Adiponectin: a key playmaker adipocytokine in non-alcoholic fatty liver disease

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and can progress to cirrhosis, liver failure, and hepatocellular carcinoma. In the last two decades, the prevalence of NAFLD has been growing in most developed countries, mainly as a consequence of its close association with obesity and diabetes mellitus. The exact pathogenesis of NAFLD and especially the mechanisms leading to disease progression have not been completely understood. Adipocytes produce and secrete several bioactive substances known as adipocytokines which are implicated in the pathogenesis of the disease. Among them, adiponectin is an insulin-sensitizing adipocytokine possessing multiple beneficial effects on obesity-related medical complication. This review focuses on the role of adiponectin in NAFLD pathogenesis and its potential use as a diagnostic tool but also as therapeutic target for NAFLD management.

Metabolic phenotype and adipose and liver features in a high-fat Western diet-induced mouse model of obesity-linked NAFLD

“…Our observation that adiponectin was reduced at the gene expression and protein levels in the HFWDϩF/S group suggests that adiponectin may be a potential link between adipose tissue dysfunction and NAFLD progression. This hypothesis is consistent with the known role of adiponectin in modulating steatosis, inflammation, and fibrosis (9). However, further experimentation is required to determine whether a reduction in adiponectin mediates the effects of the HFWDϩF/S combination in NAFLD progression.…”

Association of Circulating Adipsin, Visfatin, and Adiponectin with Nonalcoholic Fatty Liver Disease in Adults: A Case-Control Study

“…Consistent with the above studies, our data found that circulating adiponectin levels were significantly lower in NAFLD patients compared with those in controls, and adiponectin was negatively associated with NAFLD. The study indicated that the inhibition of phosphorylation of AMP-activated protein kinase or peroxisome proliferator-activated receptor α may increase the synthesis and accumulation of hepatic lipid and glucose, as well as attenuate fatty acid β-oxidation, which made it develop into NAFLD [42].…”

The Riddle of Nonalcoholic Fatty Liver Disease: Progression From Nonalcoholic Fatty Liver to Nonalcoholic Steatohepatitis

“…Adiponectin decrease, as well as adiponectin gene deletion, induces hepatic steatosis progression, fibrosis, and tumor development. 95 Moreover, KCs have also metabolic function, regulating fatty acids oxidation, increasing hepatic lipid storage and insulin resistance (IR), as mechanisms of adaptation to increased caloric intake. This event which is triggered by secretion of inflammatory cytokines, suggests a beneficial role for alternatively M2-activated KCs in metabolic derangements.…”