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. 2018 Oct 27;10(10):708–718. doi: 10.4254/wjh.v10.i10.708

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©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

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The biological effects of adiponectin on the liver. Adiponectin interacts with adiponectin receptors to prompt a number of signaling pathways. AdipoR1 and R2 dependent signaling is mediated via adaptor protein phosphotyrosine interaction (APPL) 1. The signaling activates AMP-activated protein kinase (AMPK), ceramidase activity, and peroxisome proliferator-activated receptor-alpha (PPAR-α) to suppress the accumulation of lipids and regulate glucose homeostasis. The adiponectin-adipoR2 axis can reduce inflammation by inhibiting tumor necrosis factor-alpha (TNF-α) activity. Importantly, activated adiponectin also limits the activation of hepatic stellate cells (HSCs) via both AMPK and PPAR-α activation, leading to the inhibition of liver fibrogenesis. ACC: Acetyl-CoA carboxylase; ACO: Acyl-CoA oxidase; AdipoR: Adiponectin receptor; fAPN: Full-length adiponectin; gAPN: Globular adiponectin; PEPCK: Phosphoenolpyruvate carboxykinase; SREBP-1c: Sterol regulatory element binding protein-1c.