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Influence of insulin on cholesterol removal from macrophages and cholesterol ester uptake by HepG2 cells
Author(s) -
WYBRAŃSKA I.,
BACZYŃSKA E.,
CIAŁOWICZ U.,
POLUS A.,
DEMBIŃSKAKIEĆ A.
Publication year - 1996
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1996.2350584.x
Subject(s) - insulin , cholesterol , medicine , endocrinology , chemistry , efflux , reverse cholesterol transport , lipoprotein , biology , biochemistry
The fact that an increased blood insulin level is observed in patients with coronary artery disease (CAD) confirms the hypothesis that insulin promotes the development of atherosclerosis. The low high‐density lipoprotein (HDL) concentration observed in such patients may contribute to alteration in reverse cholesterol transport and promote the accumulation of sterols in vascular tissue. We examined the effect of insulin (20−1000μUmL −1 ) on cholesterol efflux into HDL 3 particles from human blood monocyte/macrophages and rat peritoneal macrophages preloaded with labelled cholesterol esters, and the influence of insulin on the accumulation of sterols by rat liver cells and HepG2 cell line in vitro models. Insulin at concentrations up to 250μUmL −1 inhibited the efflux of cholesterol from rat macrophages and promoted high uptake of sterols by both types of hepatic cells. Pharmacological concentrations higher than 250μU mL −1 exerted the opposite effect. In the case of human macrophages, an insulin concentration of 20μUmL −1 increased cholesterol removal, whereas 100−200μU mL −1 insulin inhibited cholesterol removal from cells, and very high concentrations (>350μUmL −1 ) again increased cholesterol removal. We have shown that insulin excess counteracts the beneficial effects of HDL in removing cellular cholesterol and, therefore, may promote development of atherogenesis.