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Liver-derived endocrine IGF-I is not critical for activation of skeletal muscle protein synthesis following oral feeding

机译:肝源性内分泌IGF-I对口服喂养后骨骼肌蛋白合成的激活并不关键

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Background Insulin-like growth factor-1 (IGF-1) is produced in various tissues to stimulate protein synthesis under different conditions. It is however, difficult to distinguish effects by locally produced IGF-1 compared to liver-derived IGF-1 appearing in the circulation. In the present study the role of liver-derived endocrine IGF-I for activation of skeletal muscle protein synthesis following feeding was evaluated. Results Transgenic female mice with selective knockout of the IGF-I gene in hepatocytes were freely fed, starved overnight and subsequently refed for 3 hours and compared to wild types (wt). Liver IGF-I knockout mice had 70% reduced plasma IGF-I. Starvation decreased and refeeding increased muscle protein synthesis (p?0.05). mTOR mRNA increased in knockouts only during starvation. Plasma glucose decreased during starvation in all groups in parallel to insulin, while plasma IGF-I and GH did not change significantly among the groups during starvation-refeeding. Plasma amino acids declined and increased during starvation-refeeding in wild type mice (p?(?/?) knockouts (p? Conclusion This study demonstrates that re-synthesis of muscle proteins following starvation is not critically dependent on endocrine liver-derived IGF-I.
机译:背景技术胰岛素样生长因子-1(IGF-1)在各种组织中产生,以刺激不同条件下的蛋白质合成。然而,与循环中出现的肝源性IGF-1相比,很难通过局部产生的IGF-1来区分效果。在本研究中,评估了肝源性内分泌IGF-1在进食后激活骨骼肌蛋白合成中的作用。结果将具有选择性敲除肝细胞中IGF-I基因的转基因雌性小鼠自由喂养,挨饿过夜,随后再饲养3小时,并与野生型(wt)进行比较。肝脏IGF-1敲除小鼠血浆IGF-1降低了70%。饥饿减少,而进食增加肌肉蛋白质合成(p?0.05)。仅在饥饿期间,mTOR mRNA在基因敲除中增加。饥饿期间,与胰岛素平行,所有组的血浆葡萄糖均下降,而在饥饿补给过程中,各组之间的血浆IGF-I和GH没有明显变化。结论:饥饿后进食的野生型小鼠血浆氨基酸含量下降和增加(p?(?/?)敲除(p?)结论本研究表明,饥饿后肌肉蛋白的重新合成并非严格依赖内分泌肝脏衍生的IGF-I。

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