Expression of human apolipoprotein A-II in apolipoprotein E-deficient mice induces features of familial combined hyperlipidemia
نویسندگان
چکیده
منابع مشابه
Combined hyperlipidemia in transgenic mice overexpressing human apolipoprotein Cl.
We have generated transgenic mice over-expressing human apolipoprotein CI (apo CI) using the native gene joined to the downstream 154-bp liver-specific enhancer that we defined for apo E. Human apo CI (HuCI)-transgenic mice showed elevation of plasma triglycerides (mg/dl) compared to controls in both the fasted (211 +/- 81 vs 123 +/- 52, P = 0.0001) and fed (265 +/- 105 vs 146 +/- 68, P < 0.000...
متن کاملAntioxidative and antiatherosclerotic effects of human apolipoprotein A-IV in apolipoprotein E-deficient mice.
Mice expressing human apolipoprotein A-IV (apoA-IV) mainly in the intestine were obtained in an apolipoprotein E-deficient (apoE(0)) background (apoA-IV/E(0) mice). Quantification of aortic lesions and plasma lipid determination showed that compared with their control apoE(0) counterparts, the apoA-IV/E(0) mice are protected against atherosclerosis without an increase in HDL cholesterol. Becaus...
متن کاملBiochemical and genetic association of plasma apolipoprotein A-II levels with familial combined hyperlipidemia.
Apolipoprotein A-II (apoA-II) is a major protein on high-density lipoprotein (HDL) particles, and in mice, its levels are associated with triglyceride and glucose metabolism. In particular, transgenic mice overexpressing apoA-II exhibit hypertriglyceridemia, increased body fat, and insulin resistance, whereas apoA-II-null mice have decreased triglycerides and increased insulin sensitivity. Give...
متن کاملApolipoprotein A-II: active or passive role in familial combined hyperlipidemia.
Familial combined hyperlipidemia (FCH) was originally identified as a new phenotype in studies of survivors of myocardial infarctions and their relatives.1–3 Patients with FCH were found to present with any of three patterns of lipoprotein distribution: elevated plasma levels of very lowdensity lipoprotein (VLDL) or low-density lipoprotein (LDL) or both. Within kindred, affected individuals oft...
متن کاملMacrophage-specific expression of human apolipoprotein E reduces atherosclerosis in hypercholesterolemic apolipoprotein E-null mice.
apoE deficiency causes hyperlipidemia and premature atherosclerosis. To determine if macrophage-specific expression of apoE would decrease the extent of atherosclerosis, we expressed human apoE in macrophages of apoE-null mice (apoE-/-) and assessed the effect on lipid accumulation in cells of the arterial wall. Macrophage-specific expression of human apoE in normal mice was obtained by use of ...
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ژورنال
عنوان ژورنال: Journal of Lipid Research
سال: 2000
ISSN: 0022-2275
DOI: 10.1016/s0022-2275(20)33441-6