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.

Original languageEnglish (US)
Pages (from-to)1992-2000
Number of pages9
Issue number3
StatePublished - Mar 2015


  • Acetic Acid
  • Adipose Tissue
  • Alcoholic Beverages
  • Blood Glucose
  • Cardiovascular Diseases
  • Cholesterol, HDL
  • Ethanol
  • Humans
  • Insulin
  • Receptors, G-Protein-Coupled


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