Adipokine Mediators in Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum from simple steatosis to nonalcoholic steatohepatitis (NASH), fibrosis and cirrhosis, driven largely by metabolic dysfunction in adipose tissue. Adipokines, bioactive peptides secreted by adipocytes, orchestrate cross-talk between adipose depots and the liver, modulating lipid handling, insulin sensitivity and inflammatory responses. An imbalance between anti-inflammatory mediators such as adiponectin and pro-inflammatory factors like leptin fosters hepatic lipid accumulation, oxidative stress and recruitment of immune cells. Emerging adipokines—including resistin, chemerin, visfatin, retinol-binding protein 4, omentin and irisin—further refine the hepatic microenvironment through signalling pathways centred on AMPK, JAK2-STAT3 and NF-κB. Dysregulation of these signals underlies the transition from benign steatosis to progressive fibrosis, heightening the global burden of chronic liver disease. Understanding adipokine networks offers routes to diagnostic biomarkers and targeted therapies that reset metabolic inflammation and halt disease evolution.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Adipokine Mediators in Nonalcoholic Fatty Liver Disease publication trend

The graph below shows the total number of articles in adipokine mediators in nonalcoholic fatty liver disease across all publications each year (not limited to Nature Index journals).

Technical terms

Adipokine: A cytokine or hormone secreted by adipose tissue that influences metabolic and inflammatory processes.

Nonalcoholic fatty liver disease (NAFLD): A spectrum of liver disorders characterised by excessive hepatic fat accumulation in individuals with minimal alcohol intake.

Nonalcoholic steatohepatitis (NASH): An advanced form of NAFLD marked by hepatocellular injury, inflammation and variable fibrosis.

AMP-activated protein kinase (AMPK): A cellular energy sensor that regulates lipid and glucose metabolism, with protective roles in hepatic steatosis.

JAK2-STAT3 pathway: A signalling cascade activated by cytokines and growth factors, implicated in hepatocyte survival and fibrogenesis.

Oxidative stress: An imbalance between reactive oxygen species production and antioxidant defences, contributing to liver cell damage.

References

1. Modelling porcine NAFLD by deletion of leptin and defining the role of AMPK in hepatic fibrosis. Cell & Bioscience (2023).
2. Association of circulating omentin level and metabolic-associated fatty liver disease: a systematic review and meta-analysis. Frontiers in Endocrinology (2023).
3. Adipokines and Non-Alcoholic Fatty Liver Disease: Multiple Interactions. International Journal of Molecular Sciences (2017).