Abstract
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.
Highlights
Numerous studies have shown that cardiovascular disease is lower among alcohol consumers than among nonconsumers
These findings suggest that mild-to-moderate alcohol consumption (≤one to two drinks per day) might be a reasonable consumption rate for some persons with low plasma
Alcohol consumption modestly activates hepatic De Novo Lipogenesis (DNL), but hepatic acetate production and the release into plasma inhibits lipolysis and alters tissue fuel selection; acetate is the major quantitative fate of ingested ethanol. These studies show how alcohol modifies lipid metabolism, they remain confounded by the likelihood that the anti-diabetic and cardioprotective effects are mediated by acetate, effects that might by shrouded by separate effects of the precursors, alcohol and acetaldehyde
Summary
Beer, and spirits have been a component of the diet in many cultures over the ages. Alcohol has one well-known salutary effect; people who consume alcohol in moderation, two drinks/day for men and one drink/day for women, live longer and experience less cardiovascular disease (CVD); with higher alcohol intake life expectancy decreases, an effect that is due not to CVD but rather to well-known alcohol-promoted conditions, cirrhosis, and cancers of the mouth, esophagus, pharynx, larynx, and liver; breast cancer in women; injuries and other external causes in men [1]. These data and many other observational studies would suggest that moderate alcohol consumption is healthful. What are the mechanisms by which alcohol reduces the CVD rates? Are there other healthful alternatives to alcohol consumption that could provide the positive CVD effects of alcohol without the occurrence of other diseases, including psychosocial effects that occur at high rates of consumption?
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