期刊
TRENDS IN ENDOCRINOLOGY AND METABOLISM
卷 27, 期 1, 页码 44-53出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2015.11.004
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资金
- NHLBI NIH HHS [R01 HL056865, R01 HL030914] Funding Source: Medline
Although high-density lipoprotein-cholesterol (HDL-C) concentration is a negative risk factor for atherosclerotic cardiovascular disease (CVD), efforts to reduce CVD risk by raising HDL-C have not been uniformly successful. Many studies have shown that alcohol consumption, that increases plasma HDL-C concentration, reduces CVD incidence. However, recent genetic studies in large populations have not only removed HDL-C from the causal link between plasma HDL-C concentration and reduced CVD risk, but also suggest that the association is weak. We propose here that the cardioprotective effects of alcohol are mediated by the interaction of its terminal metabolite, acetate, with the adipocyte free fatty acid receptor 2 (FFAR2), which elicits a profound antilipolytic effect that may increase insulin sensitivity without necessarily raising plasma HDL-C concentration.
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