Adipokines and Non-Alcoholic Fatty Liver Disease: Multiple Interactions

被引：171

作者：

Adolph, Timon E. ^{[1
]}

Grander, Christoph ^{[1
]}

Grabherr, Felix ^{[1
]}

Tilg, Herbert ^{[1
]}

机构：

[1] Med Univ Innsbruck, Dept Internal Med Gastroenterol Hepatol & Endocri, A-6020 Innsbruck, Austria

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2017年 / 18卷 / 08期

基金：

奥地利科学基金会;

关键词：

Adipokines; hepatocellular cancer; metabolism; metabolic inflammation; non-alcoholic fatty liver disease (NAFLD); MESSENGER-RNA EXPRESSION; HEPATOCELLULAR-CARCINOMA; ADIPOSE-TISSUE; INSULIN-RESISTANCE; WEIGHT-LOSS; METABOLIC SYNDROME; SERUM ADIPONECTIN; HEPATIC STEATOSIS; LEPTIN RECEPTOR; GENE-EXPRESSION;

D O I：

10.3390/ijms18081649

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页数：15

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