Apolipoprotein E allele frequencies in non-insulin-dependent diabetes mellitus with hypertriglyceridemia (type IIb, III, IV, and V hyperlipoproteinemia).
Apolipoprotein E genetic variants interact with Mediterranean diet to modulate postprandial hypertriglyceridemia in coronary heart disease patients: CORDIOPREV study.
Adenovirus-mediated gene transfer of apoE4-mut1 (apoE4 (L261A, W264A, F265A, L268A, V269A)) in apoE-deficient mice (apoE(-/-)) corrected plasma cholesterol levels and did not cause hypertriglyceridemia.
Compared to apoE3 carriers, the apoE4 allele significantly increased the risk of expressing the "hyperTG/hyperapoB" phenotype [odds ratio (OR)=1.95; p=0.014].
Family studies failed to demonstrate cosegregation between the new mutations and severe hyperlipoproteinemia, although a number of carriers for the APOE*3(Cys112-->Arg; Arg251-->Gly) allele and the APOE*1(Arg158-->Cys; Leu252-->Glu) allele expressed hypertriglyceridemia and/or hypercholesterolemia.
Given the important role of apolipoprotein E (apoE) in triglyceride metabolism, we analyzed plasma levels and degree of sialylation of apoE in subjects with the acquired immunodeficiency syndrome (AIDS), a disorder accompanied by hypertriglyceridemia.
However, APOE4- women decreased high-density lipoprotein-cholesterol (HDL-C) by 17% +/- 11% and increased triglycerides by 20% +/- 41% in response to the diet, while APOE4+ women had a smaller decrease in HDL-C (-8% +/- 12%) and no change in plasma triglyceride.
In contrast, a low dose of 5 x 10(8) pfu of the apoE4-expressing adenovirus corrected hypercholesterolemia in apoE(-/-) mice and did not trigger hypertriglyceridemia.
In contrast, an adenovirus expressing the truncated apoE 1-185 form normalized the cholesterol levels of E(-)(/)(-) mice and did not cause hypertriglyceridemia.
It is concluded that the genetic polymorphism of apoE modulates the effects of obesity on lipids and lipoproteins and that allele epsilon 4 increases the risk of obesity-induced hypertriglyceridemia.
None of the family members carrying APOE*3-(Cys-112-->Arg; Arg-251-->Gly) and/or APOE*2(Val-236-->Glu) exhibited lipoprotein abnormalities characteristic of familial dysbetalipoproteinaemia, although three family members carrying APOE*3-(Cys-112-->Arg; Arg-251-->Gly) showed hypertriglyceridaemia.