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首页> 外文期刊>The Journal of Nutritional Biochemistry >Maternal malnutrition programs pancreatic islet mitochondrial dysfunction in the adult offspring.
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Maternal malnutrition programs pancreatic islet mitochondrial dysfunction in the adult offspring.

机译：产妇营养不良会导致成年后代胰腺胰岛线粒体功能异常。

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Accumulating evidence has shown that maternal malnutrition increases the risk of metabolic disease in the progeny. We previously reported that prenatal exposure to a low-protein diet (LP) leads to mitochondrial dysfunction in pancreatic islets from adult rodent offspring that could relate physiological and cellular alterations due to early diet. We aim to determine whether mitochondrial dysfunction could be a common consequence of prenatal nutritional unbalances. Pregnant Wistar rats received either a global food restriction (GFR), consisting in the reduction by 50% of the normal daily food intake, or a high-fat diet (HF) throughout gestation. GFR or HF diet during pregnancy leads to a lack of increase in insulin release and ATP content in response to glucose stimulation in islets from 3-month-old male and female offspring. These similar consequences originated from impairment in either glucose sensing or glucose metabolism, depending on the type of early malnutrition and on the sex of the progeny. Indeed, the glucose transport across beta-cell membrane seemed compromised in female HF offspring, since GLUT-2 gene was markedly underexpressed. Additionally, for each progeny, consequences downstream the entry of glucose were also apparent. Expression of genes involved in glycolysis, TCA cycle and oxidative phosphorylations was altered in GFR and HF rats in a sex- and diet-dependent manner. Moreover, prenatal malnutrition affected the regulators of mitochondrial biogenesis, namely, PPAR coactivator 1 alpha (PGC-1 alpha), since its expression was higher in islets from GFR rats. In conclusion, programming of mitochondrial dysfunction is a consequence of maternal malnutrition, which may predispose to glucose intolerance in the adult offspring. All rights reserved, Elsevier.
机译：越来越多的证据表明，母亲营养不良会增加后代发生代谢性疾病的风险。我们先前曾报道，产前接触低蛋白饮食（LP）会导致成年啮齿动物后代的胰岛胰岛线粒体功能异常，这可能与早期饮食导致的生理和细胞改变有关。我们旨在确定线粒体功能障碍是否可能是产前营养失衡的常见后果。怀孕的Wistar大鼠接受了全球食物限制（GFR）（包括将每日正常食物摄入量减少50％）或整个妊娠期间的高脂饮食（HF）。怀孕期间的GFR或HF饮食导致3个月大的雄性和雌性后代的胰岛中的葡萄糖刺激导致胰岛素释放和ATP含量缺乏增加。这些类似的后果源自葡萄糖感测或葡萄糖代谢的损害，这取决于早期营养不良的类型和后代的性别。实际上，由于GLUT-2基因的表达明显不足，因此在雌性HF后代中，跨β细胞膜的葡萄糖转运似乎受到损害。另外，对于每个后代，葡萄糖进入下游的后果也很明显。 GFR和HF大鼠以性别和饮食依赖性方式改变参与糖酵解，TCA循环和氧化磷酸化的基因的表达。此外，产前营养不良影响线粒体生物发生的调节因子，即PPAR共激活因子1α（PGC-1α），因为它在GFR大鼠的胰岛中的表达较高。总之，线粒体功能障碍的编程是母体营养不良的结果，可能导致成年后代对葡萄糖的耐受不良。保留所有权利，Elsevier。

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