Adipose tissue-liver axis in alcoholic liver disease

doi:10.4291/wjgp.v7.i1.17

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World Journal of Gastrointestinal Pathophysiology

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2150-5330

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Gastrointest Pathophysiol. Feb 15, 2016; 7(1): 17-26
Published online Feb 15, 2016. doi: 10.4291/wjgp.v7.i1.17

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Figure 1 Intracellular methionine metabolism. Chronic alcohol consumption causes SAM deficiency, but enhancement of homocysteine and SAH. MAT: Methionine adenosyl-transferase; SAM: S-adenosylmethionine; SAH: S-adenosylhomocysteine; Hcy: Homocysteine; CBS: Cystathionine beta synthase; SAHH: S-adensylmonocysteine hydrolase; MS: Methionine synthase; BHMT: Betaine-homocysteine methyltransferase.

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Figure 2 S-adenosylmethionine-dependent methylation reactions are required for protein phosphatase 2A activation, which dephosphorylates (inhibits) hormone sensitive lipase. Chronic alcohol consumption induces intracellular hypomethylation status in adipocytes, which suppresses PP2A activity, leading to uncontrolled HSL activation. SAM: S-adenosylmethionine; Me: Methyl group; PP2A: Protein phosphatase 2A; HSL: Hormone sensitive lipase.

Citation: Wang ZG, Dou XB, Zhou ZX, Song ZY. Adipose tissue-liver axis in alcoholic liver disease. World J Gastrointest Pathophysiol 2016; 7(1): 17-26
URL: https://www.wjgnet.com/2150-5330/full/v7/i1/17.htm
DOI: https://dx.doi.org/10.4291/wjgp.v7.i1.17