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Maternal High Fat Diet Alters Skeletal Muscle Mitochondrial Catalytic Activity in Adult Male Rat Offspring

机译:母体高脂饮食改变成年雄性大鼠后代骨骼肌线粒体的催化活性

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A maternal high-fat (HF) diet during pregnancy can lead to metabolic compromise, such as insulin resistance in adult offspring. Skeletal muscle mitochondrial dysfunction is one mechanism contributing to metabolic impairments in insulin resistant states. Therefore, the present study aimed to investigate whether mitochondrial dysfunction is evident in metabolically compromised offspring born to HF-fed dams. Sprague-Dawley dams were randomly assigned to receive a purified control diet (CD; 10% kcal from fat) or a high fat diet (HFD; 45% kcal from fat) for 10 days prior to mating, throughout pregnancy and during lactation. From weaning, all male offspring received a standard chow diet and soleus muscle was collected at day 150. Expression of the mitochondrial transcription factors nuclear respiratory factor-1 (NRF1) and mitochondrial transcription factor A (mtTFA) were downregulated in HF offspring. Furthermore, genes encoding the mitochondrial electron transport system (ETS) respiratory complex subunits were suppressed in HF offspring. Moreover, protein expression of the complex I subunit, NDUFB8, was downregulated in HF offspring (36%), which was paralleled by decreased maximal catalytic linked activity of complex I and III (40%). Together, these results indicate that exposure to a maternal HF diet during development may elicit lifelong mitochondrial alterations in offspring skeletal muscle.
机译:孕妇在怀孕期间的高脂(HF)饮食会导致代谢受损,例如成年后代的胰岛素抵抗。骨骼肌线粒体功能障碍是导致胰岛素抵抗状态下代谢受损的一种机制。因此,本研究旨在调查线粒体功能障碍在HF喂养的大坝所生的代谢受损的后代中是否明显。在交配之前,整个怀孕期间和哺乳期间,将Sprague-Dawley大坝随机分配为接受纯饮食(CD;脂肪中10%大卡)或高脂饮食(HFD;脂肪中45%大卡)饮食10天。从断奶开始,所有雄性后代均接受标准的日常饮食,并在第150天收集比目鱼肌。在HF后代中,线粒体转录因子核呼吸因子-1(NRF1)和线粒体转录因子A(mtTFA)的表达下调。此外,在HF后代中,编码线粒体电子转运系统(ETS)呼吸系统复杂亚基的基因被抑制。此外,在HF后代(36%)中,复合物I亚基NDUFB8的蛋白表达被下调,这与复合物I和III的最大催化连接活性降低(40%)平行。总之,这些结果表明,在发育过程中接触母体高脂饮食可能会引起后代骨骼肌的终生线粒体改变。

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