{"title":"为什么胆囊收缩素和胃泌素也是肠促素","authors":"J. Rehfeld","doi":"10.1097/XCE.0000000000000095","DOIUrl":null,"url":null,"abstract":"This review argues that cholecystokinin (CCK) and gastrin are incretins. The insulin cells are equipped with CCK2/gastrin receptors. CCK/gastrin peptides stimulate insulin secretion and potentiate the incretin effect of glucagon-like peptide-1. CCK/gastrin and insulin are released in significant amounts during normal mixed meals even at modest changes in blood glucose concentrations. Treatment of diabetes patients with combinatorial glucagon-like peptide-1 and CCK or gastrin-derived constructs therefore provides an expedient option.","PeriodicalId":72529,"journal":{"name":"Cardiovascular endocrinology","volume":"56 1","pages":"99–101"},"PeriodicalIF":0.0000,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"7","resultStr":"{\"title\":\"Why cholecystokinin and gastrin are also incretins\",\"authors\":\"J. Rehfeld\",\"doi\":\"10.1097/XCE.0000000000000095\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"This review argues that cholecystokinin (CCK) and gastrin are incretins. The insulin cells are equipped with CCK2/gastrin receptors. CCK/gastrin peptides stimulate insulin secretion and potentiate the incretin effect of glucagon-like peptide-1. CCK/gastrin and insulin are released in significant amounts during normal mixed meals even at modest changes in blood glucose concentrations. Treatment of diabetes patients with combinatorial glucagon-like peptide-1 and CCK or gastrin-derived constructs therefore provides an expedient option.\",\"PeriodicalId\":72529,\"journal\":{\"name\":\"Cardiovascular endocrinology\",\"volume\":\"56 1\",\"pages\":\"99–101\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2016-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"7\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cardiovascular endocrinology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1097/XCE.0000000000000095\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cardiovascular endocrinology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1097/XCE.0000000000000095","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Why cholecystokinin and gastrin are also incretins
This review argues that cholecystokinin (CCK) and gastrin are incretins. The insulin cells are equipped with CCK2/gastrin receptors. CCK/gastrin peptides stimulate insulin secretion and potentiate the incretin effect of glucagon-like peptide-1. CCK/gastrin and insulin are released in significant amounts during normal mixed meals even at modest changes in blood glucose concentrations. Treatment of diabetes patients with combinatorial glucagon-like peptide-1 and CCK or gastrin-derived constructs therefore provides an expedient option.
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