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Elimination of Glucagon-Like Peptide 1R Signaling Does Not Modify Weight Gain and Islet Adaptation In Mice With Combined Disruption of Leptin and GLP-1 Action

机译:消除胰高血糖素样肽1R信号并不会改变小鼠的瘦素和GLP-1作用,从而改变体重增加和胰岛适应。

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摘要

Leptin and glucagon-like peptide 1 (GLP-1) exhibit opposing actions in the endocrine pancreas. GLP-1 stimulates insulin biosynthesis, secretion, and islet growth, whereas lepth inhibits glucose-dependent insulin secretion and insulin gene transcription. In con- trast, GLP-1 and leptin actions overlap in the central nervous system, where leptin has been shown to acti- vate GLP-1 circuits that inhibit food intake.
机译:瘦素和胰高血糖素样肽1(GLP-1)在内分泌胰腺中表现出相反的作用。 GLP-1刺激胰岛素的生物合成,分泌和胰岛生长,而深度抑制葡萄糖依赖性胰岛素分泌和胰岛素基因转录。相反,中枢神经系统中GLP-1和瘦素的作用重叠,已显示瘦素可激活抑制食物摄入的GLP-1回路。

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