Effects of ethanol consumption on brown adipose tissue thermogenic capacity in mice

Dv, Muralidhara; Desautels, M.

doi:10.1016/s0031-9384(96)80042-4

Cited by 9 publications

(13 citation statements)

References 21 publications

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“…In a proof of concept experiment, overexpression of CYP2E1 in 3T3-L1 adipocytes incubated with alcohol decreased adiponectin secretion similar to that seen in vivo in rodents [21]. ADH is primarily expressed in the liver, but also found at low levels in eWAT and BAT and is almost undetectable in sWAT [19,72]. Although ADH expression was unchanged in chronic alcohol-fed mice, it may still be important in the production of acetaldehyde and the effects of that metabolite on WAT [19].…”

Section: Alcohol Metabolismmentioning

confidence: 94%

“…Alcohol easily permeates BAT as measurable levels have been reported in alcohol-fed mice [45]. Compared with the liver, BAT has a low level of ADH activity which is unchanged after 10 days of chronic alcohol intake [72,111]. …”

Section: Brown Adipose Tissuementioning

confidence: 99%

“…The effects of alcohol on BAT mass of the interscapular depot are inconsistent as no change, an increase and decrease have all been reported depending on the experimental conditions [72,112,113,114]. No change in BAT mass has been observed after 10 days (male mice) [72], 14 days (male rats) [112], or 5 weeks (mice) [46] of alcohol, while one report observed a decrease after 25 days (male mice) [72].…”

Section: Brown Adipose Tissuementioning

confidence: 99%

“…No change in BAT mass has been observed after 10 days (male mice) [72], 14 days (male rats) [112], or 5 weeks (mice) [46] of alcohol, while one report observed a decrease after 25 days (male mice) [72]. In mice categorized as being obese (body weight (BW) > 40 g), 5 weeks of alcohol in the drinking water prevented the increase in BAT observed in the control mice, suggesting that alcohol may suppress expansion of this fat depot during periods of over-nutrition [46].…”

Section: Brown Adipose Tissuementioning

confidence: 99%

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Alcohol, Adipose Tissue and Lipid Dysregulation

Steiner

Lang

2017

Biomolecules

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Chronic alcohol consumption perturbs lipid metabolism as it increases adipose tissue lipolysis and leads to ectopic fat deposition within the liver and the development of alcoholic fatty liver disease. In addition to the recognition of the role of adipose tissue derived fatty acids in liver steatosis, alcohol also impacts other functions of adipose tissue and lipid metabolism. Lipid balance in response to long-term alcohol intake favors adipose tissue loss and fatty acid efflux as lipolysis is upregulated and lipogenesis is either slightly decreased or unchanged. Study of the lipolytic and lipogenic pathways has identified several regulatory proteins modulated by alcohol that contribute to these effects. Glucose tolerance of adipose tissue is also impaired by chronic alcohol due to decreased glucose transporter-4 availability at the membrane. As an endocrine organ, white adipose tissue (WAT) releases several adipokines that are negatively modulated following chronic alcohol consumption including adiponectin, leptin, and resistin. When these effects are combined with the enhanced expression of inflammatory mediators that are induced by chronic alcohol, a pro-inflammatory state develops within WAT, contributing to the observed lipodystrophy. Lastly, while chronic alcohol intake may enhance thermogenesis of brown adipose tissue (BAT), definitive mechanistic evidence is currently lacking. Overall, both WAT and BAT depots are impacted by chronic alcohol intake and the resulting lipodystrophy contributes to fat accumulation in peripheral organs, thereby enhancing the pathological state accompanying chronic alcohol use disorder.

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Section: Alcohol Metabolismmentioning

confidence: 94%

Section: Brown Adipose Tissuementioning

confidence: 99%

Section: Brown Adipose Tissuementioning

confidence: 99%

Section: Brown Adipose Tissuementioning

confidence: 99%

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Alcohol, Adipose Tissue and Lipid Dysregulation

Steiner

Lang

2017

Biomolecules

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“…However, this so-called hypothermic effect of alcohol has primarily been studied in response to acute alcohol exposure1213. A limited number of chronic studies have reported decreased BAT weight in response to chronic alcohol exposure, but this phenomenon has not been rigorously studied141516. The current work tests the hypothesis that chronic alcohol consumption impairs retinoic acid signaling in BAT, leading to impaired BAT function and thermoregulation.…”

mentioning

confidence: 89%

Chronic alcohol consumption decreases brown adipose tissue mass and disrupts thermoregulation: a possible role for altered retinoid signaling

Blaner

Gao

Jiang

et al. 2017

Sci Rep

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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.

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