How does your fat affect your liver when you drink?
Seonghwan Hwang, Bin Gao
Seonghwan Hwang, Bin Gao
Published June 3, 2019; First published April 29, 2019
Citation Information: J Clin Invest. 2019;129(6):2181-2183. https://doi.org/10.1172/JCI128984.
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Commentary

How does your fat affect your liver when you drink?

Abstract

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.

Authors

Seonghwan Hwang, Bin Gao

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Figure 1

Role of adipose tissue in the pathogenesis of ALD.

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Role of adipose tissue in the pathogenesis of ALD. Excessive alcohol int...
Excessive alcohol intake induces white adipocyte death and macrophage infiltration, which trigger lipolysis via the elevation of epinephrine and norepinephrine. Alcohol and dysfunctional white adipocytes can also promote lipolysis by induction of insulin resistance and elevation of FGF21. WAT lipolysis subsequently elevates the circulating FFA levels, thereby inducing hepatic FFA influx, lipotoxicity, steatosis, hepatocyte death, and liver inflammation. As opposed to the detrimental effect on WAT, alcohol consumption switches on defensive mechanisms in BAT against ALD development. UCP1-mediated FFA oxidation and thermogenesis are activated by alcohol, which reduces the circulating FFA pool and attenuates FFA-induced hepatocyte death as well as hepatic fat accumulation. Alcohol intake elevates the expression of adiponectin in BAT, which reduces the burden of ALD at multiple levels by suppressing hepatic fat accumulation, hepatocyte death, and liver inflammation. CPT1, carnitine palmitoyltransferase I.