Abstract
Retinoic acid, an active metabolite of dietary vitamin A, acts as a ligand for nuclear receptor transcription factors with more than 500 known target genes. It is becoming increasingly clear that alcohol has a significant impact on cellular retinoic acid metabolism, with resultant effects on its function. Here, we test the hypothesis that chronic alcohol consumption impairs retinoic acid signaling in brown adipose tissue (BAT), leading to impaired BAT function and thermoregulation. All studies were conducted in age-matched, male mice consuming alcohol-containing liquid diets. Alcohol’s effect on BAT was assessed by histology, qPCR, HPLC, LC/MS and measures of core body temperature. Our data show that chronic alcohol consumption decreases BAT mass, with a resultant effect on thermoregulation. Follow-up mechanistic studies reveal a decreased triglyceride content in BAT, as well as impaired retinoic acid homeostasis, associated with decreased BAT levels of retinoic acid in alcohol-consuming mice. Our work highlights a hitherto uncharacterized effect of alcohol on BAT function, with possible implications for thermoregulation and energy metabolism in drinkers. Our data indicate that alcohol’s effects on brown adipose tissue may be mediated through altered retinoic acid signaling.
Highlights
To chronic alcohol exposure, but this phenomenon has not been rigorously studied[14,15,16]
This hypothesis is based on three pieces of information: (1) retinoic acid’s putative role in controlling UCP1 expression and brown adipose tissue (BAT) function; (2) altered BAT homeostasis following acute and chronic alcohol exposure; and (3) our preliminary data demonstrating that chronic alcohol consumption decreases BAT weight in mice
An important conclusion drawn from our experimental data is that the alcohol-induced decrease in BAT weight is linked to altered thermoregulation
Summary
To chronic alcohol exposure, but this phenomenon has not been rigorously studied[14,15,16]. The current work tests the hypothesis that chronic alcohol consumption impairs retinoic acid signaling in BAT, leading to impaired BAT function and thermoregulation. This hypothesis is based on three pieces of information: (1) retinoic acid’s putative role in controlling UCP1 expression and BAT function; (2) altered BAT homeostasis following acute and chronic alcohol exposure; and (3) our preliminary data demonstrating that chronic alcohol consumption decreases BAT weight in mice. We conclude that chronic alcohol consumption impairs BAT homeostasis, an effect which may be mediated by altered retinoic acid signaling and impaired lipid metabolism. Our work highlights the effects of chronic alcohol consumption on BAT, as well as the potential importance of retinoic acid signaling in the maintenance of normal BAT function
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