ArticleScientific reports2025
Exercise ameliorates nonalcoholic fatty liver disease by reducing the IGFBP5 to IGF1 ratio to activate AMPK pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Exercise elicits mitonuclear protein imbalance and UPRJournal of physiology and biochemistry · 2026Article
- Physical Activity Modifies the Association Between Atherogenic Index of Plasma and New-Onset Diabetes in Middle-Aged and Older Adults.Healthcare (Basel, Switzerland) · 2026Article
- Exercise as a Molecular Therapeutic Tool in MASLD: From Signaling Pathways to Clinical Translation-A Narrative Review.Biomedicines · 2026Review
- Integrated Machine Learning and Multi-Omics Analysis Identifies Mitophagy-Related Core Genes and Mechanisms in Non-Alcoholic Fatty Liver Disease.Journal of inflammation research · 2026Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Insulin-like growth factor-binding protein 5 (IGFBP5) is associated with nonalcoholic fatty liver disease (NAFLD). IGFBP5 has a higher binding affinity to IGF1 and modulates its effects in serum. However, the effect of exercise on its expression remains unclear. Hence, this study investigated whether exercise regulated hepatic and circulating IGFBP5 levels to ameliorate NAFLD. The NAFLD mice were regularly trained for 12 weeks on a treadmill at a 0% grade. Serum levels of IGFBP5, total IGF1, and free IGF1 were detected using proteome analyses and ELISA. Critical cytokines, such as IRS1, Akt, and AMPKα, and their phosphorylation levels mediated by IGFBP5/IGF1 were confirmed via Western blotting. The results indicated that exercise remarkably alleviated HFD-induced NAFLD and insulin resistance. Although exercise lowered serum IGFBP5 levels and the IGFBP5/total IGF1 ratio in NAFLD mice, it had no effect on the hepatic expression of IGFBP5, IGF1, and IGF1R. Moreover, exercise increased serum levels of free IGF1 in NAFLD mice, which, when bound to IGF1R, accelerated the phosphorylation levels of hepatic IRS1, Akt, and AMPKα to ameliorate NAFLD. The present study confirmed that exercise activated the effects of IGF1 by reducing the serum IGFBP5/IGF1 ratio, consequently triggering the IRS1/Akt/AMPK pathway to ameliorate HFD-induced NAFLD.
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