Pownall Henry J, Rosales Corina, Gillard Baiba K, Gotto Antonio M
Department of Cardiology, Division of Atherosclerosis, Houston Methodist Research Institute, Fondren F8-047, 6670 Bertner St., Houston, TX 77030, USA.
Department of Medicine, Weill Cornell Medical College, 1305 York Ave. Y-805, New York, NY 10021, USA.
Nutrients. 2015 Mar 18;7(3):1992-2000. doi: 10.3390/nu7031992.
Numerous studies have shown that cardiovascular disease is lower among alcohol consumers than among nonconsumers. Many of the metabolic effects of alcohol are mediated by its terminal metabolite, acetate, which has reported insulinemic properties. There have been few rational metabolic targets that underly its cardioprotective effects until it was reported that acetate, the terminal product of alcohol metabolism, is the ligand for G-protein coupled receptor 43 (GPCR43), which is highly expressed in adipose tissue. Here, we recast much of some of the major lipid and lipoprotein effects of alcohol in the context of this newly discovered G-protein and develop a mechanistic model connecting the interaction of acetate with adipose tissue-GPCR43 with these effects. According to our model, ingestions of acetate could replace alcohol as a means of improving plasma lipid risk factors, improving glucose disposal, and reducing cardiovascular disease. Future studies should include biochemical, cell, animal, and human tests of acetate on energy metabolism.
大量研究表明，饮酒者患心血管疾病的几率低于不饮酒者。酒精的许多代谢作用是由其终末代谢产物乙酸介导的，乙酸具有胰岛素样特性。在有报道称酒精代谢的终末产物乙酸是G蛋白偶联受体43（GPCR43）的配体，且该受体在脂肪组织中高表达之前，几乎没有合理的代谢靶点可以解释其心脏保护作用。在此，我们根据这一新发现的G蛋白重新阐述了酒精对一些主要脂质和脂蛋白的影响，并建立了一个机制模型，将乙酸与脂肪组织-GPCR43的相互作用与这些影响联系起来。根据我们的模型，摄入乙酸可以替代酒精，作为改善血浆脂质风险因素、改善葡萄糖代谢以及降低心血管疾病风险的一种手段。未来的研究应包括对乙酸在能量代谢方面的生化、细胞、动物和人体试验。
