Cholesterol Ester Transfer Proteins
Phospholipid Transfer Proteins
High-Density Lipoproteins, Pre-beta
Lipid Metabolism, Inborn Errors
Scavenger Receptors, Class B
ATP Binding Cassette Transporter 1
Lipid transfer inhibitor protein defines the participation of lipoproteins in lipid transfer reactions: CETP has no preference for cholesteryl esters in HDL versus LDL. (1/740)Cholesteryl ester transfer protein (CETP) catalyzes the net transfer of cholesteryl ester (CE) between lipoproteins in exchange for triglyceride (heteroexchange). It is generally held that CETP primarily associates with HDL and preferentially transfers lipids from this lipoprotein fraction. This is illustrated in normal plasma where HDL is the primary donor of the CE transferred to VLDL by CETP. However, in plasma deficient in lipid transfer inhibitor protein (LTIP) activity, HDL and LDL are equivalent donors of CE to VLDL (Arterioscler Thromb Vasc Biol. 1997;17:1716-1724). Thus, we have hypothesized that the preferential transfer of CE from HDL in normal plasma is a consequence of LTIP activity and not caused by a preferential CETP-HDL interaction. We have tested this hypothesis in lipid mass transfer assays with partially purified CETP and LTIP, and isolated lipoproteins. With a physiological mixture of lipoproteins, the preference ratio (PR, ratio of CE mass transferred from a lipoprotein to VLDL versus its CE content) for HDL and LDL in the presence of CETP alone was approximately 1 (ie, no preference). Fourfold variations in the LDL/HDL ratio or in the levels of HDL in the assay did not result in significant preferential transfer from any lipoprotein. On addition of LTIP, the PR for HDL was increased up to 2-fold and that for LDL decreased in a concentration-dependent manner. Under all conditions where LDL and HDL levels were varied, LTIP consistently resulted in a PR >1 for CE transfer from HDL. Short-term experiments with radiolabeled lipoproteins and either partially purified or homogenous CETP confirmed these observations and further demonstrated that CETP has a strong predilection to mediate homoexchange (bidirectional transfer of the same lipid) rather than heteroexchange (CE for TG); LTIP had no effect on the selection of CE or TG by CETP or its mechanism of action. We conclude, in contrast to current opinion, that CETP has no preference for CE in HDL versus LDL, suggesting that the previously reported stable binding of CETP to HDL does not result in selective transfer from this lipoprotein. These data suggest that LTIP is responsible for the preferential transfer of CE from HDL that occurs in plasma. CETP and LTIP cooperatively determine the extent of CETP-mediated remodeling of individual lipoprotein fractions. (+info)
Increased atherosclerosis in ApoE and LDL receptor gene knock-out mice as a result of human cholesteryl ester transfer protein transgene expression. (2/740)The plasma cholesteryl ester transfer protein (CETP) plays a major role in the catabolism of HDL cholesteryl ester (CE). CETP transgenic mice have decreased HDL cholesterol levels and have been reported to have either increased or decreased early atherosclerotic lesions. To evaluate the impact of CETP expression on more advanced forms of atherosclerosis, we have cross-bred the human CETP transgene into the apoE knock-out (apoE0) background with and without concomitant expression of the human apo A-I transgene. In this model the CETP transgene is induced to produce plasma CETP levels 5 to 10 times normal human levels. CETP expression resulted in moderately reduced HDL cholesterol (34%) in apoE0 mice and markedly reduced HDL cholesterol (76%) in apoE0/apoA1 transgenic mice. After injection of radiolabeled HDL CE, the CETP transgene significantly delayed the clearance of CE radioactivity from plasma in apoE0 mice, but accelerated the clearance in apoE0/apoA1 transgenic mice. ApoE0/CETP mice displayed an increase in mean atherosclerotic lesion area on the chow diet (approximately 2-fold after 2 to 4 months, and 1.4- to 1.6-fold after 7 months) compared with apoE0 mice (P<0.02). At 7 months apoA1 transgene expression resulted in a 3-fold reduction in mean lesion area in apoE0 mice (P<0.001). In the apoE0/apoA1 background, CETP produced an insignificant 1.3- to 1.7-fold increase in lesion area. In further studies the CETP transgene was bred onto the LDL receptor knock-out background (LDLR0). After 3 months on the Western diet, the mean lesion area was increased 1.8-fold (P<0.01) in LDLR0/CETP mice, compared with LDLR0 mice. These studies indicate that CETP expression leads to a moderate increase in atherosclerosis in apoE0 and LDLR0 mice, and suggest a proatherogenic effect of CETP activity in metabolic settings in which clearance of remnants or LDL is severely impaired. However, apoA1 overexpression has more dramatic protective effects on atherosclerosis in apoE0 mice, which are not significantly reversed by concomitant expression of CETP. (+info)
A cholesteryl ester transfer protein gene mutation and vascular disease in dialysis patients. (3/740)Among patients undergoing maintenance hemodialysis, a decreased high-density lipoprotein cholesterol (HDL-C) concentration is among the most common abnormalities of lipid metabolism and apparently is an independent risk factor for vascular disease. A common missense mutation of cholesteryl ester transfer protein gene, D442G (Asp 442 to Gly), increases HDL-C levels through the reduced activity of cholesteryl ester transfer from HDL to VLDL, but the mutation also may lead to reduced activity of reverse cholesterol transport. To investigate the effect of the D442G polymorphism on atherosclerotic complications in dialysis patients, the genotype and allele frequency of the polymorphism were determined in 414 unselected dialysis patients and 220 control subjects, and postprandial serum lipid levels were measured in the dialysis patients. A similar genotype distribution was found between hemodialysis patients and healthy control subjects, and in dialysis patients with and without vascular disease. Serum levels of total cholesterol and HDL-C did not differ between patients with and without the mutation and in patients with and without vascular disease. However, patients with sub-median HDL-C levels (<45 mg/dl) had an independent odds ratio of 1.8 for vascular disease (95% confidence interval, 1.04 to 3.2; P < 0.05). In this low-HDL-C subgroup, patients with the D442G mutation had a significantly higher prevalence of vascular disease than those with no mutation (54.5% versus 24.4%; P < 0.05), and an independent odds ratio of 4.9 (95% confidence interval, 1.05 to 22.65; P < 0.05). In conclusion, the D442G mutation is an independent risk factor for atherosclerotic complications in dialysis patients with HDL-C levels below 45 mg/dl. (+info)
Structure-specific inhibition of cholesteryl ester transfer protein by azaphilones. (4/740)The effect of thirteen different fungal azaphilones, which have a common 6-iso-chromane-like ring, was tested on cholesteryl ester transfer protein (CETP) activity in vitro. Chaetoviridin B showed the most potent inhibitory activity with an IC50 value of < 6.2 microM, followed by sclerotiorin with an IC50 value of 19.4 microM. Rotiorin, chaetoviridin A and rubrorotiorin had moderate inhibitory activity (IC50 ; 30 approximately 40 microM), but others showed very weak or no inhibitory activity. The relationship between the structures and their inhibitory activity indicated that the presence of an electrophilic ketone(s) and/or enone(s) at both C-6 and C-8 positions in the isochromane-like ring is essential for eliciting CETP inhibitory activity. The transfer activity of both CE and TG was inhibited by sclerotiorin to approximately the same extent (IC50: 14.4 and 10.3 microM, respectively). A model of the reaction suggested that sclerotiorin reacts with a primary amine of amino acids such as lysine in the protein to form a covalent bond. (+info)
Estrogen-mediated increases in LDL cholesterol and foam cell-containing lesions in human ApoB100xCETP transgenic mice. (5/740)The murine double transgenic mouse expressing both human apoB100 and cholesteryl ester transfer protein (CETP), has been used as a model to understand the effects mediated by various therapeutic modalities on serum lipoproteins and on atherosclerotic lesion progression. In the present study the effects of estrogen therapy on serum lipoproteins were investigated after mice were placed on an atherosclerotic diet. The daily oral administration of 20 or 100 microg/kg of 17 alpha-ethinyl estradiol resulted in a significant, dose-dependent increase in LDL cholesterol over a 20-week regimen. These differences were apparent by 6 weeks and further increases were observed through the 20-week period. Although CETP did result in a reduction in total HDL, estrogen did not have any impact on the amount of CETP activity associated with the HDL particles. The significant increase in LDL cholesterol was associated with increases in the amount of apoB100 and B48 and apoE-containing particles. Hepatic apoB message levels, however, were not different between the experimental groups. Although the extent of atherosclerotic lesions was modest, <0.5% of the aortic surface area in the vehicle group, the high-dose estrogen group, showed an increase in lesion area consistent with the elevation in LDL cholesterol. These lesions, primarily restricted to the aortic root and aortic semilunar valves, were more intensely stained with Oil Red O in the high-dose estrogen group when compared with the vehicle controls. (+info)
Wiedendiol-A inhibits cholesteryl ester binding to its transfer protein. (6/740)AIM: To study the wiedendiol-A (W-A) inhibition mechanism of plasma cholesteryl ester (CE) transfer protein (CETP) on the transfer of CE. METHODS: Using gel filtration method. RESULTS: W-A at 30 mumol.L-1 inhibited association of CE with CETP by 76% and CETP transfer activity by 81%. In addition, W-A enhanced binding of TP2, a monoclonal antibody with a CETP C-terminal epitope which is involved in CE binding, to CETP, suggesting a W-A-induced conformational change at the epitope for increased TP2 binding. When CETP activity was measured by varying high-density lipoproteins (HDL) concentration, the apparent Vmax of CE transfer was inhibited by 74% and 83% in the presence of W-A at 14 and 25 mumol.L-1, respectively, while the apparent K(m) of HDL for CETP did not change. CONCLUSION: W-A action is mediated through interaction between W-A and CETP, but not through those between W-A and lipoproteins. (+info)
Remodeling of HDL by CETP in vivo and by CETP and hepatic lipase in vitro results in enhanced uptake of HDL CE by cells expressing scavenger receptor B-I. (7/740)The transport of HDL cholesteryl esters (CE) from plasma to the liver involves a direct uptake pathway, mediated by hepatic scavenger receptor B-I (SR-BI), and an indirect pathway, involving the exchange of HDL CE for triglycerides (TG) of TG-rich lipoproteins by cholesteryl ester transfer protein (CETP). We carried out HDL CE turnover studies in mice expressing human CETP and/or human lecithin:cholesterol acyltransferase (LCAT) transgenes on a background of human apoA-I expression. The fractional clearance of HDL CE by the liver was delayed by LCAT transgene, while the CETP transgene increased it. However, there was no incremental transfer of HDL CE radioactivity to the TG-rich lipoprotein fraction in mice expressing CETP, suggesting increased direct removal of HDL CE in the liver. To evaluate the possibility that this might be mediated by SR-BI, HDL isolated from plasma of the different groups of transgenic mice was incubated with SR-BI transfected or control CHO cells. HDL isolated from mice expressing CETP showed a 2- to 4-fold increase in SR-BI-mediated HDL CE uptake, compared to HDL from mice lacking CETP. The addition of pure CETP to HDL in cell culture did not lead to increased selective uptake of HDL CE by cells. However, when human HDL was enriched with TG by incubation with TG-rich lipoproteins in the presence of CETP, then treated with hepatic lipase, there was a significant enhancement of HDL CE uptake. Thus, the remodeling of human HDL by CETP, involving CE;-TG interchange, followed by the action of hepatic lipase (HL), leads to the enhanced uptake of HDL CE by cellular SR-BI. These observations suggest that in animals such as humans in which both the selective uptake and CETP pathways are active, the two pathways could operate in a synergistic fashion to enhance reverse cholesterol transport. (+info)
Characterization of a cholesterol response element (CRE) in the promoter of the cholesteryl ester transfer protein gene: functional role of the transcription factors SREBP-1a, -2, and YY1. (8/740)Cholesteryl ester transfer protein (CETP) is expressed in human adipocytes, where it acts to promote selective uptake of HDL-CE (Benoist, F., M. McDonnell, P. Lau, R. Milne, and R. McPherson. 1997. J. Biol. Chem. 272: 23572;-23577). In contrast to other major sterol-responsive genes such as 3-hydroxy-3-methylglutaryl coenzyme A reductase CETP expression is up-regulated rather than down-regulated in response to cholesterol. To define elements involved in cholesterol-mediated up-regulation of CETP gene expression, deletion derivatives of the CETP promoter were cloned into a luciferase reporter construct and transfected into the human liposarcoma cell line SW872, cultured in the presence or absence of lipoproteins. A fragment associated with a positive cholesterol response was identified between nucleotides -361 and -138 (relative to the initiation site of transcription) of the promoter. This region contains a tandem repeat of a sequence known to mediate sterol dependent regulation of the hamster HMG-CoA reductase gene. We have putatively denoted this region, the cholesterol response element (CRE). Using gel mobility shift assays we demonstrate that both YY1 and SREBP-1 interact with the CRE of CETP. Furthermore, in transient co-transfection experiments, both YY1 and SREBP-1a were found to trans-activate, in a dose-dependent manner, the luciferase activity of constructs harboring the CRE. We also demonstrate that SREBP-2, is able to trans-activate a luciferase construct harboring the CRE although much less effectively as compared to SREBP-1. Finally, functional analysis of the CRE confirms its regulatory role in modulating CETP gene expression through its interaction with YY1 and SREBP-1a. (+info)
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 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.
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.
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.
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.
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.
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.
Cholesteryl ester transfer protein
Reverse cholesterol transport
Very low-density lipoprotein
Pancreatic lipase family
Ethanol-induced non-lamellar phases in phospholipids
Donald S. Fredrickson
Pharmacology of bicalutamide
Coherent Raman scattering microscopy
Fatty acid synthesis
Phospholipid transfer protein
Role of cholesteryl ester transfer protein in reverse cholesterol transport - PubMed
Interaction of the cholesterol ester transfer protein I405V polymorphism with alcohol consumption in smoking and non-smoking...
HDL Revisited: Biological Functions and Clinical Relevance
Crosstalk between reverse cholesterol transport and innate immunity - PubMed
Dr Martin Whyte | University of Surrey
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Cholesterol Genes Tied to Age-Related Macular Degeneration | National Institutes of Health (NIH)
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Astounding Number of Medical Procedures Have No Benefit, Even Harm - JAMA Study | From the Trenches World Report
Institute for Informatics, Data Science and Biostatistics - Research output - Research Profiles at Washington University...
- Finally, we illustrate our approach by analyzing the relationship between coding variants and levels of high-density lipoprotein (HDL) cholesterol in 11,556 individuals from the HUNT and SardiNIA studies, demonstrating association for coding variants in the APOC3, CETP, LIPC, LIPG, and LPL genes and illustrating the value of family samples, meta-analysis, and gene-level tests. (nih.gov)
- However, several large randomized trials utilizing cholesteryl ester transfer protein (CETP) inhibitors did not show benefit for reducing cardiovascular events in spite of raising HDL levels. (medscape.com)
- The study has also shed light on a new biological pathway for AMD disease development, by uncovering two genes associated with AMD risk in the high-density lipoprotein (HDL) cholesterol pathway: human hepatic lipase (LIPC) and cholesterol ester transfer protein (CETP). (nih.gov)
- Cholesterol ester transfer protein (CETP) gene polymorphism and selected parameters of lipid metabolism in children from families with history of cardiovascular system diseases. (cdc.gov)
- Association of cholesteryl ester transfer protein (CETP) gene polymorphism, high density lipoprotein cholesterol and risk of coronary artery disease: a meta-analysis using a Mendelian randomization approach. (cdc.gov)
- A meta-analytic evaluation of cholesteryl ester transfer protein (CETP) C-629A polymorphism in association with coronary heart disease risk and lipid changes. (cdc.gov)
- Background: We aimed to identify independent genetic determinants of circulating CETP (cholesteryl ester transfer protein) to assess causal effects of variation in CETP concentration on circulating lipid concentrations and cardiovascular disease risk. (tilburguniversity.edu)
- Therefore, the results of our study are fully consistent with the notion that CETP concentration is causally associated with CAD through low-density lipoprotein cholesterol. (tilburguniversity.edu)
- The patients had reduced postheparin hepatic triglyceride lipase (HTGL) activities, and one of them has recently been identified to be homozygous for a missense mutation in exon 15 (D442: G) in the cholesteryl ester transfer protein (CETP) gene. (qxmd.com)
- LDL are formed from IDL with the involvement of hepatic lipase (HL) and are enriched with HDL cholesterol, with the involvement of the cholesterol ester transfer protein (CETP) [ 1 - 3 ]. (archivesofmedicalscience.com)
- ABCA1 - ATP-binding cassette transporter A1, CETP - cholesterol ester transfer protein, EL - endothelial lipase, HL - hepatic lipase, LCAT - lecithin cholesterol acyltransferase, LPL - lipoprotein lipase, PLTP - phospholipid transfer protein, TG - triglycerides. (archivesofmedicalscience.com)
- Fats, or lipids, such as cholesterol and triglycerides, are carried in the blood in particles called lipoproteins. (nih.gov)
- Apolipoproteins (plasma proteins involved in metabolism of cholesterol, triglycerides, phospholipids, and proteins in the blood) and enzymes involved in lipid metabolism are measured. (nih.gov)
- In the previously cited study by Khan et al 9 , type 2 diabetics who were given 1, 3 or 6 grams of cinnamon a day for 60 days experienced significant drops in triglycerides (23 to 30 percent), low-density lipoprotein (LDL) cholesterol (7 to 27 percent), and total cholesterol (12 to 26 percent). (totalhealthmagazine.com)
- There are 2 major types of lipids in the blood: cholesterol and triglycerides. (who.int)
- Hyperlipidemia is a set of metabolic disorders that can be genetic or acquired that are characterized by excess lipids in the blood which can include cholesterol and/or triglycerides. (igenomix.fr)
- Objective - Niacin potently decreases plasma triglycerides and LDL-cholesterol. (tno.nl)
Cholesteryl ester hydrolase2
- Selected genes corresponded to folate metabolism, vitamins B-12, A, and E, and cholesterol pathways or lipid metabolism. (usda.gov)
- Many oxazoles showed a higher CYP450 dependent microsomal metabolism than the corresponding ethyl esters. (bvsalud.org)
- The maternal lipid metabolism during pregnancy is characterized by progressive increases in plasma cholesterol and triglyceride levels accompanied by increases in low density lipoprotein (LDL) and very low density lipoprotein (VLDL), leading to maternal hyperlipidemia during late pregnancy [ 4 ]. (biomedcentral.com)
- Metabolism: Metabolized by ester hydrolysis to active metabolite which undergoes glucuronide conjugation in liver. (medicineindia.org)
- 25 mg/dl includes patients with deficiency of cholesteryl ester transfer protein, lecithin cholesterol acyltransferase, phospholipid transfer protein, lipoprotein lipase, hepatic lipase, or apo-CII, ANGPTL3, and Tangier disease. (nih.gov)
- Lecithin: cholesterol acyltransferase (LCAT) activity is associated with HDL containing apo A-I. Google Scholar. (jmir-inc.com)
- Hepatic lipase and cholesteryl ester transfer protein mass and activity remained unchanged. (ox.ac.uk)
- We used a mathematical technique called linear regression to determine which gene deviations were associated with higher or lower HDL cholesterol levels. (usda.gov)
- About a dozen genetic markers have been found, including the Cholesterol Ester Transfer Protein gene, which indicates lower risk of heart disease and dementia, as well as the APOC3 gene that protects against cardiovascular disease and diabetes. (yoyenta.com)
- The protein encoded by this gene is found in plasma, where it is involved in the transfer of cholesteryl ester from high density lipoprotein (HDL) to other lipoproteins. (nih.gov)
- Description of the protein which includes the UniProt Function and the NCBI Gene Summary. (nih.gov)
- Publication: Quantile-Dependent Expressivity and Gene-Lifestyle Interactions Involving High-Density Lipoprotein Cholesterol. (nih.gov)
- Key Message: Quantile-dependent expressivity provides a potential explanation for some reported gene-lifestyle interactions for HDL-cholesterol. (nih.gov)
- The lipid part is bound to specific proteins - apolipoproteins (apo), which determine the physical and biological properties of lipoproteins [ 3 ]. (archivesofmedicalscience.com)
- Endogenous TG are synthesized in hepatocytes, where jointly with cholesterol and apolipoproteins (apoB 100, apoE, apoC) constitute building material for VLDL secreted into the blood, where their remnants (IDL) are formed by an action of endothelial lipase (EL). (archivesofmedicalscience.com)
- A potential liability of these compounds was their generally high in vivo clearance due to ethyl ester hydrolysis. (bvsalud.org)
- Within the circulation, THs are mainly bound to proteins (3) and appear only in minor free fractions (FT3, FT4), which are considered as the biologically active pool. (deepdyve.com)
- HDLs are among a family of lipoproteins that transport essential fats, such as cholesterol, through the bloodstream. (nih.gov)
- Complementing the AHA Presidential Advisory's focus on fats, this document found plant-based proteins to be significantly more heart healthy than animal-based proteins. (wordpress.com)
- Serum retinol binding protein transports ingested retinol from the intestine to the liver and other tissues. (elifesciences.org)
- Regulates the reverse cholesterol transport, by which excess cholesterol is removed from peripheral tissues and returned to the liver for elimination (PubMed:17237796). (nih.gov)
- Supply of cholesterol to the peripheral tissues, where it is essential for the formation of cell membranes and biosynthesis of steroid hormones, and to the liver, where it is used for the synthesis of bile acids ( hepatic pathway ) ( Figure 2 ). (archivesofmedicalscience.com)
- Reverse cholesterol transport is a mechanism by which the body removes excess cholesterol from peripheral tissues and delivers them to the liver, where it will be redistributed to other tissues or removed from the body by the gallbladder. (jmir-inc.com)
- As cholesterol in HDL becomes esterified, it creates a concentration gradient and draws in cholesterol from tissues and from other lipoproteins (Figures 26-5 and 26-6), thus enabling HDL to function in reverse cholesterol transport (Figure 25-5). (jmir-inc.com)
- 1] Cholesterol from non-hepatic peripheral tissues is transferred to HDL by the ABCA1 (ATP-binding cassette transporter). (jmir-inc.com)
- Reverse cholesterol transport is a multi-step process resulting in the net movement of cholesterol from peripheral tissues back to the liver first via entering the lymphatic system, then the bloodstream. (jmir-inc.com)
- Cholesterol -- A white crystalline substance found in animal tissues and various foods that is normally synthesized by the liver and is important as a constituent of cell membranes and a precursor to steroid hormones. (nih.gov)
- It is believed to affect blood cholesterol levels by removing cholesterol from plasma and tissues and carrying it back to the liver for action by bile and eventual excretion. (nih.gov)
- Enhanced cholesterol efflux to HDL through the ABCA1 transporter in hypertriglyceridemia of type 2 diabetes. (nih.gov)
- Our objective was to examine the role of hypertriglyceridemia on the capacity of HDL to facilitate ABCA-1 mediated cholesterol efflux in type 2 diabetes (T2DM).HDL mediated cholesterol efflux through the ABCA-1 transporter was measured using BHK cell lines in samples of 71 participants with T2DM in the presence or absence of high triglyceride levels (TG). (nih.gov)
- Scientists identified two additional genes, lipoprotein lipase (LPL) and ATP binding cassette transporter 1 (ABCA1), that may be involved in the cholesterol pathway as well, but more research is needed to confirm these findings. (nih.gov)
- Lipoproteins are a family of large particles composed of an "envelope", which contains phospholipids and free cholesterol, and a core containing TG and cholesterol esters. (archivesofmedicalscience.com)
- Serum amyloid A (SAA) proteins are strongly induced in the liver by systemic infection and in the intestine by bacterial colonization, but their exact functions remain unclear. (elifesciences.org)
- It had been suggested that Serum Amyloid A (SAA) proteins, a family of proteins made by some liver and intestinal cells, could be involved in the response to infection, because these proteins' levels increase during infection. (elifesciences.org)
- Plasma proteins -- Proteins present in blood serum, including serum albumin, blood coagulation factors, and many other types of proteins. (nih.gov)
- Involved in the transfer of neutral lipids, including cholesteryl ester and triglyceride, among lipoprotein particles. (nih.gov)
- BACKGROUND: The phenotypic expression of a high-density lipoprotein (HDL) genetic risk score has been shown to depend upon whether the phenotype (HDL-cholesterol) is high or low relative to its distribution in the population (quantile-dependent expressivity). (nih.gov)
- Proteins that specifically bind to IRON. (umassmed.edu)
- Retinol must bind to specific proteins to be able to move through the bloodstream and be transported around the body. (elifesciences.org)
- went on to solve the crystal structure of a mouse SAA protein, and showed that four SAA molecules bind together to form a 'pocket' that can hold a retinol molecule. (elifesciences.org)
- found that mice fed a diet poor in vitamin A produced fewer SAA proteins in their liver and intestinal cells. (elifesciences.org)
- We evaluated key steps of the reverse cholesterol transport, ie, cellular free cholesterol efflux, cholesteryl ester transfer protein-mediated cholesteryl ester (CE) transfer from HDL to apolipoprotein B-containing lipoproteins, and hepatic HDL-CE uptake, in patients displaying FH (n = 12) and in healthy normolipidemic control subjects (n = 12). (jmir-inc.com)
- Reverse cholesterol transport designates the process by which cholesterol from lipid-loaded peripheral cells, such as macrophage foam cells, passages through the plasma high-density lipoprotein (HDL) compartment to the liver and is excreted via the feces . (jmir-inc.com)
- Instead a microsomal triglyceride transfer protein, which exists as a complex with protein disulphide isomerase in the endoplasmic reticulum, has been implicated. (ox.ac.uk)
- We have cloned and sequenced the human cDNA encoding microsomal triglyceride transfer protein. (ox.ac.uk)
- Microsomal triglyceride transfer protein is expressed in ovary, testis and kidney, in addition to liver and small intestine. (ox.ac.uk)
- SR-BI is an 82-kDa integral membrane protein, belonging to the CD36 family, whose physiologicalrole isrelated totheselective uptake ofHDL cholesteryl ester, the process by which the core cholesteryl ester is taken into the cell without the endocytic uptake and degradation of the whole HDL. (jmir-inc.com)
- It lowers circulating triglyceride levels by activating lipoprotein lipase which is a key enzyme in the degradation of VLDL (very low density lipoprotein) cholesterol. (medicineindia.org)
- The amount of cholesterol carried in blood in high density lipoprotein (HDL) particles is an indicator of heart disease risk, with high levels being favorable. (usda.gov)
- We report here that personal counseling resulted in significant (p=0.0001) reductions in plasma concentrations of total cholesterol, LDL, fasting glucose and 2h glucose. (nih.gov)
- A tight regulation of both placental ApoD transcription and protein content is most probably at the basis of the low circulating ApoD concentrations in women with excessive GWG. (biomedcentral.com)
- The selected examples showed larger genetic effect sizes for lifestyle conditions associated with higher vis-à-vis lower average HDL-cholesterol concentrations. (nih.gov)
Levels of total cholesterol1
- Plasma levels of total cholesterol, HDL cholesterol, and triglyceride in all subjects were 6.28 +/- 1.78, 3.15 +/- 0.90, and 1.08 +/- 0.53 mmol/L, respectively. (qxmd.com)
- A large genetic study of age-related macular degeneration (AMD) has identified three new genes associated with this blinding eye disease-two involved in the cholesterol pathway. (nih.gov)
- We suspect that these genetic variations found in the cholesterol pathway impact the retina differently from the circulatory system, so cholesterol levels in the blood may not provide meaningful information about AMD risk," Swaroop explained. (nih.gov)
- Start studying Unit 9 reverse cholesterol transport pathway. (jmir-inc.com)
- Reverse cholesterol transport (RCT) is a pathway by which accumulated cholesterol is transported from the vessel wall to the liver for excretion, thus preventing atherosclerosis. (jmir-inc.com)
- Exacerbated postprandial hypertriglyceridemia (PP-HTG) and metabolic context both modulate the overall efficacy of the reverse cholesterol transport (RCT) pathway, but the specific contribution of exaggerated PP-HTG on RCT efficacy remains indeterminate. (jmir-inc.com)
- Therefore, we investigated deviations in genes that code for proteins involved in physiologic pathways related to HDL cholesterol. (usda.gov)
- Blood samples were drawn from 759 individuals, and HDL cholesterol levels were measured, and deviations in 23 genes were determined. (usda.gov)
- Deviations in many genes were associated with HDL cholesterol levels, including cholesterol ester transfer protein (which moves cholesterol among lipoproteins), beta-carotene mono-oxygenase 1 (which converts beta-carotene to vitamin A), and transporters that move the vitamin folate into cells. (usda.gov)
- Additionally, HDL mediated efflux was measured in 13 diabetic and non-diabetic participants fasting and four hours after a high-fat test challenge.HDL mediated cholesterol efflux function was increased in participants with T2DM with hypertriglyceridemia when compared to participants with T2DM without hypertriglyceridemia (efflux ratio mean±standard deviation (SD), T2DM+TG: 1.17±0.25 vs. T2DM - TG: 1.03±0.19, p=0.0098). (nih.gov)
- Iron-Binding Proteins" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
- Allows the net movement of cholesteryl ester from high density lipoproteins/HDL to triglyceride-rich very low density lipoproteins/VLDL, and the equimolar transport of triglyceride from VLDL to HDL (PubMed:3600759, PubMed:24293641). (nih.gov)
- Genetic analysis of long-lived families reveals novel variants influencing high density-lipoprotein cholesterol. (cdc.gov)
- This suggests these reported interactions could be the result of selecting subjects for conditions that differentiate high from low HDL-cholesterol (e.g., lean vs. overweight, active vs. sedentary, high-fat vs. high-carbohydrate diets, alcohol drinkers vs. abstainers, nonsmokers vs. smokers) producing larger versus smaller genetic effect sizes. (nih.gov)
- Molecular biology -- The branch of biology dealing with the formation, structure, and function of macromolecules essential to life, such as DNA, RNA, and proteins, especially their role in cell replication and the transmission of genetic information. (nih.gov)
Reverse cholesterol transport5
- This review aims to summarize recent studies demonstrating … San Francisco, U.S.A. Reverse cholesterol transport in insulin resistance and type 2 diabetes mellitus. (jmir-inc.com)
- macrophage- reverse cholesterol transport (m-RCT), is an important anti-atherogenic mechanism. (jmir-inc.com)
- Increasing reverse cholesterol transport may someday be a way to reduce atherosclerosis and heart disease. (jmir-inc.com)
- Initial steps in reverse cholesterol transport: the role of short-lived cholesterol acceptors O. L. Francone Search for other works by this author on: Oxford Academic. (jmir-inc.com)
- The reverse cholesterol transport (RCT) is the process that may counteract the pathogenic events leading to the formation of atheroma. (jmir-inc.com)
- Factors affecting high-density lipoprotein cholesterol in HIV-infected patients on nevirapine-based antiretroviral therapy. (cdc.gov)
- Although high-density lipoprotein cholesterol is not a causal risk factor for CAD, it has been unequivocally demonstrated that low-density lipoprotein cholesterol lowering is proportionally associated with a lower CAD risk. (tilburguniversity.edu)
- 0.05), and high-density lipoprotein subfraction 2 cholesterol remained unchanged. (ox.ac.uk)
- It is prodrug which has greater LDL (low density lipoprotein) cholesterol lowering potential. (medicineindia.org)
- It also reduces VLDL levels and increases HDL (high density lipoprotein) cholesterol. (medicineindia.org)
- High-density lipoprotein cholesterol (HDLC) -- The portion of plasma lipoprotein cholesterol with most density. (nih.gov)
- Low-density lipoprotein cholesterol (LDLC) -- The protein-lipid combination that transports the major amount of the cholesterol in the blood. (nih.gov)
Amount of cholesterol1
- The cells are grown in the laboratory and the amount of cholesterol that enters or leaves the cells is measured, providing information on abnormalities in cholesterol transport. (nih.gov)
- The increase in HDL cholesterol is partly due to transfer of surface lipid components from catabolised VLDL to HDL and also due to increased production of HDL apoproteins by liver. (medicineindia.org)
- But there is a correlation between certain types of cholesterol in the blood and heart disease, like high levels of the small, dense LDL are connected to an increased risk of heart attacks. (thehealthyskeptic.org)
- The cholesterol in your diet doesn't necessarily effect the levels of these different types of cholesterol in your blood right? (thehealthyskeptic.org)
- But is it right to say that cholesterol in the diet doesn't effect heart disease but certain levels of certain types of cholesterol in the blood can lead to heart disease? (thehealthyskeptic.org)
- However, the relationship between HDL cholesterol levels in the blood and AMD is still unclear. (nih.gov)
- The most common risk factors are cigarette smoking, diabetes, high blood pressure and elevated cholesterol. (wordpress.com)
- While LDLC helps in synthesis of bile acid and steroid hormones, elevated blood levels of LDLC--or 'bad cholesterol'--have been linked to heart disease because it carries the cholesterol through the blood to the cells. (nih.gov)
- The structure of lipoproteins is maintained primarily by hydrophobic interactions between nonpolar components of lipids and proteins. (archivesofmedicalscience.com)
- explain why LDL and total cholesterol are not useful markers for heart disease. (thehealthyskeptic.org)
- In daily practice, non-HDL cholesterol level (ie, LDL + very LDL cholesterol [total cholesterol - HDL cholesterol]) is the most readily available measure of the total pool of these atherogenic lipoproteins. (medscape.com)
- This graph shows the total number of publications written about "Iron-Binding Proteins" by people in this website by year, and whether "Iron-Binding Proteins" was a major or minor topic of these publications. (umassmed.edu)
- Atherosclerosis accounts for up to 80% of cholesterol (LDL-C) and the total choles- deaths in diabetic patients due to coronary terol/HDL-C ratio (TC/HDL-C) [ 1 ]. (who.int)
- Synthesis of cholesterol in the abnormal tonsil was brisk, but not obviously greater than in similar unaffected tissue (7). (nih.gov)
- Protein chemistry -- A branch of chemistry which encompasses a range of techniques and approaches that can aid the investigation of protein structure and function. (nih.gov)
- Dyslipidaemia obesity and insulin changes highly acceler- encompasses changes in HDL-cholesterol ate the progression to atherosclerosis [ 2 ]. (who.int)
- It is believed that early stages of AMD are affected by accumulation of oxidation products of cholesterol and other lipids in the retinal pigment epithelium, a layer of cells in the back of the eye. (nih.gov)
- Patients with established coronary disease and low HDL cholesterol levels are at high risk for recurrent events and should be targeted for aggressive nonpharmacological (ie, dietary modification, weight loss, physical exercise) and pharmacological treatment. (medscape.com)