胃排空
胰高血糖素样肽-1
肠内分泌细胞
食欲
医学
血糖性
2型糖尿病
胰高血糖素样肽1受体
药理学
内科学
内分泌学
糖尿病
肽
生物
胰高血糖素样肽-2
受体
生物信息学
兴奋剂
内分泌系统
激素
生物化学
胃
出处
期刊:Cell Metabolism
[Cell Press]
日期:2018-04-01
卷期号:27 (4): 740-756
被引量:1215
标识
DOI:10.1016/j.cmet.2018.03.001
摘要
Glucagon-like peptide-1 (GLP-1) released from gut enteroendocrine cells controls meal-related glycemic excursions through augmentation of insulin and inhibition of glucagon secretion. GLP-1 also inhibits gastric emptying and food intake, actions maximizing nutrient absorption while limiting weight gain. Here I review the circuits engaged by endogenous versus pharmacological GLP-1 action, highlighting key GLP-1 receptor (GLP-1R)-positive cell types and pathways transducing metabolic and non-glycemic GLP-1 signals. The role(s) of GLP-1 in the benefits and side effects associated with bariatric surgery are discussed and actions of GLP-1 controlling islet function, appetite, inflammation, and cardiovascular pathophysiology are highlighted. Refinement of the risk-versus-benefit profile of GLP-1-based therapies for the treatment of diabetes and obesity has stimulated development of orally bioavailable agonists, allosteric modulators, and unimolecular multi-agonists, all targeting the GLP-1R. This review highlights established and emerging concepts, unanswered questions, and future challenges for development and optimization of GLP-1R agonists in the treatment of metabolic disease.
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