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首页> 外文期刊>American Journal of Physiology >Maternal low-protein diet alters pancreatic islet mitochondrial function in a sex-specific manner in the adult rat.
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Maternal low-protein diet alters pancreatic islet mitochondrial function in a sex-specific manner in the adult rat.

机译：母体低蛋白饮食以成年大鼠的性别特异性方式改变胰岛线粒体功能。

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摘要

Mitochondrial dysfunction may be a long-term consequence of a poor nutritional environment during early life. Our aim was to investigate whether a maternal low-protein (LP) diet may program mitochondrial dysfunction in islets of adult progeny before glucose intolerance ensues. To address this, pregnant Wistar rats were fed isocaloric diets containing either 20% protein (control) or 8% protein (LP diet) throughout gestation. From birth, offspring received the control diet. The mitochondrial function was analyzed in islets of 3-mo-old offspring. Related to their basal insulin release, cultured islets from both male and female LP offspring presented a lower response to glucose challenge and a blunted ATP production compared with control offspring. The expression of malate dehydrogenase as well as the subunit 6 of the ATP synthase encoded by mitochondrial genome (mtDNA) was lower in these islets, reducing the capacity of ATP production through the Krebs cycle and oxidative phosphorylation. However, mtDNA content was unchanged in LP islets compared with control. Several consequences of protein restriction during fetal life were more marked in male offspring. Only LP males showed an increased reactive oxygen species production associated with a higher expression of mitochondrial subunits of the electron transport chain NADH-ubiquinone oxireductase subunit 4L, an overexpression of peroxisome proliferator-activated receptor-gamma and uncoupling protein-2, and a strongly reduced beta-cell mass. In conclusion, mitochondrial function is clearly altered in islets from LP adult offspring in a sex-specific manner. That may provide a cellular explanation for the earlier development of glucose intolerance in male than in female offspring of dams fed an LP diet.
机译：线粒体功能障碍可能是生命早期不良营养环境的长期后果。我们的目的是调查在葡萄糖耐量不足之前，母亲的低蛋白饮食是否可能导致成人后代胰岛中的线粒体功能障碍。为了解决这个问题，在怀孕期间，给怀孕的Wistar大鼠喂食等热量饮食，其中含有20％的蛋白质（对照）或8％的蛋白质（LP饮食）。从出生起，后代就接受对照饮食。分析了3个月大的后代的胰岛中的线粒体功能。与它们的基础胰岛素释放有关，雄性和雌性LP后代的培养胰岛与对照后代相比，对葡萄糖激发的反应较低，ATP生成减弱。在这些胰岛中，苹果酸脱氢酶以及由线粒体基因组（mtDNA）编码的ATP合酶的亚基6的表达较低，从而降低了通过克雷布斯循环和氧化磷酸化产生ATP的能力。然而，与对照相比，LP胰岛中的mtDNA含量没有变化。胎儿后代中蛋白质限制的几种后果在雄性后代中更为明显。只有LP男性表现出增加的活性氧产生，与电子转运链NADH-泛醌氧化还原酶亚基4L的线粒体亚基的更高表达，过氧化物酶体增殖物激活受体-γ和解偶联蛋白2的过表达，以及强烈降低的β细胞质量。总之，线粒体功能在LP成年后代的胰岛中以性别特定的方式明显改变。这可能为在饲喂低脂饮食的水坝中雄性比雌性后代中葡萄糖不耐症的早期发展提供了细胞学解释。

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