Apolipoproteins E
Apolipoproteins C
Apolipoproteins
Apolipoprotein C-III
Apolipoprotein E3
Apolipoproteins A
Lipoproteins
Apolipoproteins B
Apolipoprotein A-I
Apolipoprotein A-II
Apolipoprotein C-II
Lipoproteins, HDL
Apolipoproteins D
Apolipoprotein C-I
Cholesterol
Lipoproteins, VLDL
Lipids
Apolipoprotein B-100
Apolipoprotein B-48
Cholesterol, HDL
Lipoproteins, HDL3
Tangier Disease
Phosphatidylcholine-Sterol O-Acyltransferase
Lipoproteins, LDL
Nephelometry and Turbidimetry
ATP Binding Cassette Transporter 1
Cholesterol Esters
Isoelectric Focusing
Receptors, Lipoprotein
Lipid Metabolism
Chylomicrons
Cholesterol, LDL
Phospholipids
Ultracentrifugation
Hypolipoproteinemias
Lipoproteins, HDL2
Lipoprotein(a)
Electrophoresis, Polyacrylamide Gel
Apoproteins
Liver
Immunodiffusion
Lipoprotein Lipase
Hyperlipoproteinemia Type IV
Phosphatidylcholines
ATP-Binding Cassette Transporters
Hyperlipoproteinemias
Chemistry, Clinical
Cholesterol, VLDL
Cholesterol Ester Transfer Proteins
Lipoproteins, IDL
Reference Values
Scavenger Receptors, Class B
Freeze Drying
Ethinyl Estradiol
Immunoassay
Serum Amyloid A Protein
Dietary Fats
Microscopy, Electron
Immunoelectrophoresis
Hyperlipoproteinemia Type V
Abetalipoproteinemia
Dimyristoylphosphatidylcholine
Receptors, Scavenger
Amino Acid Sequence
Oleic Acid
Chromatography, Gel
Arteriosclerosis
Biological Transport
Lipolysis
Sterol O-Acyltransferase
Rats, Inbred Strains
Callitrichinae
High-Density Lipoproteins, Pre-beta
Lipase
Liposomes
Receptors, LDL
Oleic Acids
Carrier Proteins
Molecular Sequence Data
Lecithin Acyltransferase Deficiency
Hyperlipidemia, Familial Combined
Protein Binding
Antigens, CD36
Specific regional transcription of apolipoprotein E in human brain neurons. (1/5038)
In central nervous system injury and disease, apolipoprotein E (APOE, gene; apoE, protein) might be involved in neuronal injury and death indirectly through extracellular effects and/or more directly through intracellular effects on neuronal metabolism. Although intracellular effects could clearly be mediated by neuronal uptake of extracellular apoE, recent experiments in injury models in normal rodents and in mice transgenic for the human APOE gene suggest the additional possibility of intraneuronal synthesis. To examine whether APOE might be synthesized by human neurons, we performed in situ hybridization on paraffin-embedded and frozen brain sections from three nondemented controls and five Alzheimer's disease (AD) patients using digoxigenin-labeled antisense and sense cRNA probes to human APOE. Using the antisense APOE probes, we found the expected strong hybridization signal in glial cells as well as a generally fainter signal in selected neurons in cerebral cortex and hippocampus. In hippocampus, many APOE mRNA-containing neurons were observed in sectors CA1 to CA4 and the granule cell layer of the dentate gyrus. In these regions, APOE mRNA containing neurons could be observed adjacent to nonhybridizing neurons of the same cell class. APOE mRNA transcription in neurons is regionally specific. In cerebellar cortex, APOE mRNA was seen only in Bergmann glial cells and scattered astrocytes but not in Purkinje cells or granule cell neurons. ApoE immunocytochemical localization in semi-adjacent sections supported the selectivity of APOE transcription. These results demonstrate the expected result that APOE mRNA is transcribed and expressed in glial cells in human brain. The important new finding is that APOE mRNA is also transcribed and expressed in many neurons in frontal cortex and human hippocampus but not in neurons of cerebellar cortex from the same brains. This regionally specific human APOE gene expression suggests that synthesis of apoE might play a role in regional vulnerability of neurons in AD. These results also provide a direct anatomical context for hypotheses proposing a role for apoE isoforms on neuronal cytoskeletal stability and metabolism. (+info)Transcription factor AP-2 activity is modulated by protein kinase A-mediated phosphorylation. (2/5038)
We recently reported that APOE promoter activity is stimulated by cAMP, this effect being mediated by factor AP-2 [Garcia et al. (1996) J. Neurosci. 16, 7550-7556]. Here, we study whether cAMP-induced phosphorylation modulates the activity of AP-2. Recombinant AP-2 was phosphorylated in vitro by protein kinase A (PKA) at Ser239. Mutation of Ser239 to Ala abolished in vitro phosphorylation of AP-2 by PKA, but not the DNA binding activity of AP-2. Cotransfection studies showed that PKA stimulated the effect of AP-2 on the APOE promoter, but not that of the S239A mutant. Therefore, cAMP may modulate AP-2 activity by PKA-induced phosphorylation of this factor. (+info)Age of onset in Huntington disease: sex specific influence of apolipoprotein E genotype and normal CAG repeat length. (3/5038)
Age of onset (AO) of Huntington disease (HD) is known to be correlated with the length of an expanded CAG repeat in the HD gene. Apolipoprotein E (APOE) genotype, in turn, is known to influence AO in Alzheimer disease, rendering the APOE gene a likely candidate to affect AO in other neurological diseases too. We therefore determined APOE genotype and normal CAG repeat length in the HD gene for 138 HD patients who were previously analysed with respect to CAG repeat length. Genotyping for APOE was performed blind to clinical information. In addition to highlighting the effect of the normal repeat length upon AO in maternally inherited HD and in male patients, we show that the APOE epsilon2epsilon3 genotype is associated with significantly earlier AO in males than in females. Such a sex difference in AO was not apparent for any of the other APOE genotypes. Our findings suggest that subtle differences in the course of the neurodegeneration in HD may allow interacting genes to exert gender specific effects upon AO. (+info)Competition of Abeta amyloid peptide and apolipoprotein E for receptor-mediated endocytosis. (4/5038)
The genetic polymorphism of apolipoprotein E (apoE) is associated with the age of onset and relative risk of Alzheimer's disease (AD). In contrast to apoE3, the wild type allele, apoE4 confers an increased risk of late-onset AD. We demonstrate that the beta-amyloid peptide isoforms Abeta (1-28), Abeta (1-40), and Abeta (1-43) compete for the cellular metabolism of apoE3 and apoE4 containing beta-very low density lipoproteins. An antibody raised against Abeta (1-28) cross-reacted with recombinant apoE. Epitope mapping revealed positive amino acid clusters as common epitopes of Abeta (13 through 17; HHQKL) and apoE (residues 144 through 148; LRKRL), both regions known to be heparin binding domains. Abeta in which amino acids 13 through 17 (HHQKL) were replaced by glycine (GGQGL) failed to compete with the cellular uptake of apoE enriched betaVLDL. These observations indicate that Abeta and apoE are taken up into cells by a common pathway involving heparan sulfate proteoglycans. (+info)Mass spectral study of polymorphism of the apolipoproteins of very low density lipoprotein. (5/5038)
New isoforms of apolipoprotein (apo)C-I and apoC-III have been detected in delipidated fractions from very low density lipoprotein (VLDL) using matrix-assisted laser desorption (MALDI) and electrospray ionization (ESI) mass spectrometry (MS). The cleavage sites of truncated apoC-III isoforms have also been identified. The VLDL fractions were isolated by fixed-angle single-spin ultracentrifugation using a self-generating sucrose density gradient and delipidated using a newly developed C18 solid phase extraction protocol. Fifteen apoC isoforms and apoE were identified in the MALDI spectra and the existence of the more abundant species was verified by ESI-MS. The relative intensities of the apoCs are closely correlated in three normolipidemic subjects. A fourth subject with type V hyperlipidemia exhibited an elevated apoC-III level and a suppressed level of the newly discovered truncated apoC-I isoform. ApoC-II was found to be particularly sensitive to in vitro oxidation. The dynamic range and specificity of the MALDI assay shows that the complete apoC isoform profile and apoE phenotype can be obtained in a single measurement from the delipidated VLDL fraction. (+info)beta-amyloid load is not influenced by the severity of cardiovascular disease in aged and demented patients. (6/5038)
BACKGROUND AND PURPOSE: This study was conducted to analyze the association between reported risk factors for Alzheimer's disease, apolipoprotein E epsilon4 allele, and cardiovascular disease and neuropathological changes essential for the diagnosis of Alzheimer's disease. METHODS: Our data are based on clinical and postmortem evaluations of a cohort of nondemented (n=118) and demented (n=107) individuals. A cardiovascular index was calculated at autopsy to estimate the extent of cardiovascular disease. Neuropathological lesions such as senile/neuritic plaques, neurofibrillary tangles, beta-amyloid load, cerebral amyloid angiopathy, and the load of paired helical filaments were determined. RESULTS: The aforementioned neuropathological lesions did not show any positive significant correlation with cardiovascular index. In contrast, the extent of Alzheimer's lesions was significantly higher in those nondemented and demented patients carrying the apolipoprotein E epsilon4 allele than in those without this allele. CONCLUSIONS: Our results demonstrate that the apolipoprotein E epsilon4 allele, but not cardiovascular disease, indeed influences the extent of Alzheimer's lesions seen in the brain tissue of demented patients as well as asymptomatic controls. (+info)Apo E phenotype and changes in serum lipids in adult patients during growth hormone replacement. (7/5038)
OBJECTIVE: To determine whether apo E phenotype influences changes in lipid profiles induced by growth hormone replacement in growth hormone (GH)-deficient adults. DESIGNS: Patients were treated for 6 months with recombinant human GH (hGH), given in a dose of 0.125 U/kg per week for 4 weeks followed by 0.25 U/kg per week thereafter. The effects on serum lipids and the influence of apo E phenotype were examined. METHODS: Thirty patients (aged 35.1+/-11.8 years: mean +/- S.D.) with adult growth hormone deficiency with included in the study. Fasting serum samples were analysed for apo E phenotype total cholesterol, high-density lipoprotein (HDL)-cholesterol, triglycerides, lipoprotein (a) (Lp(a)) and IGF-I. Low-density lipoprotein (LDL)-cholesterol was calculated using the Friedwald formula. RESULTS: Six months of replacement treatment with hGH resulted in a reduction in HDL-cholesterol from 0.90+/-0.10 to 0.68+/-0.08 mmol/l (P<0.01), and a small, non-significant reduction in total cholesterol from 6.14+/-0.40 to 5.99+/-0.35 mmol/l (P = 0.06). There was no significant change in the other lipid parameters. The decrease in HDL-cholesterol concentration was greater in patients carrying the apo E2 allele (0.40+/-0.07 mmol/l, P<0.05) than in patients homozygous for the apo E3 allele (0.23+/-0.04 mmol/l) and patients carrying the apo E4 allele (0.15+/-0.36 mmol/l). Patients with the apo E4 allele had lower baseline cholesterol concentrations than patients lacking the apo E4 allele, and this persisted after treatment with hGH (P<0.05). CONCLUSIONS: Apo E phenotype may be a determining factor in the response of HDL-cholesterol to hGH in GH-deficient adults. (+info)Iron-deficient diet reduces atherosclerotic lesions in apoE-deficient mice. (8/5038)
BACKGROUND: Iron deposition is evident in human atherosclerotic lesions, suggesting that iron may play a role in the development of atherosclerosis. To test this idea, the correlation between the extent of iron deposition and the severity of atherosclerosis in apolipoprotein E (apoE)-deficient mice was investigated. Furthermore, the effect of a low-iron diet on the progression of atherosclerotic lesions in these animals was evaluated. METHODS AND RESULTS: Iron deposition in tissues of apoE-deficient mice was examined by Perls' staining method. The results clearly demonstrated that iron deposits are present in atherosclerotic lesions and tissue sections of heart and liver in an age-dependent manner. When the young mice received a low-iron diet for 3 months, the hematocrit, serum iron, hemoglobin, and cholesterol concentrations were not significantly altered compared with those of littermates placed on a chow diet. However, the serum ferritin level of animals in the iron-restricted group was 27% to 30% lower than that of the control group in either sex. Furthermore, the lipoproteins isolated from the iron-restricted group exhibited greater resistance to copper-induced oxidation. Histological examination revealed that atherosclerotic lesions developed in mice fed a low-iron diet were significantly smaller than those found in control littermates. Likewise, the iron deposition as well as tissue iron content was much less in aortic tissues of the iron-restricted animals. Circulating autoantibodies to oxidized LDL and immunostains for epitopes of malondialdehyde-modified LDL detected on lesions were also significantly lower in mice fed a low-iron diet. CONCLUSIONS: Iron deposition is closely associated with the progression of atherosclerosis in apoE-deficient mice. Restriction in dietary iron intake leads to significant inhibition of lesion formation in these animals. These results suggest that the beneficial effect of a low-iron diet may be mediated, at least in part, by the reduction of iron deposition as well as LDL oxidation in vascular lesions. (+info)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.
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.
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.
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 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.
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.
People with hyperlipoproteinemia type V often have a history of low birth weight and growth retardation, and may experience a range of health problems including fatigue, muscle weakness, and liver disease. The disorder is usually inherited in an autosomal recessive pattern, meaning that a person must inherit two copies of the mutated gene - one from each parent - to develop the condition.
Treatment for hyperlipoproteinemia type V typically involves a combination of dietary changes and medication. Dietary recommendations may include avoiding foods high in saturated fats and cholesterol, and increasing intake of unsaturated fats, such as those found in nuts and vegetable oils. Medications may include drugs that raise HDL levels or lower LDL levels, such as niacin or statins. In severe cases, liver transplantation may be necessary.
In summary, hyperlipoproteinemia type V is a rare genetic disorder that affects the metabolism of lipids and lipoproteins in the body, leading to extremely low levels of LDL cholesterol and high levels of HDL cholesterol. Treatment typically involves a combination of dietary changes and medication, and may include liver transplantation in severe cases.
The main symptom of abetalipoproteinemia is a complete absence of chylomicrons, which are small particles that carry triglycerides and other lipids in the bloodstream. This results in low levels of triglycerides and other lipids in the blood, as well as an impaired ability to absorb vitamins and other nutrients from food.
Abetalipoproteinemia is usually diagnosed during infancy or early childhood, when symptoms such as fatigue, weakness, and poor growth become apparent. The disorder can be identified through blood tests that measure lipid levels and genetic analysis.
Treatment for abetalipoproteinemia typically involves a combination of dietary changes and supplements to ensure adequate nutrition and prevent complications such as malnutrition and liver disease. In some cases, medications may be prescribed to lower triglyceride levels or improve the absorption of fat-soluble vitamins.
The prognosis for abetalipoproteinemia varies depending on the severity of the disorder and the presence of any complications. In general, early diagnosis and appropriate treatment can help to manage symptoms and prevent long-term health problems. However, some individuals with abetalipoproteinemia may experience ongoing health issues throughout their lives.
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 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.
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.
Apolipoprotein
Apolipoprotein L1
Apolipoprotein D
Apolipoprotein H
Apolipoprotein E
Apolipoprotein B
Apolipoprotein AI
Apolipoprotein L
Apolipoprotein C
Apolipoprotein O
Apolipoprotein C-II
Apolipoprotein C-IV
Apolipoprotein B deficiency
Anti-apolipoprotein antibodies
Apolipoprotein C-III
Apolipoprotein C-I
Apolipoprotein A-II
Apolipoprotein B (apoB) 5′ UTR cis-regulatory element
Gladys Maestre
Lipocalin
ApoA-1 Milano
Low-density lipoprotein receptor-related protein 8
APOM
Björn Dahlbäck
Susan Serjeantson
APOL3
Gladstone Institutes
APOL2
APOL6
Chylomicron
Genetic association of apolipoprotein E with age-related macular degeneration
NHANES 2011-2012: Apolipoprotein B Data Documentation, Codebook, and Frequencies
Apolipoprotein B100: MedlinePlus Medical Encyclopedia
Anti-Apolipoprotein B antibody [F2C13] (GTX15663) | GeneTex
Longitudinal SPECT study in Alzheimer's disease: relation to apolipoprotein E polymorphism | Journal of Neurology, Neurosurgery...
RePub, Erasmus University Repository:
Serum levels of apolipoproteins and incident type 2 diabetes: A prospective cohort study
Genetic Variation Associated with Differences in the Response of Plasma Apolipoprotein B Levels to Dietary Fibre | Clinical...
Knowledge of the Biological Actions of Extra Virgin Olive Oil Gained From Mice Lacking Apolipoprotein E | Revista Española de...
WHO EMRO | Effects of omega-3 fatty acid supplements on serum lipids, apolipoproteins and malondialdehyde in type 2 diabetes...
Cell autonomous mechanisms of Apolipoprotein E isoform-dependent neurodegeneration - JPND Neurodegenerative Disease Research
Apolipoproteins A | Profiles RNS
The role of apolipoprotein N-acyl transferase, Lnt, in the lipidation of factor H binding protein of Neisseria meningitidis...
APolipoprotein II Archives - Xcode Life
T3DB: Apolipoprotein D
Apolipoprotein Evaluation - True Health Labs
Hypertriglyceridemia: Practice Essentials, Pathophysiology, Etiology
Alzheimer Disease in Down Syndrome: Overview, Pathophysiology/Risk Factors, Epidemiology
Apolipoprotein A-1 - Own Your Labs
Apolipoprotein A | UCLA Health Library, Los Angeles, CA
Recombinant Human Apolipoprotein C-II Protein - enQuire BioReagents
CIENCIASMEDICASNEWS: Apolipoprotein E polymorphism in cerebrovascular & coronary heart diseases.
Human APOL1(Apolipoprotein L) ELISA Kit - Jemsec International NGS
What is Apolipoprotein B (Apo B)? - Dr Mike MacDonald
China good quality Infectious Disease Rapid Tests on sales
Apolipoprotein A 1 Apo A 1 Lab Test Online In USA
Molecular Genetics 01 - Apolipoprotein E (E2, E3, E4) - INSTAND e.V.
Modulation of Apolipoprotein D levels in human pregnancy and association with gestational weight gain | Reproductive Biology...
Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis....
Apolipoprotein A2 isoforms associated with exocrine pancreatic insufficiency in early chronic pancreatitis. | J Gastroenterol...
OHIO Open Library - Student Research and Creative Activity Expo: Apolipoprotein A4 Regulates Lipid Metabolism
ApoE9
- We studied the association of HDL cholesterol (HDL-C), apoA1, apoCIII, apoD, and apoE as well as the ratios of apolipoproteins with apoA1 with the risk of T2D. (eur.nl)
- To examine the association of self-reported health (SRH) with the apolipoprotein E (APOE) gene, life stress, and sociobehavioural factors in adults aged 55 and over. (bmj.com)
- Description: A sandwich quantitative ELISA assay kit for detection of Rat Apolipoprotein E (APOE) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates or other biological fluids. (isogem.org)
- Description: Quantitative sandwich ELISA kit for measuring Dog Apolipoprotein E (APOE) in samples from serum, plasma, tissue homogenates. (isogem.org)
- Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Dog Apolipoprotein E (APOE) in serum, plasma and other biological fluids. (isogem.org)
- Apolipoprotein E (APOE) is found in VLDL and binds to potential receptors involved in HCV entry into cells, the LDL receptor, and the scavenger receptor protein SR-B1. (ncl.ac.uk)
- [ 5 ] Only 10% of amyloidosis deposits consist of components such as glycosaminoglycans (GAGs), apolipoprotein-E (apoE), and serum amyloid P-component (SAP), while nearly 90% of the deposits consist of amyloid fibrils that are formed by the aggregation of misfolded proteins. (medscape.com)
- BACKGROUND AND AIMS: The human Apolipoprotein E (APOE) gene is polymorphic. (nih.gov)
- Apolipoprotein E (ApoE) genotype is the strongest genetic risk factor for late-onset Alzheimer's disease, with the ε4 allele increasing risk in a dose-dependent fashion. (nih.gov)
Allele5
- The ε4 allele of apolipoprotein E is a risk factor for Alzheimer's disease. (bmj.com)
- CONCLUSION Apolipoprotein E polymorphism is involved in the pathogenesis and heterogeneity of Alzheimer's disease as the most severe cerebral hypoperfusion was found in the ε4 allele subgroups. (bmj.com)
- 1-4 The ε4 allele of apolipoprotein E is a risk factor for Alzheimer's disease and accelerates the onset of dementia. (bmj.com)
- The ultimate goal is to gain an in depth understanding of the mechanisms by which the Apolipoprotein E e4 allele confers increased AD risk for the purpose of advancing the overall search for efficacious AD treatments and Apolipoprotein E e4-directed therapeutics in particular. (nih.gov)
- The apolipoprotein E4 (APOE4) allele was significantly associated with poor SRH overall (odds ratio (OR) 1.54, 95% confidence interval (CI) 1.03 to 2.35), but the association was stronger in women (OR 2.13, 95% CI 1.17 to 3.88) than in men. (bmj.com)
Lipids3
- We conducted a Mendelian randomization (MR) study to disentangle the comparative effects of lipids and apolipoproteins on ischemic stroke. (nih.gov)
- Month-to-month variability of lipids, lipoproteins, and apolipoproteins and the impact of acute infection in adolescents. (uchicago.edu)
- Moreover, menopause is also associated with alterations in the levels of various lipids circulating in the blood, such as lipoproteins, apolipoproteins, low-density lipoproteins (LDLs), high-density lipoproteins (HDL) and triacylglycerol (TG). (mdpi.com)
CIII4
- Genotypes were determined using DNA markers for the low-density lipoprotein receptor, apolipoprotein B, apolipoprotein CIII and hepatic lipase gene loci. (portlandpress.com)
- Hypertriglyceridemia and the apolipoprotein CIII gene locus: lack of association with the variant insulin response element in Italian school children. (uchicago.edu)
- Recent Apolipoprotein CIII trials. (bvsalud.org)
- PURPOSE OF REVIEW This review will briefly revise the evidence concerning the pharmacological inhibition of Apolipoprotein CIII (ApoCIII) in patients with hypertriglyceridemia . (bvsalud.org)
Serum1
- In an immunochemical reaction, Apolipoprotein B in the human serum sample form immune complexes with specific antibodies. (cdc.gov)
Gene7
- This patent covers cellular models expressing variants of the human gene Apolipoprotein E. This invention not only allows for the evaluation of cellular phenotypes but also enables the creation of models for genetic and chemical screening. (nih.gov)
- This gene product is the main apolipoprotein of chylomicrons and low density lipoproteins. (genetex.com)
- 5-8 The apolipoprotein E gene, located on chromosome 19, has three major alleles: ε2, ε3, and ε4. (bmj.com)
- Although there have been some recent cell and animal experiments indicating that expression of the gene encoding apolipoprotein B mRNA editing enzyme catalytic subunit 3B ( APOBEC3B ) is closely related to cancer, it still lacks pan-cancer analysis. (biomedcentral.com)
- The apolipoprotein B mRNA editing enzyme catalytic subunit 3B ( APOBEC3B ) protein, also known as A3B or ARP4, is a member of the cytidine deaminase gene family [ 6 ]. (biomedcentral.com)
- Apolipoprotein A5 gene variants and the risk of coronary heart disease: a case-control study and meta-analysis. (uchicago.edu)
- In a mutant with markedly reduced binding, the transposon was located in the lnt gene which encodes apolipoprotein N-acyl transferase, Lnt, responsible for the addition of the third fatty acid to apolipoproteins prior to their sorting to the outer membrane. (nottingham.ac.uk)
Lipoproteins2
- Regulation and clearance of apolipoprotein B-containing lipoproteins. (medlineplus.gov)
- ApoCIII is a plasma apolipoprotein playing a major role in the metabolism of triglyceride -rich lipoproteins , namely chylomicrons and very-low-density lipoproteins as well as in the pathological processes involved in atherosclerosis . (bvsalud.org)
Amyloid2
- Apolipoprotein E is present in senile plaques, neurofibrillary tangles, and cerebrovascular amyloid, the major neuropathological changes seen in Alzheimer's disease. (bmj.com)
- Different binding properties of the apolipoprotein isoforms to β-amyloid and tau protein also suggests that it is involved in the pathogenesis of Alzheimer's disease. (bmj.com)
Polymorphism1
- The effect of apolipoprotein E polymorphism on cerebral perfusion was studied. (bmj.com)
MRNA1
- Holzfeind P, Merschak P, Dieplinger H, Redl B: The human lacrimal gland synthesizes apolipoprotein D mRNA in addition to tear prealbumin mRNA, both species encoding members of the lipocalin superfamily. (t3db.ca)
Alleles1
- There was no significant variation in the reduction of plasma total cholesterol, low-density lipoprotein cholesterol or apolipoprotein B concentrations for alleles of other genes tested. (portlandpress.com)
Cholesterol3
- Apolipoprotein E (Apo-E) is a major cholesterol carrier that supports lipid transport and injury repair in the brain. (nih.gov)
- Apolipoprotein B100 (apoB100) is a protein that plays a role in moving cholesterol around your body. (medlineplus.gov)
- The effects of apolipoprotein F deficiency on high density lipoprotein cholesterol metabolism in mice. (nih.gov)
Neurodegeneration1
- This FOA encouarges multidisciplinary and interdisciplinary research to elucidate how Apolipoprotein E, lipoprotein receptors and CNS lipid homeostasis influence brain aging and the transition to neurodegeneration in Alzheimers disease (AD). (nih.gov)
ApoB2
- The analyst should use the special sampling weights in this file to analyze Apolipoprotein B (ApoB). (cdc.gov)
- What are the relationships between apolipoprotein (apo) A-I and apoB concentrations, the apoB/apoA-I ratio and the prevalences of dyslipidemia and metabolic syndrome (MS) in south-west Chinese women with polycystic ovary syndrome (PCOS). (unboundmedicine.com)
Pathogenesis1
- There is now much evidence implicating apolipoprotein E (apo E) in the pathogenesis of CAD and AD. (europa.eu)
Metabolism1
- 1. We hypothesized that differences within genes whose protein products are involved in apolipoprotein B metabolism could influence the response of plasma apolipoprotein B-containing lipoprotein concentrations to increases in dietary fibre. (portlandpress.com)
Metabolic syndrome1
- Publication: Apolipoprotein E4 association with metabolic syndrome depends on body fatness. (nih.gov)
Genetic1
- 4. Thus, genetic variability is associated with inter-individual differences in the fibre-related reduction in plasma apolipoprotein B and apolipoprotein B-containing lipoprotein concentrations. (portlandpress.com)
Proportional2
Profiles1
- Below are the most recent publications written about "Apolipoproteins A" by people in Profiles. (uchicago.edu)
Protein component2
- Apolipoprotein B is the main protein component of LDL and accounts for approximately 95% of the total protein content of LDL. (cdc.gov)
- Balbin M, Freije JM, Fueyo A, Sanchez LM, Lopez-Otin C: Apolipoprotein D is the major protein component in cyst fluid from women with human breast gross cystic disease. (t3db.ca)
Human4
- Elements in the C terminus of apolipoprotein [a] responsible for the binding to the tenth type III module of human fibronectin. (uchicago.edu)
- Lysine-phosphatidylcholine adducts in kringle V impart unique immunological and potential pro-inflammatory properties to human apolipoprotein(a). (uchicago.edu)
- Cloning and expression of human apolipoprotein D cDNA. (t3db.ca)
- Yang CY, Gu ZW, Blanco-Vaca F, Gaskell SJ, Yang M, Massey JB, Gotto AM Jr, Pownall HJ: Structure of human apolipoprotein D: locations of the intermolecular and intramolecular disulfide links. (t3db.ca)
Concentrations2
- Fasting blood lipid, lipoprotein and apolipoprotein concentrations were measured at the start and end of the 2 week metabolic period. (portlandpress.com)
- 3. Reductions in plasma concentrations of apolipoprotein B were significantly different depending on genotype determined with a low-density lipoprotein receptor DNA marker ( P = 0.03). (portlandpress.com)
Role1
- OBJECTIVE We aimed to investigate the role of serumlevels of various apolipoproteins on the risk for type 2 diabetes (T2D). (eur.nl)
Cells1
- ICC/IF analysis of HepG2 cells using GTX15663 Apolipoprotein B antibody [F2C13]. (genetex.com)
Major1
- This graph shows the total number of publications written about "Apolipoproteins A" by people in this website by year, and whether "Apolipoproteins A" was a major or minor topic of these publications. (uchicago.edu)
Levels2
- As such, we hypothesized that apoC-II and apolipoprotein C-III (apoC-III) levels were related to BP abnormalities and CVD in children suffering from mild-to-moderate CKD. (frontiersin.org)
- All apolipoproteins, ratios, and HDL-C levels were naturally logtransformed to reach normal distribution. (eur.nl)
Type1
- Nous avons réalisé un essai en double aveugle contre placebo sur 50 patients atteints de diabète de type 2 randomisés pour recevoir 2 g/jour d'acides gras oméga 3 purifiés ou un placebo pendant 10 semaines. (who.int)
Patients1
- These apolipoproteins are low in atherosclerotic patients. (uchicago.edu)
TARGET1
- Apolipoprotein E has been nominated as a potential target for AD. (nih.gov)
Panel1
- Apolipoprotein measurements may provide more detail about your risk for heart disease, but the added value of this test beyond a lipid panel is unknown. (medlineplus.gov)