Glucagon-like peptide-1, glucose homeostasis and diabetes

被引：129

作者：

Holst, Jens J. ^{[1
,4
,5
]}

Deacon, Carolyn F. ^{[1
]}

Vilsboll, Tina ^{[2
]}

Krarup, Thure ^{[2
]}

Madsbad, Sten ^{[3
]}

机构：

[1] Univ Copenhagen, Panum Inst, Dept Biomed Sci, DK-2200 Copenhagen, Denmark

[2] Univ Hosp, Dept Internal Med F, DK-2900 Copenhagen, Denmark

[3] Hvidovre Univ Hosp, Dept Endocrinol, DK-2650 Hvidovre, Denmark

[4] Novo Nordisk AS, Copenhagen, Denmark

[5] Merck Sharp & Dohme Ltd, Copenhagen, Denmark

来源：

TRENDS IN MOLECULAR MEDICINE | 2008年 / 14卷 / 04期

关键词：

D O I：

10.1016/j.molmed.2008.01.003

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Incretins, enhancers of insulin secretion, are essential for glucose tolerance, and a reduction in their function might contribute to poor P-cell function in patients with type-2 diabetes mellitus. However, at supraphysiollogical doses, the incretin glucagon-like peptide-1 (GLP-1) protects pancreatic P cells, and inhibits glucagon secretion, gastric emptying and food intake, leading to weight loss. GLP-1 mimetics, which are stable-peptide-based activators of the GLP-1 receptor, and incretin enhancers, which inhibit the incretin-degrading enzyme dipeptidyl peptidase-4, have emerged as therapies for type-2 diabetes and have recently reached the market. The pathophysiollogical basis the clinical use of these therapeutics is reviewed here.

引用

页码：161 / 168

页数：8

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