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<p>This study investigates the potential mechanisms by which maternal chromium (Cr) supplementation mitigates offspring obesity through identification of key regulatory genes. Sixteen pregnant C57BL/6 mice were randomly allocated to either control (CON) or chromium-supplemented (CR) dietary groups, with nutritional interventions administered throughout gestation and lactation. Post-weaning, all offspring received CR diets until 32&#xa0;weeks of age. Comparative analysis revealed significant reductions in adipose tissue mass and 136 differentially expressed genes (DEGs) in CR offspring adipose tissue, identified through GEO2R analysis. Functional enrichment analyses revealed significant involvement of these DEGs in critical metabolic pathways: lipid metabolism regulation (PPAR signaling), steroid hormone biosynthesis, cholesterol homeostasis, and fatty acid oxidation processes. Protein–protein interaction network analysis identified 14 hub genes central to adipocyte regulation, including <i>ACSL1</i>, <i>DGAT1</i>, <i>ADIPOQ</i>, <i>PPARD</i>, <i>PPARG</i>, <i>SREBF1</i>, <i>APOC2</i>, and <i>FABP1</i>, which collectively demonstrate synergistic effects in suppressing lipid accumulation. These findings elucidate molecular mechanisms underlying chromium-mediated protection against metabolic disorders and propose novel therapeutic targets for intergenerational obesity prevention. The identified gene network provides a framework for developing maternal nutritional strategies and pharmacological interventions targeting epigenetic regulation of lipid metabolism.</p>

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Gene Dynamics in Maternal Nutrition: The Role of Chromium in Mitigating Offspring Obesity

  • 期刊论文

  • 发表日期：

    2025年6月19日

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  • Xiaofeng Li,
  • Tao Wang,
  • Wei Wang,
  • Zhongyuan Wang,
  • Hongyan Wang,
  • Kewei Fan,
  • Bing Yang

摘要

This study investigates the potential mechanisms by which maternal chromium (Cr) supplementation mitigates offspring obesity through identification of key regulatory genes. Sixteen pregnant C57BL/6 mice were randomly allocated to either control (CON) or chromium-supplemented (CR) dietary groups, with nutritional interventions administered throughout gestation and lactation. Post-weaning, all offspring received CR diets until 32 weeks of age. Comparative analysis revealed significant reductions in adipose tissue mass and 136 differentially expressed genes (DEGs) in CR offspring adipose tissue, identified through GEO2R analysis. Functional enrichment analyses revealed significant involvement of these DEGs in critical metabolic pathways: lipid metabolism regulation (PPAR signaling), steroid hormone biosynthesis, cholesterol homeostasis, and fatty acid oxidation processes. Protein–protein interaction network analysis identified 14 hub genes central to adipocyte regulation, including ACSL1, DGAT1, ADIPOQ, PPARD, PPARG, SREBF1, APOC2, and FABP1, which collectively demonstrate synergistic effects in suppressing lipid accumulation. These findings elucidate molecular mechanisms underlying chromium-mediated protection against metabolic disorders and propose novel therapeutic targets for intergenerational obesity prevention. The identified gene network provides a framework for developing maternal nutritional strategies and pharmacological interventions targeting epigenetic regulation of lipid metabolism.