Moderately decreased maternal dietary energy intake during pregnancy reduces fetal skeletal muscle mitochondrial biogenesis in the pigs.
Moderately decreased maternal dietary energy intake during pregnancy reduces fetal skeletal muscle mitochondrial biogenesis in the pigs.
复制标题
怀孕期间适度减少母体膳食能量摄入会减少猪的胎儿骨骼肌线粒体生物发生
DOI：
10.1186/s12263-016-0535-1
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发表时间：
2016
影响因子：
3.5
通讯作者：
Chen D
中科院分区：
文献类型：
--
作者：
Zou T;Yu B;Yu J;Mao X;Zheng P;He J;Huang Z;Liu Y;Chen D
背景线粒体在卵母细胞和早期胚胎中非常重要，在维持能量稳态中发挥着关键作用。流行病学研究结果表明，孕期母亲营养不良引起的线粒体功能障碍与后代代谢紊乱的发生有关。在此，我们以猪为模型，研究了妊娠期间适度减少母体能量摄入对子代骨骼肌线粒体生物合成的影响。方法将怀孕的梅山母猪按照国家研究委员会（NRC；2012）的建议分为标准能量（SE）摄入组和低能量（LE）摄入组。妊娠第90天采集胎儿脐静脉血清和最长肌样本进行进一步分析。结果LE组母猪和胎儿体重以及血清生长激素（GH）和葡萄糖浓度降低。母亲 LE 饮食降低了参与线粒体生物合成和功能的基因的信使 RNA (mRNA) 表达，例如过氧化物酶体增殖物激活受体 γ 共激活剂 1α (PPARGC1A)、核呼吸因子 1 (NRF1)、线粒体转录因子 A (TFAM)、线粒体 H+-ATP 合成酶的 β 亚基 (ATB5B)、sirtuin 1 (Sirt1) 和柠檬酸合酶 (CS)。 LE组PPARGC1A和Sirt1蛋白表达、细胞内NAD+与NADH比值和CS活性降低，线粒体DNA（mtDNA）含量相应降低。此外，LE组中铜/锌超氧化物歧化酶（CuZn-SOD）mRNA和蛋白质水平的表达以及SOD和过氧化氢酶（CAT）活性均降低。结论观察到的肌肉线粒体生物合成和抗氧化防御能力下降表明，妊娠期间母体能量摄入的适度减少会损害胎猪的线粒体功能。
BackgroundMitochondria are of major importance in oocyte and early embryo, playing a key role in maintaining energy homeostasis. Epidemiological findings indicate that maternal undernutrition-induced mitochondrial dysfunction during pregnancy is associated with the development of metabolic disorders in offspring. Here, we investigated the effects of moderately decreased maternal energy intake during pregnancy on skeletal muscle mitochondrial biogenesis in fetal offspring with pig as a model.MethodsPregnant Meishan sows were allocated to a standard-energy (SE) intake group as recommended by the National Research Council (NRC; 2012) and a low-energy (LE) intake group. Fetal umbilical vein serum and longissimus muscle samples were collected for further analysis on day 90 of pregnancy.ResultsSow and fetal weights and the concentrations of serum growth hormone (GH) and glucose were reduced in LE group. Maternal LE diet decreased the messenger RNA (mRNA) expression of genes involved in mitochondrial biogenesis and function such as peroxisome proliferator-activated receptor gamma coactivator 1α (PPARGC1A), nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (TFAM), β subunit of mitochondrial H+-ATP synthase (ATB5B), sirtuin 1 (Sirt1), and citrate synthase (CS). The protein expression of PPARGC1A and Sirt1, intracellular NAD+-to-NADH ratio, and CS activity was reduced in LE group, and accordingly, mitochondrial DNA (mtDNA) content was decreased. Moreover, copper/zinc superoxide dismutase (CuZn-SOD) expression at both mRNA and protein levels and SOD and catalase (CAT) activities were reduced in LE group as well.ConclusionsThe observed decrease in muscle mitochondrial biogenesis and antioxidant defense capacity suggests that moderately decreased maternal energy intake during pregnancy impairs mitochondrial function in fetal pigs.