Glucagon-like peptide-1, glucose homeostasis and diabetes.

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Glucagon-like peptide-1, glucose homeostasis and diabetes. / Holst, Jens Juul; Deacon, Carolyn F; Vilsbøll, Tina; Krarup, Thure; Madsbad, Sten.

In: Trends in Molecular Medicine, Vol. 14, No. 4, 2008, p. 161-8.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Holst, JJ, Deacon, CF, Vilsbøll, T, Krarup, T & Madsbad, S 2008, 'Glucagon-like peptide-1, glucose homeostasis and diabetes.', Trends in Molecular Medicine, vol. 14, no. 4, pp. 161-8. https://doi.org/10.1016/j.molmed.2008.01.003

APA

Holst, J. J., Deacon, C. F., Vilsbøll, T., Krarup, T., & Madsbad, S. (2008). Glucagon-like peptide-1, glucose homeostasis and diabetes. Trends in Molecular Medicine, 14(4), 161-8. https://doi.org/10.1016/j.molmed.2008.01.003

Vancouver

Holst JJ, Deacon CF, Vilsbøll T, Krarup T, Madsbad S. Glucagon-like peptide-1, glucose homeostasis and diabetes. Trends in Molecular Medicine. 2008;14(4):161-8. https://doi.org/10.1016/j.molmed.2008.01.003

Author

Holst, Jens Juul ; Deacon, Carolyn F ; Vilsbøll, Tina ; Krarup, Thure ; Madsbad, Sten. / Glucagon-like peptide-1, glucose homeostasis and diabetes. In: Trends in Molecular Medicine. 2008 ; Vol. 14, No. 4. pp. 161-8.

Bibtex

@article{1632e760ab4911ddb5e9000ea68e967b,
title = "Glucagon-like peptide-1, glucose homeostasis and diabetes.",
abstract = "Incretins, enhancers of insulin secretion, are essential for glucose tolerance, and a reduction in their function might contribute to poor beta-cell function in patients with type-2 diabetes mellitus. However, at supraphysiological doses, the incretin glucagon-like peptide-1 (GLP-1) protects pancreatic beta 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 pathophysiological basis the clinical use of these therapeutics is reviewed here.",
author = "Holst, {Jens Juul} and Deacon, {Carolyn F} and Tina Vilsb{\o}ll and Thure Krarup and Sten Madsbad",
note = "Keywords: Diabetes Mellitus; Glucagon-Like Peptide 1; Glucose; Homeostasis; Humans",
year = "2008",
doi = "10.1016/j.molmed.2008.01.003",
language = "English",
volume = "14",
pages = "161--8",
journal = "Trends in Molecular Medicine",
issn = "1471-4914",
publisher = "Elsevier Ltd. * Trends Journals",
number = "4",

}

RIS

TY - JOUR

T1 - Glucagon-like peptide-1, glucose homeostasis and diabetes.

AU - Holst, Jens Juul

AU - Deacon, Carolyn F

AU - Vilsbøll, Tina

AU - Krarup, Thure

AU - Madsbad, Sten

N1 - Keywords: Diabetes Mellitus; Glucagon-Like Peptide 1; Glucose; Homeostasis; Humans

PY - 2008

Y1 - 2008

N2 - Incretins, enhancers of insulin secretion, are essential for glucose tolerance, and a reduction in their function might contribute to poor beta-cell function in patients with type-2 diabetes mellitus. However, at supraphysiological doses, the incretin glucagon-like peptide-1 (GLP-1) protects pancreatic beta 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 pathophysiological basis the clinical use of these therapeutics is reviewed here.

AB - Incretins, enhancers of insulin secretion, are essential for glucose tolerance, and a reduction in their function might contribute to poor beta-cell function in patients with type-2 diabetes mellitus. However, at supraphysiological doses, the incretin glucagon-like peptide-1 (GLP-1) protects pancreatic beta 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 pathophysiological basis the clinical use of these therapeutics is reviewed here.

U2 - 10.1016/j.molmed.2008.01.003

DO - 10.1016/j.molmed.2008.01.003

M3 - Journal article

C2 - 18353723

VL - 14

SP - 161

EP - 168

JO - Trends in Molecular Medicine

JF - Trends in Molecular Medicine

SN - 1471-4914

IS - 4

ER -

ID: 8416785