Abstract
Alcoholic liver disease (ALD) remains an important health problem in the United States. The disease process is featured by early steatosis, steatohepatitis (steatosis with inflammatory cells infiltration and necrosis), with some individuals ultimately progressing to fibrosis/cirrhosis. Although the disease progression is well characterized, no FDA-approved therapies are currently available to halt or reverse this process in humans. The mechanisms underlying the initiation and progression of ALD are complex and multifactorial. Emerging evidence supports that adipose tissue dysfunction contributes to the pathogenesis of ALD. It has been long known that aberrant hepatic methionine metabolism is a major metabolic abnormality induced by chronic alcohol exposure and plays an etiological role in the pathogenesis of ALD. The recent studies in our group documented the similar effect of chronic alcohol drinking in adipose tissue. In this article, we briefly reviewed the recent research progress in the field with a focus on how abnormal methionine metabolism in adipose tissue contributes to adipose tissue dysfunction and liver damage.
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