Adiponectin and PPAR: a setup for intricate crosstalk between obesity and non-alcoholic fatty liver disease.

Abstract

Adiponectin, a soluble adipocytokine, plays an important role in the functioning of adipose tissue and in the regulation of inflammation, particularly hepatic inflammation. The adiponectin subsequently imparts a crucial role in metabolic and hepato-inflammatory diseases. The most recent evidences indicate that lipotoxicity-induced inflammation in the liver is associated with obesity-derived alterations and remolding in adipose tissue that culminates in most prevalent liver pathology named as non-alcoholic fatty liver disease (NAFLD). A comprehensive crosstalk of adiponectin and its cognate receptors, specifically adiponectin receptor-2 in the liver mediates ameliorative effects in obesity-induced NAFLD by interaction with hepatic peroxisome proliferator-activated receptors (PPARs). Recent studies highlight the implication of molecular mediators mainly involved in the pathogenesis of obesity and obesity-driven NAFLD, however, the plausible mechanisms remain elusive. The present review aimed at collating the data regarding mechanistic approaches of adiponectin and adiponectin-activated PPARs as well as PPAR-induced adiponectin levels in attenuation of hepatic lipoinflammation. Understanding the rapidly occurring adiponectin-mediated pathophysiological outcomes might be of importance in the development of new therapies that can potentially resolve obesity and obesity-associated NAFLD.