Departamento de Biología de la Reproducción, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City 14080, Mexico.
CONACyT-Cátedras, Investigador por México, Departamento de Biología de la Reproducción, Instituto Nacional de Ciencias Médicas y Nutrición SZ, Mexico City 14080, Mexico.
Nutrients. 2023 May 9;15(10):2245. doi: 10.3390/nu15102245.
We investigated whether excessive retroperitoneal adipose tissue (AT) expansion programmed by maternal obesity (MO) affects adipocyte size distribution and gene expression in relation to adipocyte proliferation and differentiation in male and female offspring (F1) from control (F1C) and obese (F1MO) mothers. Female Wistar rats (F0) ate a control or high-fat diet from weaning through pregnancy and lactation. F1 were weaned onto a control diet and euthanized at 110 postnatal days. Fat depots were weighed to estimate the total AT. Serum glucose, triglyceride, leptin, insulin, and the insulin resistance index (HOMA-IR) were determined. Adipocyte size and adipogenic gene expression were examined in retroperitoneal fat. Body weight, retroperitoneal AT and adipogenesis differed between male and female F1Cs. Retroperitoneal AT, glucose, triglyceride, insulin, HOMA-IR and leptin were higher in male and female F1MO vs. F1C. Small adipocytes were reduced in F1MO females and absent in F1MO males; large adipocytes were increased in F1MO males and females vs. F1C. Wnt, PI3K-Akt, and insulin signaling pathways in F1MO males and in F1MO females were downregulated vs. F1C. MO induced metabolic dysfunction in F1 through different sex dimorphism mechanisms, including the decreased expression of pro-adipogenic genes and reduced insulin signaling in males and lipid mobilization-related genes in females.
我们研究了母体肥胖（MO）引起的过度腹膜后脂肪组织（AT）扩张是否会影响雄性和雌性后代（F1）脂肪细胞的大小分布和基因表达，进而影响脂肪细胞的增殖和分化。雌性 Wistar 大鼠（F0）从断奶到怀孕和哺乳期均食用对照或高脂肪饮食。F1 断奶后接受对照饮食，并在出生后 110 天安乐死。称重脂肪组织以估计总 AT。测定血清葡萄糖、甘油三酯、瘦素、胰岛素和胰岛素抵抗指数（HOMA-IR）。检查腹膜后脂肪中的脂肪细胞大小和脂肪生成基因表达。F1C 的雄性和雌性之间的体重、腹膜后 AT 和脂肪生成存在差异。F1MO 的雄性和雌性的腹膜后 AT、葡萄糖、甘油三酯、胰岛素、HOMA-IR 和瘦素均高于 F1C。F1MO 雌性的小脂肪细胞减少，F1MO 雄性的小脂肪细胞不存在；F1MO 的雄性和雌性的大脂肪细胞增加。与 F1C 相比，F1MO 的雄性和雌性的 Wnt、PI3K-Akt 和胰岛素信号通路均下调。MO 通过不同的性别二态性机制导致 F1 代谢功能障碍，包括雄性中促脂肪生成基因表达减少和胰岛素信号降低，以及雌性中脂质动员相关基因减少。
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