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首页> 外文期刊>Biology of Reproduction: Offical Journal of the Society for the Study of Reproduction >Oxidative metabolism of pyruvate is required for meiotic maturation of murine oocytes in vivo.
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Oxidative metabolism of pyruvate is required for meiotic maturation of murine oocytes in vivo.

机译：丙酮酸氧化代谢的需要减数分裂成熟小鼠卵母细胞的体内。

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摘要

The requirement for oxidative metabolism of pyruvate during oogenesis in vivo was evaluated by inactivating Pdha1, a gene encoding an enzymatic subunit of pyruvate dehydrogenase complex, in murine oocytes at the beginning of the follicular growth phase. Immunohistochemical analysis revealed that Pdha1(-) oocytes have dramatically reduced amounts of pyruvate dehydrogenase enzyme by the secondary follicle stage. Despite this reduction, these oocytes grow to normal size, are ovulated, and can be fertilized. Pdha1(-) oocytes are, however, impaired in their ability to support embryonic development, as demonstrated by the failure of fertilized oocytes to develop beyond the one-cell zygote stage in vivo. Immunocytochemical evaluation showed that almost all (98.4%) ovulated Pdha1(-) oocytes have not completed meiotic maturation and/or have gross abnormalities of the meiotic spindle and chromatin. Meiotic maturation is even more compromised when these oocytes are matured in vitro in the absence of cumulus cellsor in the presence of the gap junction inhibitor 18-alpha glycyrrhetinic acid, indicating that cumulus cells can partially compensate for this enzymatic deficiency through a gap junction-mediated mechanism. Ovulated Pdha1(-) oocytes were also shown to have reduced levels of total ATP content and NAD(P)H autofluorescence relative to oocytes without this enzymatic deficiency. These studies demonstrate that oxidative metabolism of pyruvate is essential for proper completion of oogenesis, serving as a vital source of energy during meiotic maturation. At earlier stages of oogenesis this metabolic pathway may not be necessary due to metabolic compensation by the granulosa cells.
机译：氧化代谢的需求丙酮酸在体内卵子发生评估由基因编码一种灭活Pdha1丙酮酸脱氢酶的酶亚基复杂,在小鼠卵母细胞的开始卵泡生长阶段。分析显示,Pdha1(-)卵母细胞大大减少了大量的丙酮酸脱氢酶酶通过次级卵泡阶段。,排卵正常大小,都可以受精。支持胚胎的能力受损说明开发的失败受精卵子发展超出了一个细胞体内受精卵阶段。评估显示,几乎所有人(98.4%)Pdha1排卵(-)卵母细胞还没有完成减数分裂成熟和/或有毛异常的减数分裂纺锤体染色质。当这些卵母细胞成熟在妥协体外没有积云cellsor缝隙连接的抑制剂18-alpha甘草次酸,表明积云这个酶的细胞可以部分弥补通过间隙连接调控不足机制。减少了总ATP含量水平和NAD (P) H相对于卵母细胞自体荧光如果没有这种酶缺乏症。表明,丙酮酸的氧化代谢正常完成卵子发生的必要条件,作为重要的能源来源减数分裂成熟。卵子发生代谢途径可能不是由于代谢补偿的必要颗粒细胞。

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