Resistin mediates the hepatic stellate cell phenotype.

Aim: To describe the role of resistin in liver fibrosis.

Methods: For the in vivo animal study, Sprague Dawley rats were subjected to bile duct ligation (BDL) for 4 wk. Rat liver, adipose tissue (epididymal fat) and serum were analyzed for resistin expression.

Leptin and acetaldehyde synergistically promotes αSMA expression in hepatic stellate cells by an interleukin 6-dependent mechanism.

Background: The mechanisms whereby patients with obesity/overweight are more susceptible to alcohol-associated liver fibrosis are unclear. Leptin, a peptide hormone secreted by white adipose tissue is increased in association with overweight/obesity and is recognized as mediator of liver fibrosis. We sought to assess whether leptin contributes to alcoholic liver fibrosis by in vitro studies in hepatic stellate cells (HSC).

Kupffer cells mediate leptin-induced liver fibrosis.

Background & Aims: Leptin has profibrogenic effects in liver, although the mechanisms of this process are unclear. We sought to elucidate the direct and indirect effects of leptin on hepatic stellate cells (HSCs).

Methods: HSCs from Sprague-Dawley rats were exposed to leptin and expression of collagen-I, tissue inhibitor of matrix metalloproteinases-1 (TIMP1), transforming growth factor beta1 (TGF-beta1), and connective tissue growth factor (CTGF/CCN2) was assessed.

Roles of adipokines in liver injury and fibrosis.

Adipose tissue is now recognized as the largest endocrine organ in the body, secreting over 100 proteins termed adipokines that influence energy homeostasis, lipid physiology, inflammation, immune function and wound healing. Some of these proteins, such as TNFalpha, have important proinflammatory effects, but during hepatic injury are principally secreted at a local level within the liver. Their role in liver injury and fibrosis is beyond the scope of this review.