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首页> 美国卫生研究院文献>Endocrinology >Absence of the Glucagon-Like Peptide-1 Receptor Does Not Affect the Metabolic Phenotype of Mice with Liver-Specific Gsα Deficiency
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Absence of the Glucagon-Like Peptide-1 Receptor Does Not Affect the Metabolic Phenotype of Mice with Liver-Specific Gsα Deficiency

机译：胰高血糖素样肽-1受体的缺乏不会影响小鼠肝特异性Gsα缺乏症的代谢表型。

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The stimulatory G protein α-subunit (Gsα) couples hormone and other receptors to the generation of intracellular cAMP. We previously showed that mice with liver-specific Gsα deficiency [liver-specific Gsα knockout (LGsKO) mice] had reduced adiposity and improved glucose tolerance associated with increased glucose-stimulated insulin secretion, pancreatic islet hyperplasia, and very high serum glucagon and glucagon-like peptide 1 (GLP-1) levels. Because GLP-1 is known to stimulate insulin secretion and to have effects on energy balance, we mated LGsKO mice with germline GLP-1 receptor (GLP-1R) knockout mice (Glp1r−/−) and compared LGsKO to double-knockout (LGs/Glp1r−/−) mice to determine the contribution of excess GLP-1R signaling to the LGsKO phenotype. Loss of the GLP-1R failed to reverse most of the metabolic features of LGsKO mice, including reduced fat mass, increased glucose tolerance, and second-phase glucose-stimulated insulin secretion, islet cell hyperplasia, and very high glucagon and GLP-1 levels. However, loss of GLP-1R impaired first-phase insulin secretion in mice with or without liver-specific Gsα deficiency. Thus, excess GLP-1 action (or at least through GLP-1R) does not contribute to the LGsKO metabolic phenotype, and other unknown factors involved in the cross talk between the liver Gsα/cAMP pathway and pancreatic islet function need to be further elucidated.
机译：刺激性G蛋白α亚基（Gsα）将激素和其他受体与细胞内cAMP的产生结合。我们先前曾发现具有肝脏特异性Gsα缺乏症的小鼠[肝脏特异性Gsα敲除（LGsKO）小鼠]减少了肥胖症，并改善了糖耐量，与葡萄糖刺激的胰岛素分泌增加，胰岛增生以及非常高的血清胰高血糖素和胰高血糖素-像肽1（GLP-1）的水平。因为已知GLP-1刺激胰岛素分泌并影响能量平衡，所以我们将LGsKO小鼠与种系GLP-1受体（GLP-1R）剔除小鼠（Glp1r -/-）进行了配对并进行了比较LGsKO双敲除（LGs / Glp1r -/-）小鼠，以确定过量的GLP-1R信号对LGsKO表型的贡献。 GLP-1R的丧失未能逆转LGsKO小鼠的大多数代谢特征，包括脂肪减少，葡萄糖耐量增加和第二阶段葡萄糖刺激的胰岛素分泌，胰岛细胞增生以及胰高血糖素和GLP-1水平很高。但是，GLP-1R的缺失会损害有或没有肝脏特异性Gsα缺乏症的小鼠的第一阶段胰岛素分泌。因此，过量的GLP-1作用（或至少通过GLP-1R）不会促进LGsKO代谢表型，还需要进一步阐明参与肝脏Gsα/ cAMP途径与胰岛功能之间的相互影响的其他未知因素。 。

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