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首页> 外文期刊>The Journal of Nutritional Biochemistry >Hypothalamic insulin receptor expression and DNA promoter methylation are sex- specifically altered in adult offspring of high-fat diet (HFD)-overfed mother rats
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Hypothalamic insulin receptor expression and DNA promoter methylation are sex- specifically altered in adult offspring of high-fat diet (HFD)-overfed mother rats

机译：下丘脑胰岛素受体表达和DNA启动子甲基化是性别的 - 在高脂饮食（HFD）-oved母语大鼠的成人后代

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Maternal overnutrition around reproduction has been shown to increase the offspring's risk for "diabesity," mediated by altered hypothalamic neuropeptide expression. In this report, a possible contribution of altered hypothalamic sensing capacity for the peripheral satiety signals glucose, insulin and leptin will be addressed, taking into account potential sex differences. Specifically, we evaluated the effects a maternal high-fat diet (HFD) overfeeding has in rats pre- and during pregnancy and lactation on the hypothalamic gene expression patterns of insulin and leptin receptors (InsR, ObRb) and glucose transporter 3 (Glut3) as well as DNA methylation in the offspring at adult age (day 200 of life). Maternal HFD consumption resulted in a metabolic syndrome phenotype, i.e., obesity, hyperleptinemia, hyperinsulinemia, impaired glucose tolerance and increased homeostatic model assessment of insulin resistance. Interestingly, in turn, insulin resistance was more pronounced in male offspring, accompanied by decreased hypothalamic InsR-mRNA. This was linked with hypermethylation of an activating transcription factor binding site within the hypothalamic InsR promoter. The degree of methylation correlated inversely with respective InsR expression, while InsR expression itself was inversely related to phenotypic "diabesity." Expression of ObRb and Glut3 mRNA was not significantly changed. In conclusion, sex-specific alterations of hypothalamic InsR expression and DNA promoter methylation in adult offspring of HFD-overfed dams may lead to hypothalamic insulin resistance and "diabesity," with males predisposed to this epigenetic malprogramming. (C) 2019 Elsevier Inc. All rights reserved.
机译：已经显示出繁殖的孕产妇过量，以提高后代“糖尿病”的后代风险，由改变的下丘脑神经肽表达介导。在本报告中，考虑到潜在的性别差异，将解决外周饱腹感测葡萄糖，胰岛素和瘦蛋白的改变的下丘脑感测能力的可能贡献。具体而言，我们评估了在胰岛素和瘦蛋白受体（INSR，OBRB）和葡萄糖转运蛋白3（Glut3）的胰岛素和乳蛋白受体（INSR，OBRB）和葡萄糖转运蛋白3（Glut3）上的妊娠和哺乳期妊娠和哺乳期患者的母体高脂饮食（HFD）过度喂养。以及成人年龄（生命日第200天的后代DNA甲基化。母体HFD消费导致代谢综合征表型，即肥胖，高层血症，高胰岛素血症，葡萄糖耐量受损和胰岛素抵抗的稳态模型评估增加。有趣的是，又血液后代胰岛素抵抗更加明显，伴随着下丘脑insr-mRNA减少。这与下丘脑INSR启动子内的激活转录因子结合位点的高甲基化有关。甲基化程度与相应的INSR表达相反相关，而INSR表达本身与表型“糖尿病性”相反。 OBRB和Glut3 mRNA的表达没有显着改变。总之，HFD综合坝的成人后代下丘脑INSR表达和DNA启动子甲基化的特异性改变可能导致下丘脑胰岛素抗性和“仿糖尿病”，令人讨论的血液抑制患者令人讨厌的胰岛素患者。 （c）2019 Elsevier Inc.保留所有权利。

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