Gastrointestinal peptides and insulin secretion

Ebert, R.; Creutzfeldt, W.

doi:10.1002/dmr.5610030101

Cited by 84 publications

(42 citation statements)

References 165 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Type 2 diabetes mellitus is characterized by a decrease in glucose-stimulated insulin secretion in association with a reduced incretin effect (Ebert and Creutzfeldt, 1987). However, the levels of intact circulating GIP are only minimally reduced or normal in subjects with type 2 diabetes (Rask et al, 2001;Vilsboll et al, 2001).…”

Section: E Glucose-dependent Insulinotropic Peptide Receptor and Typmentioning

confidence: 99%

International Union of Pharmacology. XXXV. The Glucagon Receptor Family

et al. 2003

View full text Add to dashboard Cite

Section: E Glucose-dependent Insulinotropic Peptide Receptor and Typmentioning

confidence: 99%

International Union of Pharmacology. XXXV. The Glucagon Receptor Family

et al. 2003

View full text Add to dashboard Cite

“…The gut endocrine cells, which secrete the gluco-incretin hormones GIP and GLP-1 after absorption of nutrients, particularly glucose (1,2), represent such a secondary control system. The glucoincretin hormones play different roles in the control of whole-body glucose homeostasis.…”

Section: Introductionmentioning

confidence: 99%

Gluco-incretins control insulin secretion at multiple levels as revealed in mice lacking GLP-1 and GIP receptors

Preitner¹,

Ibberson²,

Franklin³

et al. 2004

J. Clin. Invest.

116

View full text Add to dashboard Cite

The role of the gluco-incretin hormones GIP and GLP-1 in the control of β cell function was studied by analyzing mice with inactivation of each of these hormone receptor genes, or both. Our results demonstrate that glucose intolerance was additively increased during oral glucose absorption when both receptors were inactivated. After intraperitoneal injections, glucose intolerance was more severe in double-as compared to single-receptor KO mice, and euglycemic clamps revealed normal insulin sensitivity, suggesting a defect in insulin secretion. When assessed in vivo or in perfused pancreas, insulin secretion showed a lack of first phase in Glp-1R -/-but not in Gipr -/-mice. In perifusion experiments, however, first-phase insulin secretion was present in both types of islets. In double-KO islets, kinetics of insulin secretion was normal, but its amplitude was reduced by about 50% because of a defect distal to plasma membrane depolarization. Thus, gluco-incretin hormones control insulin secretion (a) by an acute insulinotropic effect on β cells after oral glucose absorption (b) through the regulation, by GLP-1, of in vivo first-phase insulin secretion, probably by an action on extra-islet glucose sensors, and (c) by preserving the function of the secretory pathway, as evidenced by a β cell autonomous secretion defect when both receptors are inactivated.

show abstract

“…The augmented response to oral glucose defines the entero-insular axis, also referred to as the glucoincretin effect. It is thought to be mediated in part by the release of gut hormones into the blood which potentiate glucoseinduced ,Q-cell insulin secretion (1)(2)(3). A number of gut peptides have been suggested as being insulinotropic, such as secre-tin, gastrin-releasing peptide, vasoactive intestinal peptide (VIP),' and cholecystokinin (1)(2)(3).…”

Section: Introductionmentioning

confidence: 99%

Glucagon-like peptide-1 is a physiological incretin in rat.

Wang¹,

Wang²,

Owji³

et al. 1995

J. Clin. Invest.

187

112

View full text Add to dashboard Cite

Glucagon-like peptide-1 7-36 amide (GLP-1) has been postulated to be the primary hormonal mediator of the enteroinsular axis but evidence has been indirect. The discovery of exendin (9-39), a GLP-1 receptor antagonist, allowed this to be further investigated. The IC5o for GLP-1 receptor binding, using RIN 5AH fl-cell membranes, was found to be 0.36 nmol/l for GLP-1 and 3.44 nmol/l for exendin (9-39). There was no competition by exendin (9-39) at binding sites for glucagon or related peptides. In the anaesthetized fasted rat, insulin release after four doses of GLP-1 (0.1, 0.2, 0.3, and 0.4 nmol/kg) was tested by a 2-min intravenous infusion. Exendin (9-39) (1.5, 3.0, and 4.5 nmol/kg) was administered with GLP-1 0.3 nmol/kg, or saline, and only the highest dose fully inhibited insulin release. Exendin (9-39) at 4.5 nmol/kg had no effect on glucose, arginine, vasoactive intestinal peptide or glucose-dependent insulinotropic peptide stimulated insulin secretion. Postprandial insulin release was studied in conditioned conscious rats after a standard meal. Exendin (9-39) (0.5 nmol/kg) considerably reduced postprandial insulin concentrations, for example by 48% at 15 min (431±21 pmol/ I saline, 224±32 pmol/l exendin, P < 0.001). Thus, GLP-1 appears to play a major role in the entero-insular axis. (J. Clin. Invest. 1995.95:417-421.)

show abstract

Gastrointestinal peptides and insulin secretion

Cited by 84 publications

References 165 publications

International Union of Pharmacology. XXXV. The Glucagon Receptor Family

International Union of Pharmacology. XXXV. The Glucagon Receptor Family

Gluco-incretins control insulin secretion at multiple levels as revealed in mice lacking GLP-1 and GIP receptors

Glucagon-like peptide-1 is a physiological incretin in rat.

Contact Info

Product

Resources

About