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Int. J. Mol. Sci. 2017, 18(8), 1649; doi:10.3390/ijms18081649

Adipokines and Non-Alcoholic Fatty Liver Disease: Multiple Interactions

Department of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University Innsbruck, A-6020 Innsbruck, Austria
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Received: 18 July 2017 / Revised: 18 July 2017 / Accepted: 26 July 2017 / Published: 29 July 2017
(This article belongs to the Special Issue Adipokines)
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Abstract

Accumulating evidence links obesity with low-grade inflammation which may originate from adipose tissue that secretes a plethora of pro- and anti-inflammatory cytokines termed adipokines. Adiponectin and leptin have evolved as crucial signals in many obesity-related pathologies including non-alcoholic fatty liver disease (NAFLD). Whereas adiponectin deficiency might be critically involved in the pro-inflammatory state associated with obesity and related disorders, overproduction of leptin, a rather pro-inflammatory mediator, is considered of equal relevance. An imbalanced adipokine profile in obesity consecutively contributes to metabolic inflammation in NAFLD, which is associated with a substantial risk for developing hepatocellular carcinoma (HCC) also in the non-cirrhotic stage of disease. Both adiponectin and leptin have been related to liver tumorigenesis especially in preclinical models. This review covers recent advances in our understanding of some adipokines in NAFLD and associated HCC. View Full-Text
Keywords: Adipokines; hepatocellular cancer; metabolism; metabolic inflammation; non-alcoholic fatty liver disease (NAFLD) Adipokines; hepatocellular cancer; metabolism; metabolic inflammation; non-alcoholic fatty liver disease (NAFLD)
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MDPI and ACS Style

Adolph, T.E.; Grander, C.; Grabherr, F.; Tilg, H. Adipokines and Non-Alcoholic Fatty Liver Disease: Multiple Interactions. Int. J. Mol. Sci. 2017, 18, 1649.

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