Commentary 10.1172/JCI128984
Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, Maryland, USA.
Address correspondence to: Bin Gao, Laboratory of Liver Diseases, NIAAA/NIH, 5625 Fishers Lane, Bethesda, Maryland 20892, USA; Phone: 301.443.3998; Email: bgao@mail.nih.gov.
Find articles by Hwang, S. in: JCI | PubMed | Google Scholar
Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, Maryland, USA.
Address correspondence to: Bin Gao, Laboratory of Liver Diseases, NIAAA/NIH, 5625 Fishers Lane, Bethesda, Maryland 20892, USA; Phone: 301.443.3998; Email: bgao@mail.nih.gov.
Find articles by Gao, B. in: JCI | PubMed | Google Scholar
First published April 29, 2019 - More info
White adipose tissue (WAT) dysfunction is generally thought to promote the development of alcoholic liver disease (ALD) in alcoholics by releasing free fatty acids and inflammatory mediators. This explains, at least in part, the synergistic or additive effects of alcohol and obesity on liver disease progression. In this issue of the JCI, Shen et al. establish a previously unrecognized concept that brain alcohol sensing enhances thermogenesis of brown adipose tissue (BAT) through sympathetic nerve activation. BAT functions as hepatoprotective machinery to counteract the development of ALD, implying a therapeutic potential of BAT activity modulation for the treatment of ALD.
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