Mechanism-Based Biomarker Prediction for Low-Grade Inflammation in Liver and Adipose Tissue

Sympathetic nervous system control of triglyceride metabolism: Novel concepts derived from recent studies

Aspirin reduces hypertriglyceridemia by lowering VLDL-triglyceride production in mice fed a high-fat diet

The expression of type III hyperlipoproteinemia: Involvement of lipolysis genes

Niacin increases HDL by reducing hepatic expression and plasma levels of cholesteryl ester transfer protein in APOE*3Leiden.CETP mice

ApoE2-associated hypertriglyceridemia is ameliorated by increased levels of apoA-V but unaffected by apoC-III deficiency

Plasma apoAV levels are markedly elevated in severe hypertriglyceridemia and positively correlated with the APOA5 S19W polymorphism

The Hyplip2 locus causes hypertriglyceridemia by decreased clearance of triglycerides

Ritonavir impairs lipoprotein lipase-mediated lipolysis and decreases uptake of fatty acids in adipose tissue

Apolipoprotein AV: Low concentration, high impact

Generation of a recombinant apolipoprotein E variant with improved biological functions: Hydrophobic residues (LEU-261, TRP-264, PHE-265, LEU-268, VAL-269) of apoE can account for the apoE-induced hypertriglyceridemia

Severe hypertriglyceridemia in human APOC1 transgenic mice is caused by apoC-I-induced inhibition of LPL

Modulating effect of the A-278C promoter polymorphism in the cholesterol 7alpha-hydroxylase gene on serum lipid levels in normolipidaemic and hypertriglyceridaemic individuals

ApoAV reduces plasma triglycerides by inhibiting very low density lipoprotein-triglycerides (VLDL-TG) production and stimulating lipoprotein lipase-mediated VLDL-TG hydrolysis

Stimulation of lipogenesis by pharmacological activation of the liver X receptor leads to production of large, triglyceride-rich very low density lipoprotein particles

Apolipoprotein E2 (Lys146→Gln) causes hypertriglyceridemia due to an apolipoprotein E variant-specific inhibition of lipolysis of very low density lipoproteins-triglycerides

Normal oxidative stress and enhanced lipoprotein resistance to in vitro oxidation in hypertriglyceridemia Effects of bezafibrate therapy

Hyperlipidemia of ApoE2(Arg158-Cys) and ApoE3-Leiden transgenic mice is modulated predominantly by LDL receptor expression

In LDL receptor-deficient mice, catabolism of remnant lipoproteins requires a high level of apoE but is inhibited by excess apoE

Hyperlipidemia and cutaneous abnormalities in transgenic mice overexpressing human apolipoprotein C1