ArticleThe Journal of endocrinology2013
Involvement of exercise-induced macrophage migration inhibitory factor in the prevention of fatty liver disease.
Article in The Journal of endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Mechanisms underpinning the effect of exercise on the non-alcoholic fatty liver disease: review.EXCLI journal · 2025Review
- Unraveling the underlying pathogenic factors driving nonalcoholic steatohepatitis and hepatocellular carcinoma: an in-depth analysis of prognostically relevant gene signatures in hepatocellular carcinoma.Journal of translational medicine · 2024Article
- Intermittent fasting activates macrophage migration inhibitory factor and alleviates high-fat diet-induced nonalcoholic fatty liver disease.Scientific reports · 2023Article
- Exerkines and osteoarthritis.Frontiers in physiology · 2023Review
- Single-cell dissection of the obesity-exercise axis in adipose-muscle tissues implies a critical role for mesenchymal stem cells.Cell metabolism · 2022Article
- Exercise inhibits JNK pathway activation and lipotoxicityFrontiers in endocrinology · 2022Article
- Exercise and Organ Cross Talk.Advances in experimental medicine and biology · 2020Review
- The Effects of Physical Exercise on Fatty Liver Disease.Gene expression · 2018Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Physical inactivity can lead to obesity and fat accumulation in various tissues. Critical complications of obesity include type II diabetes and nonalcoholic fatty liver disease (NAFLD). Exercise has been reported to have ameliorating effects on obesity and NAFLD. However, the underlying mechanism is not fully understood. We showed that liver expression of macrophage migration inhibitory factor (MIF) was increased after 4 weeks of treadmill exercise. Phosphorylation of AMP-activated protein kinase and acetyl-CoA carboxylase in human hepatocyte cell lines was enhanced after MIF treatment. These responses were accompanied by increases in lipid oxidation. Moreover, inhibition of either AMPK or cluster of differentiation 74 resulted in inhibition of MIF-induced lipid oxidation. Furthermore, the administration of MIF to a human hepatocyte cell line and mice liver reduced liver X receptor agonist-induced lipid accumulation. Taken together, these results indicate that MIF is highly expressed in the liver during physical exercise and may prevent hepatic steatosis by activating the AMPK pathway.
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