What is the role of adiponectin in obesity related non-alcoholic fatty liver disease?

Abstract

Non-alcoholic fatty liver disease (NAFLD) is recognized as the most common type of chronic liver disease in Western countries. Insulin resistance is a key factor in the pathogenesis of NAFLD, the latter being considered as the hepatic component of insulin resistance or obesity. Adiponectin is the most abundant adipose-specific adipokine. There is evidence that adiponectin decreases hepatic and systematic insulin resistance, and attenuates liver inflammation and fibrosis. Adiponectin generally predicts steatosis grade and the severity of NAFLD; however, to what extent this is a direct effect or related to the presence of more severe insulin resistance or obesity remains to be addressed. Although there is no proven pharmacotherapy for the treatment of NAFLD, recent therapeutic strategies have focused on the indirect upregulation of adiponectin through the administration of various therapeutic agents and/or lifestyle modifications. In this adiponectin-focused review, the pathogenetic role and the potential therapeutic benefits of adiponectin in NAFLD are analyzed systematically.

Association between hemoglobin glycation index and hepatic steatosis in non-diabetic individuals

“…Obesity may lead to an imbalanced production of pro-and antiinflammatory adipokines secreted from adipose tissue, which contributes to the pathogenesis of NAFLD. In particular a decreased release of adiponectin, an adipokine known to exert anti-inflammatory and insulin-sensitizing effects, has been found to play a crucial role in the pathogenesis of NAFLD [43,44]. Accordingly we found that HGI levels were positively associated with measures of visceral obesity such as BMI, waist circumference and % fat mass.…”

“…Moreover, visceral obesity and the consequent adipose metabolic dysfunction represent important risk factors for the development and progression of NAFLD [43,44]. Obesity may lead to an imbalanced production of pro-and antiinflammatory adipokines secreted from adipose tissue, which contributes to the pathogenesis of NAFLD.…”

Moderate to vigorous physical activity volume is an important factor for managing nonalcoholic fatty liver disease: A retrospective study

“…Low adiponectin levels are implicated in hepatic lipid accumulation and associated with NAFLD severity. 32 On the other hand, elevated adiponectin levels improve insulin sensitivity and enhance fatty acid oxidation, which in turn improve NAFLD pathology. 32 In addition, in one report, hepatic adiponectin signaling played a protective role against progression from simple steatosis to NASH in mice.…”

“…32 On the other hand, elevated adiponectin levels improve insulin sensitivity and enhance fatty acid oxidation, which in turn improve NAFLD pathology. 32 In addition, in one report, hepatic adiponectin signaling played a protective role against progression from simple steatosis to NASH in mice. 33 It is likely that the increased serum adiponectin level resulting from MVPA for !250 minÁwk 21 contributes to the improved pathophysiology of NAFLD.…”

Diabetic foot syndrome: Immune-inflammatory features as possible cardiovascular markers in diabetes

“…Furthermore, visceral fat plays a central role in the pathogenesis of insulin resistance and NAFLD owing to the fact that adipose tissue is not an inert tissue but it acts as a real active endocrine organ, thus furtherly impairing insulin resistance and influencing cytokine/adipokine pathways in terms of increased levels of FFA, adiponectin, leptin, TNF-α, IL-6. In particular adiponectin acts as a leading mediator in this pathogenetic events and its decreased levels are directly related to steatosis grade owing to the fact that adiponectin has a protective role decreasing lipid accumulation and fibrosis processes in liver [79] . Fatty free acids represent a well demonstred pathogenetic markers of insulin resistance and of its complications such as NAFLD owing to the fact that FFA cause liver cellular apoptosis and impair interplay between hepatic cells and immune system, cytokines, ROS and finally also impairing insulin production and signaling mechanisms [80][81][82][83][84][85][86] .…”