Li Xiaofeng, Wang Tao, Wang Wei, Wang Zhongyuan, Wang Hongyan, Fan Kewei, Yang Bing
College of Animal Science and Technology, Ningxia University, Yinchuan, 750021, China.
College of Animal Science, Anhui Science and Technology University, Chuzhou, 233100, China.
Biol Trace Elem Res. 2025 Jun 19. doi: 10.1007/s12011-025-04711-0.
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.
本研究通过鉴定关键调控基因，探究母体补充铬（Cr）减轻子代肥胖的潜在机制。将16只怀孕的C57BL/6小鼠随机分为对照组（CON）或补充铬（CR）饮食组，在整个妊娠期和哺乳期进行营养干预。断奶后，所有子代均给予CR饮食直至32周龄。通过GEO2R分析，比较分析显示CR组子代脂肪组织质量显著降低，且脂肪组织中有136个差异表达基因（DEG）。功能富集分析表明，这些DEG显著参与关键代谢途径：脂质代谢调节（PPAR信号通路）、类固醇激素生物合成、胆固醇稳态和脂肪酸氧化过程。蛋白质-蛋白质相互作用网络分析确定了14个对脂肪细胞调节至关重要的枢纽基因，包括ACSL1、DGAT1、ADIPOQ、PPARD、PPARG、SREBF1、APOC2和FABP1，它们共同发挥协同作用抑制脂质积累。这些发现阐明了铬介导的预防代谢紊乱的分子机制，并为预防代际肥胖提出了新的治疗靶点。所鉴定的基因网络为制定针对脂质代谢表观遗传调控的母体营养策略和药物干预提供了框架。
