Maternal Obesity Leads to Muscle Dysfunction via <i>H19</i> -Mediated Programming of Insulin-Like Growth Factor 2 Signaling

H19-mediated epigenetic modifications alter Igf2 promoter activity, leading to persistent Igf2 suppression in maternal obesity (MO) offspring, causing long-term muscle dysfunction. MO increases H19 expression and enhances EZH2 recruitment and H3K27me3 deposition in the Igf2 P3 promoter, leading to higher DNA methylation. H19-EZH2 axis provides a potential therapeutic target for mitigating MO-induced muscle dysfunction and improving offspring metabolic health.

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Publication Details

Journal
Diabetes
Published
2025-12-03
DOI
https://doi.org/10.2337/db25-0271
Primary Topic
Gestational Diabetes Research and Management
Type
article
Field-Weighted Citation Impact
0.00
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article

Maternal Obesity Leads to Muscle Dysfunction via H19 -Mediated Programming of Insulin-Like Growth Factor 2 Signaling

‬Min Du, Li Wei Chen, Jeanene M. de Avila, Zhongyun Kou et al.
Diabetes
Gestational Diabetes Research and Management
article

Maternal Obesity Leads to Muscle Dysfunction via H19 -Mediated Programming of Insulin-Like Growth Factor 2 Signaling

‬Min Du, Li Wei Chen, Jeanene M. de Avila, Zhongyun Kou, Xinrui Li, MohammadSowkat Hossain, Mei-Jun Zhu, S Islam
article en

Abstract

H19-mediated epigenetic modifications alter Igf2 promoter activity, leading to persistent Igf2 suppression in maternal obesity (MO) offspring, causing long-term muscle dysfunction. MO increases H19 expression and enhances EZH2 recruitment and H3K27me3 deposition in the Igf2 P3 promoter, leading to higher DNA methylation. H19-EZH2 axis provides a potential therapeutic target for mitigating MO-induced muscle dysfunction and improving offspring metabolic health.

DiabetesVol. 75(2)
Washington State University (US)
Openalex Percentile: Top 52%
Gestational Diabetes Research and Management
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