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Circulating IGFBP-2 levels are inversely associated with the incidence of nonalcoholic fatty liver disease: A cohort study

Objective The insulin-like growth factor (IGF) axis is essential for the body’s metabolism. The hepatokine, insulin-like growth factor-binding protein 2 (IGFBP-2), acts as a major regulator of this metabolism. We aimed to evaluate the role of serum IGFBP-2 in the incidence of nonalcoholic fatty live...

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Published in:Journal of international medical research 2020-08, Vol.48 (8), p.300060520935219-300060520935219
Main Authors: Yang, Ji, Zhou, Wenjing, Wu, Yue, Xu, Liqian, Wang, Yuming, Xu, Zherong, Yang, Yunmei
Format: Article
Language:English
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Summary:Objective The insulin-like growth factor (IGF) axis is essential for the body’s metabolism. The hepatokine, insulin-like growth factor-binding protein 2 (IGFBP-2), acts as a major regulator of this metabolism. We aimed to evaluate the role of serum IGFBP-2 in the incidence of nonalcoholic fatty liver disease (NAFLD). Methods This hospital-based prospective cohort study recruited residents from a health program from January to November 2013, and re-invited them for follow-up in 2016. The occurrence of NAFLD was noted and IGFBP-2 levels were evaluated by enzyme-linked immunosorbent assay at both visits. Results Of 763 participants at baseline, 296 completed the re-evaluation. Baseline serum IGFBP-2 levels were significantly lower in subjects with NAFLD compared with those without NAFLD. Circulating IGFBP-2 levels were negatively correlated with body mass index, waist-to-hip ratio, alanine transaminase, triglycerides, fasting glucose, and insulin. IGFBP-2 levels at follow-up decreased in subjects who developed NAFLD compared with those who did not. Higher circulating levels of IGFBP-2 at baseline were negatively associated with the incidence of NAFLD. Conclusion These results indicate that IGFBP-2 levels are inversely associated with the risk of NAFLD. This offers new insights into the role of circulating IGFBP-2, as an IGF-axis hepatokine, in the pathogenesis of hepatic steatosis.
ISSN:0300-0605
1473-2300
DOI:10.1177/0300060520935219