Methionine Partially Replaced by Methionyl-Methionine Dipeptide Improves Reproductive Performance over Methionine Alone in Methionine-Deficient Mice.
Methionine Partially Replaced by Methionyl-Methionine Dipeptide Improves Reproductive Performance over Methionine Alone in Methionine-Deficient Mice.
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DOI：
10.3390/nu10091190
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发表时间：
2018-09-01
期刊：
影响因子：
5.9
通讯作者：
Liu H
中科院分区：
文献类型：
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作者：
Chen Q;Dai W;Sun Y;Zhao F;Liu J;Liu H
孕妇体内蛋白质分解减少导致血浆中蛋氨酸（Met）浓度降低，引起妊娠相关代谢紊乱。其二肽甲硫氨酰-甲硫氨酸（Met-Met）可能对胎儿发育有积极影响。本研究主要探讨Met-Met是否可以作为游离Met的一部分来促进小鼠的生殖结果及其潜在机制。Met缺陷妊娠小鼠在妊娠期间单独用Met或用Met-Met处理。在15-45%剂量范围内，孕鼠每天腹腔注射35%蛋氨酸是最佳剂量。当35%Met组中25%的Met被Met-Met取代时，胚胎发育和新生儿出生体重得到增强。Met-Met替代品具有更高的血浆胰岛素、葡萄糖和游离氨基酸（AA）浓度。此外，在胎盘中，Met-Met处理组AA转运体mRNA丰度和肽转运体（PhT 1和PepT 1）蛋白水平较高。此外，Met-Met增加4 E-BP 1、S6 K1和AKT/mTOR磷酸化。这些结果表明，Met-Met可以作为Met的部分来源，以促进生殖结果在Met限制的怀孕小鼠，这可能是通过促进营养的可用性和激活AKT/mTOR介导的信号通路介导的。
Decreased protein breakdown in pregnant women results in lower concentration of methionine (Met) in plasma, causing pregnancy-related metabolic disturbance. Its dipeptide methionyl-methionine (Met-Met) may exert positive influence in fetal development. This study mainly investigated whether Met-Met can be used as part of free Met to promote reproductive outcomes in mice and the underlying mechanisms. Met-deficient pregnant mice were treated with Met alone or with Met-Met during pregnancy. Daily intraperitoneal injection of 35% dietary Met in pregnant mice was the best dose among the 15–45% doses. Embryo development and newborn birth weight were enhanced when 25% of the Met in the 35% Met group was replaced with Met-Met. Met-Met replacement had higher plasma insulin, glucose, and free amino acids (AA) concentrations. Besides, in the placenta, the AA transporter mRNA abundances and peptide transporters (PhT1 and PepT1) protein levels were higher in Met-Met treatment group. Moreover, Met-Met increased 4E-BP1, S6K1 and AKT/mTOR phosphorylation. These results suggest that Met-Met could be used as a partial source of Met to promote reproductive outcomes in Met-restricted pregnant mice, which might be mediated by promoting nutrient availability and activating AKT/mTOR-mediated signaling pathway.