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首页> 外文期刊>Endocrinology >High-fat intake during pregnancy and lactation exacerbates high-fat diet-induced complications in male offspring in mice
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High-fat intake during pregnancy and lactation exacerbates high-fat diet-induced complications in male offspring in mice

机译：妊娠和哺乳期高脂饮食加重了高脂饮食引起的雄性后代小鼠并发症

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摘要

Altered fetal environments, such as a high-fat milieu, induce metabolic abnormalities in offspring. Different postnatal environments reveal the predisposition for adult diseases that occur during the fetal period. This study investigates the ability of a maternal high-fat diet (HFD) to program metabolic responses to HFD reexposure in offspring after consuming normal chow for 23 weeks after weaning. Wild-type CD1 females were fed a HFD (H) or control (C) chow during pregnancy and lactation. At 26 weeks of age, offspring were either reexposed (H-C-H) or newly exposed (C-C-H) to the HFD for 19 weeks. Body weight was measured weekly, and glucose and insulin tolerance were measured after 10 and 18 weeks on the HFD. The metabolic profile of offspring on a HFD or C diet during pregnancy and lactation and weaned onto a low-fat diet was similar at 26 weeks. H-C-H offspring gained more weight and developed larger adipocytes after being reintroduced to the HFD later in life than C-C-H. H-C-H mice were glucose and insulin intolerant and showed reduced gene expression of cox6a2 and atp5i in muscle, indicating mitochondrial dysfunction. In adipocytes, the expression of slc2a4, srebf1, and adipoq genes was decreased in H-C-H mice compared with C-C-C, indicating insulin resistance. H-C-H showed extensive hepatosteatosis, accompanied by increased gene expression for cd36 and serpin1, compared with C-C-H. Perinatal exposure to a HFD programs a more deleterious response to a HFD challenge later in life even after an interval of normal diet in mice.
机译：胎儿环境的改变（例如高脂环境）会导致后代的代谢异常。不同的产后环境揭示了胎儿期发生成人疾病的易感性。这项研究调查了断奶后的23周食用普通食物后，母体高脂饮食（HFD）对后代HFD再暴露进行编程代谢反应的能力。在怀孕和哺乳期间，给野生型CD1雌性喂了HFD（H）或对照（C）的食物。在26周龄时，将后代重新暴露（H-C-H）或新暴露（C-C-H）19周。每周测量一次体重，在HFD上10和18周后测量葡萄糖和胰岛素耐受性。在怀孕和哺乳期间，采用HFD或C饮食的后代在断奶后和低脂饮食中的代谢状况在26周时相似。与C-C-H相比，H-C-H后代在生命后期被重新引入HFD后，体重增加并发育出更大的脂肪细胞。 H-C-H小鼠对葡萄糖和胰岛素不耐受，并且其肌肉中cox6a2和atp5i的基因表达降低，表明线粒体功能异常。在脂肪细胞中，与C-C-C相比，H-C-H小鼠中slc2a4，srebf1和adipoq基因的表达降低，表明胰岛素抵抗。与C-C-H相比，H-C-H显示出广泛的肝脂肪变性，伴有cd36和serpin1的基因表达增加。围生期暴露于HFD的程序在以后的生活中对HFD激发的编程更具有害性，即使间隔一定时间的小鼠饮食也是如此。

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