Adipokines and Non-Alcoholic Fatty Liver Disease: Multiple Interactions.
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.
['Adolph|Timon E|TE|', 'Grander|Christoph|C|', 'Grabherr|Felix|F|', 'Tilg|Herbert|H|']
D052242:Adiponectin D000818:Animals D006528:Carcinoma, Hepatocellular D006801:Humans D020738:Leptin D008113:Liver Neoplasms D009363:Neoplasm Proteins D065626:Non-alcoholic Fatty Liver Disease D009765:Obesity
Adipokines non-alcoholic fatty liver disease (NAFLD) metabolic inflammation metabolism hepatocellular cancer