotein gene cluster. Alternative splicing and the use of alternative promoters results in multiple transcript variants. [provided by RefSeq, Sep 2016 ...
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VLDL definition, very-low-density lipoprotein: a plasma lipoprotein with a high lipid content, associated with atherosclerosis. See more.
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Very low density lipoprotein is produced by the liver. It transports fat from the liver to other tissue such as adipose tissue. VLDL consists of a single layer of phospholipid and cholesterol....
Glucose. It is a primary source of energy. When its transported into the body, it stimulates pancreas to produce insulin. Our brain notices this increase, understands metabolism & gradually reduces hunger. This is mainly by the "Feed Back Mechanism". There are many processes involved when you consume glucose, but one that occurs in your liver produces very low density lipoprotein (the bad cholestoral)(VLDL) Fortunately, only about 1 out of 24 calories from glucose that are processed by the liver turn into VLDL [7].. Fructose. Fructose is considered bad because of how its processed by the body. Firstly, there is no hormone to remove fructose from our bloodstream (unlike glucose, which stimulates insulin production). Fructose can only be metabolized by liver. This means a greater number of calories which is about three times more than glucose which is metabolized in liver, results in much higher production of VLDL and fat [7]. Fructose fools metabolism by turning off bodys appetite-control ...
In a meal-eating omnivore such as the human, excess calories are ingested in the anabolic phase of the feeding cycle, followed by a period of negative caloric balance when the organism draws upon its carbohydrate and fat stores. Lipoproteins mediate this cycle by transporting lipids from the intestines as chylomicrons-and from the liver as very low density lipoproteins (VLDL)-to most tissues for oxidation and to adipose tissue for storage. Lipid is mobilized from adipose tissue as free fatty acids (FFA) bound to serum ...
குறையடர்த்தி கொழுமியப்புரதம் (Low density lipoprotein; LDL) ஐந்து பெரும் கொழுமியப்புரதத் தொகுப்புகளுள் ஒன்றாகும். கொழுமியப்புரதத் தொகுப்புகளை பெரிய அளவுகளிலிருந்து சிறிய அளவிற்கு பின்வறுமாறு வரிசைப்படுத்தலாம்: கைலோமைக்ரான்கள், மிகு-குறையடர்த்தி கொழுமியப்புரதம் (VLDL), இடைநிலையடர்த்தி கொழுமியப்புரதம் (IDL), குறையடர்த்தி கொழுமியப்புரதம் (LDL) மற்றும் உயரடர்த்தி கொழுமியப்புரதம் (HDL). ...
QUESTION: Hi Im Ma.Luisa Villareal. My vldl is 53 and my triglycerides are 265. What should I do to get normal level? ANSWER: Hello, I read your
The LDL and VLDL are not a good idea as well as your health, while High-density lipo protein may be the great one. No matter if Cholesterol lowering foods
Hepatic histology and expressions of VLDL, L-FABP and FATP4 in liver tissues.(A) Representative images (200×magnification, haematoxylin and eosin stain) of hep
Affiliation:東京大学,先端科学技術研究センター,特任准教授, Research Field:Pathological medical chemistry,Pharmacology in pharmacy,Applied health science,General pharmacology, Keywords:核内受容体,PPARδ,LRP5,very low-density lipoprotein,Acetyl-CoA synthetase,islet,SOX6,Wnt signal,PDX-1,insulin, # of Research Projects:7, # of Research Products:34
TY - JOUR. T1 - Lack of association of very low density lipoprotein receptor gene polymorphism with caucasian Alzheimers disease. AU - Okuizumi, Kaoru. AU - Onodera, Osamu. AU - Seki, Koji. AU - Tanaka, Hajime. AU - Namba, Yoshio. AU - Ikeda, Kazuhiko. AU - Saunders, Ann M.. AU - Pericak-Vance, Margaret A. AU - Roses, Allen D.. AU - Tsuji, Shoji. PY - 1996/8/1. Y1 - 1996/8/1. N2 - To determine whether the association of the very low density lipoprotein receptor (VLDL-R) gene with AIzheimers disease (AD), which has recently been identified in Japanese AD patients, is commonly observed in AD patients of other ethnic backgrounds, we have investigated the allele frequency of the polymorphic CGG repeat in the 5-UTR of the VLDL-R gene using a data set of 84 caucasian AD patients with 104 caucasian controls. Although the allele frequency of the 8-repeat allele was slightly lower, and that of 9-repeat allele was slightly higher, in the caucasian AD patients than in caucasian controls, the differences ...
Lipoproteins contain a core of hydrophobic lipids (triglycerides and cholesteryl esters) surrounded by a shell of hydrophilic lipids (phospholipids, unesterified cholesterol) and proteins (called apolipoproteins) that interact with body fluids. The plasma lipoproteins are divided into five major classes based on their relative density (Fig. 27-1 and Table 27-1): chylomicrons, very-low-density lipoproteins (VLDLs), intermediate-density lipoproteins (IDLs), low-density lipoproteins (LDLs), and high-density lipoproteins (HDLs). Each lipoprotein class comprises a family of particles that vary in density, size, and protein composition. Because lipid is less dense than water, the density of a lipoprotein particle is primarily determined by the amount of lipid per particle. Chylomicrons are the most lipid-rich and therefore least dense lipoprotein particles, whereas HDLs have the least lipid and are therefore the most dense lipoproteins. In addition to their density, lipoprotein particles can be ...
Lipoproteins contain a core of hydrophobic lipids (triglycerides and cholesteryl esters) surrounded by a shell of hydrophilic lipids (phospholipids, unesterified cholesterol) and proteins (called apolipoproteins) that interact with body fluids. The plasma lipoproteins are divided into five major classes based on their relative density (Fig. 421-1 and Table 421-1): chylomicrons, very-low-density lipoproteins (VLDLs), intermediate-density lipoproteins (IDLs), low-density lipoproteins (LDLs), and high-density lipoproteins (HDLs). Each lipoprotein class comprises a family of particles that vary in density, size, and protein composition. Because lipid is less dense than water, the density of a lipoprotein particle is primarily determined by the amount of lipid per particle. Chylomicrons are the most lipid-rich and therefore least dense lipoprotein particles, whereas HDLs have the least lipid and are therefore the most dense lipoproteins. In addition to their density, lipoprotein particles can be ...
Sixteen pigs from 2 distinct genetic lines (LGAH and VFIL) obtained after eight generations of divergent selection for high (H) and low (L) lean tissue growth rate with ad-libitum feeding (LGA) and voluntary feed intake (VFI), respectively, were used in this study. The objectives of this investigation were to establish appropriate working conditions for the postheparin plasma lipoprotein lipase (LPL) assay and to study relationships between fat deposition and plasma lipids, very low density lipoprotein (VLDL) lipids, VLDL-subfractions and postheparin plasma LPL activity in growing pigs. Four preliminary experiments were performed to determine the appropriate working conditions for the postheparin plasma LPL assays. Postheparin plasma preincubated with SDS (20-50 mM) at 26 C for 45 minutes inhibited hepatic lipase activity. A total of 2 l VLDL/assay produced maximum stimulation of LPL activity. Postheparin plasma protein and increasing incubation time contributed an optimum response. LGAH pigs ...
Patti, Lidia, Swinburn, Boyd, Riccardi, Gabriele, Rivellese, Angela A. and Howard, Barbara V. 1991, Alterations in very low density lipoprotein subfractions in normotriglyceridemic non-insulin-dependent diabetics, Atherosclerosis, vol. 91, no. 1-2, pp. 15-23, doi: 10.1016/0021-9150(91)90183-4. ...
In this report, the authors used nuclear magnetic resonance (NMR) spectroscopy to measure different apoB-containing lipoprotein particle concentrations in 11,984 subjects from the JUPITER study population. The variables of interest were LDL (large, small), intermediate-density lipoproteins (IDL), and very low-density lipoproteins (VLDL, large, medium and small) particle subclasses, VLDL-cholesterol and VLDL/chylomicron triglycerides. In the statin-treated group, in which median LDL-C was 55 mg/dl (1.4 mmol/L), there was no association between LDL or IDL particle concentration and risk for major adverse cardiovascular events (MACE). There was, however, an association for VLDL particle concentration, specifically driven by small VLDL particles. Indeed, each increase by one standard deviation in small VLDL particle concentration was associated with 68% increase in the residual risk of MACE. This finding is consistent with mechanistic studies of lipoprotein/arterial wall interactions, which show ...
This test measures the amount of very low-density lipoprotein (VLDL) in your blood.. VLDL cholesterol is a type of blood fat. Its considered one of the "bad" forms of cholesterol, along with LDL cholesterol and triglycerides. This is because high levels cholesterol can clog your arteries and lead to a heart attack. Sixty percent of a VLDL particle is a triglyceride, This test is usually used along with a series of other tests in a general lipid profile to screen for cardiovascular disease (CVD). High levels of VLDL cholesterol and triglycerides in your blood may mean you are at risk for CVD. People who are obese also have higher levels of VLDL cholesterol. ...
Very low density lipoproteins (VLDL) are smaller and more dense than chylomicrons (see Figure 2). VLDLs contain triacylglycerols, some cholesterol and cholesteryl esters and the apoproteins; apo- B100, apo-CI, apo-CII, apo-CIII, and apoE. VLDLs exist to remove triacylglycerols and cholesteryl esters from the liver and distribute them throughout the body. As VLDLs move into the circulating plasma they are converted first to intermediate density lipoproteins (IDL) and then into low density lipoproteins (LDL). Lipoprotein lipase serves to remove the majority of fatty acids from both the VLDL and IDL, thus increasing the density of the lipoproteins while maintaining cholesterol and cholesteryl ester concentrations. The removal of fatty acids and the loss of all apolipoproteins except apoB-100 and apo(a) results in LDL. LDLs are the primary plasma carriers of cholesterol for delivery to all tissues. LDL can be absorbed by the liver and other tissues via receptor mediated endocytosis.. ...
Deciphering novel pathways that regulate liver lipid content has profound implications for understanding the pathophysiology of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Recent evidence suggests that the nuclear envelope is a site of regulation of lipid metabolism, but there is limited appreciation of the responsible mechanisms and molecular components within this organelle. We showed that conditional hepatocyte deletion of the inner nuclear membrane protein lamina-associated polypeptide 1 (LAP1) causes defective VLDL secretion and steatosis, including intranuclear lipid accumulation. LAP1 binds to and activates torsinA, an AAA+ ATPase that resides in the perinuclear space and continuous main ER. Deletion of torsinA from mouse hepatocytes caused even greater reductions in VLDL secretion and profound steatosis. Mice from both of the mutant lines studied developed hepatic steatosis and subsequent steatohepatitis on a regular chow diet in the absence of ...
We have investigated whether arterial wall low density lipoprotein (LDL) metabolism in areas of disturbed flow differs from the metabolism in adjacent regions of undisturbed flow. Using the rabbit aorto-iliac bifurcation as a model, we examined the rates of LDL incorporation and catabolism in vivo and correlated them to the arterial flow patterns in these regions. The trapped ligand method was used to quantitate the rates of LDL incorporation and degradation over a 20-hour period in three hemodynamic zones of the daughter iliac branch: 1) a region of flow separation where the shearing forces are elevated along the medial wall and reduced along the lateral wall, 2) a transition region where the flow patterns begin to approach the fully established situation, and 3) a unidirectional flow region with symmetric fluid shearing forces along the medial and lateral walls. Our results indicate an elevated rate of LDL incorporation into the lateral versus the medial wall in the proximal zone of flow ...