What is apoc iii

ApoC-III content of apoB-containing lipoproteins is associated with binding to the vascular proteoglycan biglycan. A proteomic study of the apolipoproteins in LDL subclasses in patients with the metabolic syndrome and type 2 diabetes. Role of extracellular retention of low density lipoproteins in atherosclerosis.

Gustafsson M, Boren J. Mechanism of lipoprotein retention by the extracellular matrix. Retention of atherogenic lipoproteins in atherogenesis. Cell Mol Life Sci. Effects of dietary fats on the fluidity of human high-density lipoprotein: influence of the overall composition and phospholipid fatty acids. Apolipoprotein B conservation of lipid-associating amphipathic secondary structural motifs in nine species of vertebrates.

Molecular mechanism for changes in proteoglycan binding on compositional changes of the core and the surface of low-density lipoprotein-containing human apolipoprotein B Clin Biochem. Sphingomyelinase induces aggregation and fusion, but phospholipase A2 only aggregation, of low density lipoprotein LDL particles. Two distinct mechanisms leading to increased binding strength of LDL to human aortic proteoglycans.

Secretory sphingomyelinase, a product of the acid sphingomyelinase gene, can hydrolyze atherogenic lipoproteins at neutral pH. Implications for atherosclerotic lesion development. Modification of LDL with human secretory phospholipase A 2 or sphingomyelinase promotes its arachidonic acid-releasing propensity.

Macrophage uptake of cholesterol-containing particles derived from LDL and isolated from atherosclerotic lesions. Eur Heart J. E — Susceptibility of low-density lipoprotein particles to aggregate depends on particle lipidome, is modifiable, and associates with future cardiovascular deaths. Apolipoprotein CIII induces expression of vascular cell adhesion molecule-1 in vascular endothelial cells and increases adhesion of monocytic cells.

Apolipoprotein C-III strongly correlates with activated factor VII-anti-thrombin complex: an additional link between plasma lipids and coagulation. Thromb Haemost. Apolipoprotein CIII links islet insulin resistance to beta-cell failure in diabetes. Increased incidence of ischemic cerebrovascular events in cardiovascular patients with elevated apolipoprotein CIII. Effects of APOC3 heterozygous deficiency on plasma lipid and lipoprotein metabolism.

A null mutation in human APOC3 confers a favorable plasma lipid profile and apparent cardioprotection. Circ Cardiovasc Genet.

Implementing a successful data-management framework: the UK10K managed access model. Genome Med. A rare functional cardioprotective APOC3 variant has risen in frequency in distinct population isolates.

Nat Commun. Two novel mutations in apolipoprotein C3 underlie atheroprotective lipid profiles in families. Clin Genet. Characterization of the lipid-binding properties and lipoprotein lipase inhibition of a novel apolipoprotein C-III variant Ala23Thr.

APOC3 Loss-of-function mutations, remnant cholesterol, low-density lipoprotein cholesterol, and cardiovascular risk: mediation- and meta-analyses of individuals. Human knockouts and phenotypic analysis in a cohort with a high rate of consanguinity. Variations in plasma apolipoprotein C-III levels are strong correlates of the triglyceride response to a high-monounsaturated fatty acid diet and a high-carbohydrate diet. Am J Clin Nutr. Increased plasma concentrations of lipoprotein a during a low-fat, high-carbohydrate diet are associated with increased plasma concentrations of apolipoprotein C-III bound to apolipoprotein B-containing lipoproteins.

Adverse effects of fructose on cardiometabolic risk factors and hepatic lipid metabolism in subjects with abdominal obesity. J Intern Med. Dietary fructose and the metabolic syndrome. Effects of dietary fructose restriction on liver fat, de novo lipogenesis, and insulin kinetics in children with obesity.

An integrated understanding of the rapid metabolic benefits of a carbohydrate-restricted diet on hepatic steatosis in humans.

Cell Metab. Effects of fructose or glucose on circulating ApoCIII and triglyceride and cholesterol content of lipoprotein subfractions in humans. J Clin Med. Hieronimus B, Stanhope KL. Dietary fructose and dyslipidemia: new mechanisms involving apolipoprotein CIII. Overproduction of VLDL1 driven by hyperglycemia is a dominant feature of diabetic dyslipidemia.

Overproduction of large VLDL particles is driven by increased liver fat content in man. Fatty liver, insulin resistance, and dyslipidemia. Curr Diab Rep. Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management. Broad views of non-alcoholic fatty liver disease. Cell Syst. Eur J Clin Nutr. Effect of omega-3 supplements on plasma apolipoprotein C-III concentrations: a systematic review and meta-analysis of randomized controlled trials.

Ann Med. The effect of omega-3 carboxylic acids on apolipoprotein CIII-containing lipoproteins in severe hypertriglyceridemia. Oscarsson J, Hurt-Camejo E. Omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid and their mechanisms of action on apolipoprotein B-containing lipoproteins in humans: a review. Lipids Health Dis. Hypertriglyceridemia as a result of human apo CIII gene expression in transgenic mice. Postprandial concentrations and distribution of apo C-III in type 2 diabetic patients.

Effect Of bezafibrate treatment. Contribution of apo CIII reduction to the greater effect of week micronized fenofibrate than atorvastatin therapy on triglyceride levels and LDL size in dyslipidemic patients.

People with elevated triglycerides are at increased risk for cardiovascular disease and for type 2 diabetes. People with severely elevated triglycerides, such as people with familial chylomicronemia syndrome FCS , are at high risk for acute pancreatitis and other serious conditions.

Further, its presence on lipoproteins may increase their atherogenicity. A study in the New England Journal of Medicine reported that out of a sample of over , people, individuals with an apoC-III loss-of-function mutation had a reduced risk of clinical coronary heart disease. Triglycerides may also play a role in cardiovascular risk.

This gene is overexpressed in Liver x This gene is overexpressed in Serum Show more. Tissue specificity: Liver. Liver 4. Germ Layers: endoderm mesoderm. Systems: cardiovascular digestive. Regions: Head and neck: ear. Thorax: heart. Abdomen: duodenum intestine liver small intestine. General: blood vessel. This gene was present in the common ancestor of mammals. All consequence types are included: molecular consequences e. Residual Variation Intolerance Score : Gene Damage Index Score : 0.

Quality Products:. Metabolism of water-soluble vitamins and cofactors. ENSP 19 P By this way a delicate system was created where the islets rich and deficient in apoCIII coexisted in one animal model. The disagreement may be caused by the differences about experiment factors such as models and intervention methods. Although whether lipoprotein-associated phospholipase A2 Lp-PLA2 is an independent risk factor for atherosclerosis remains controversial, Lp-PLA2 activity and mass shows a strong, positive association with atherosclerosis [ 34 ].

However, the detailed mechanisms in the circle still await further investigation. The phase 2 study evaluated the pharmacodynamic effects of volanesorsen in adult patients with severe or uncontrolled HTG [ 37 ].

Similar changes occurred when volanesorsen was given as an add-on to stable fibrate therapy. No serious treatment-associated safety issues were identified. The apparent clinical benefits brought by volanesorsen presented not only in patients with HTG but also in those with familial chylomicronemia syndrome FCS. Short-term efficacy and apparent safety of volanesorsen brings light to further long-term evaluation.

These studies aim to evaluate the efficacy and safety of mg volanesorsen versus placebo administered subcutaneously once a week for 52 ,26, 52 weeks respectively in patients with corresponding diseases. The primary outcome is measured by the percent change in fasting TG from baseline to 13 weeks. In addition to the promising ASO treatment, zeolite nanoparticles, whose negative charge help it to interact electrostatically with the positively charged amino acid residues of apoCIII , selectively capture plasma apoCIII and may be a potential therapy to reduce plasma apoCIII in the future [ 40 ].

Considerable evidence indicates that apoCIII can affect the development of CVD not only by regulating triglyceride metabolism but also through its direct atherogenic effects.

Novel understanding of apoCIII in atherogenesis makes it an attractive therapy target and some innovative approaches to modifying it emerge. Although full illustration of apoCIII function still awaits further exploration, to lower the apoCIII levels in circulation via specific intervention seems to be an intriguing therapy for cardiovascular protection. Effects of combination lipid therapy in type 2 diabetes mellitus.

N Engl J Med. Article Google Scholar. Common variants associated with plasma triglycerides and risk for coronary artery disease. Nat Genet. Loss-of-function mutations in APOC3, triglycerides, and coronary disease. Loss-of-function mutations in APOC3 and risk of ischemic vascular disease. Article PubMed Google Scholar. Apolipoprotein C-III: understanding an emerging cardiovascular risk factor. Clin Sci Lond. J Lipid Res. Yao Z. Human apolipoprotein C-III: a new intrahepatic protein factor promoting assembly and secretion of very low density lipoproteins.

Cardiovasc Hematol Disord Drug Targets. Low-density lipoproteins containing apolipoprotein C-III and the risk of coronary heart disease. Increased plasma apolipoprotein C-III concentration independently predicts cardiovascular mortality: the Hoorn study. Clin Chem. D25V apolipoprotein C-III variant causes dominant hereditary systemic amyloidosis and confers cardiovascular protective lipoprotein profile. Nat Commun.