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细胞机制调控葡萄糖依赖性胰岛素多肽分泌。

Cellular mechanisms governing glucose-dependent insulinotropic polypeptide secretion.

机构信息

Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, United Kingdom.

Wellcome Trust/MRC Institute of Metabolic Science (IMS), University of Cambridge, United Kingdom.

出版信息

Peptides. 2020 Mar;125:170206. doi: 10.1016/j.peptides.2019.170206. Epub 2019 Nov 19.

DOI:10.1016/j.peptides.2019.170206
PMID:31756367
Abstract

Glucose-dependent insulinotropic polypeptide (GIP) is a gut hormone secreted from the upper small intestine, which plays an important physiological role in the control of glucose metabolism through its incretin action to enhance glucose-dependent insulin secretion. GIP has also been implicated in postprandial lipid homeostasis. GIP is secreted from enteroendocrine K-cells residing in the intestinal epithelium. K-cells sense a variety of components found in the gut lumen following food consumption, resulting in an increase in plasma GIP signal dependent on the nature and quantity of ingested nutrients. We review the evidence for an important role of sodium-coupled glucose uptake through SGLT1 for carbohydrate sensing, of free-fatty acid receptors FFAR1/FFAR4 and the monoacyl-glycerol sensing receptor GPR119 for lipid detection, of the calcium-sensing receptor CASR and GPR142 for protein sensing, and additional modulation by neurotransmitters such as somatostatin and galanin. These pathways have been identified through combinations of in vivo, in vitro and molecular approaches.

摘要

葡萄糖依赖性胰岛素多肽(GIP)是一种从小肠上部分泌的肠激素,通过其肠促胰岛素作用增强葡萄糖依赖性胰岛素分泌来控制葡萄糖代谢,从而发挥重要的生理作用。GIP 还与餐后脂质稳态有关。GIP 由存在于肠上皮中的肠内分泌 K 细胞分泌。K 细胞在进食后感知肠道腔中存在的各种成分,导致 GIP 信号的增加,这取决于摄入的营养物质的性质和数量。我们回顾了通过 SGLT1 摄取钠耦合葡萄糖对碳水化合物的感应、游离脂肪酸受体 FFAR1/FFAR4 和单酰基甘油感应受体 GPR119 对脂质的感应、钙感应受体 CASR 和 GPR142 对蛋白质的感应的重要作用的证据,以及神经递质如生长抑素和神经肽 Y 的额外调节作用。这些途径是通过体内、体外和分子方法的组合确定的。

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