Alpha cell function in health and disease: influence of glucagon-like peptide-1
(2005) In Diabetologia 48(9). p.1700-1713- Abstract
- Although there is abundant evidence that hyperglucagonaemia plays a key role in the development of hyperglycaemia in type 2 diabetes, efforts to understand and correct this abnormality have been overshadowed by the emphasis on insulin secretion and action. However, recognition that the incretin hormone glucagon-like peptide-1 (GLP-1) exerts opposing effects on glucagon and insulin secretion has revived interest in glucagon, the neglected partner of insulin, in the bihormonal hypothesis. In healthy subjects, glucagon secretion is regulated by a variety of nutrient, neural and hormonal factors, the most important of which is glucose. The defect in alpha cell function that occurs in type 2 diabetes reflects impaired glucose sensing. GLP-1... (More)
- Although there is abundant evidence that hyperglucagonaemia plays a key role in the development of hyperglycaemia in type 2 diabetes, efforts to understand and correct this abnormality have been overshadowed by the emphasis on insulin secretion and action. However, recognition that the incretin hormone glucagon-like peptide-1 (GLP-1) exerts opposing effects on glucagon and insulin secretion has revived interest in glucagon, the neglected partner of insulin, in the bihormonal hypothesis. In healthy subjects, glucagon secretion is regulated by a variety of nutrient, neural and hormonal factors, the most important of which is glucose. The defect in alpha cell function that occurs in type 2 diabetes reflects impaired glucose sensing. GLP-1 inhibits glucagon secretion in vitro and in vivo in experimental animals, and suppresses glucagon release in a glucose-dependent manner in healthy subjects. This effect is also evident in diabetic patients, but GLP-1 does not inhibit glucagon release in response to hypoglycaemia, and may even enhance it. Early clinical studies with agents acting through GLP-1 signalling mechanisms (e.g. exenatide, liraglutide and vildagliptin) suggest that GLP-1 can improve alpha cell glucose sensing in patients with type 2 diabetes. Therapeutic approaches based around GLP-1 have the potential to improve both alpha cell and beta cell function, and could be of benefit in patients with a broad range of metabolic disorders. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/224545
- author
- Dunning, B E ; Foley, J E and Ahrén, Bo LU
- organization
- publishing date
- 2005
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- IGT, dipeptidyl peptidase IV, diabetes treatment, DPP-4, GLP-1, glucagon-like peptide-1, glucagon, incretin, impaired glucose tolerance
- in
- Diabetologia
- volume
- 48
- issue
- 9
- pages
- 1700 - 1713
- publisher
- Springer
- external identifiers
-
- wos:000231939300003
- pmid:16132964
- scopus:24944577486
- pmid:16132964
- ISSN
- 1432-0428
- DOI
- 10.1007/s00125-005-1878-0
- language
- English
- LU publication?
- yes
- id
- 9041f109-2a1f-48c3-92d6-44fbbbbe2fea (old id 224545)
- date added to LUP
- 2016-04-01 11:38:22
- date last changed
- 2024-01-07 14:41:40
@article{9041f109-2a1f-48c3-92d6-44fbbbbe2fea,
abstract = {{Although there is abundant evidence that hyperglucagonaemia plays a key role in the development of hyperglycaemia in type 2 diabetes, efforts to understand and correct this abnormality have been overshadowed by the emphasis on insulin secretion and action. However, recognition that the incretin hormone glucagon-like peptide-1 (GLP-1) exerts opposing effects on glucagon and insulin secretion has revived interest in glucagon, the neglected partner of insulin, in the bihormonal hypothesis. In healthy subjects, glucagon secretion is regulated by a variety of nutrient, neural and hormonal factors, the most important of which is glucose. The defect in alpha cell function that occurs in type 2 diabetes reflects impaired glucose sensing. GLP-1 inhibits glucagon secretion in vitro and in vivo in experimental animals, and suppresses glucagon release in a glucose-dependent manner in healthy subjects. This effect is also evident in diabetic patients, but GLP-1 does not inhibit glucagon release in response to hypoglycaemia, and may even enhance it. Early clinical studies with agents acting through GLP-1 signalling mechanisms (e.g. exenatide, liraglutide and vildagliptin) suggest that GLP-1 can improve alpha cell glucose sensing in patients with type 2 diabetes. Therapeutic approaches based around GLP-1 have the potential to improve both alpha cell and beta cell function, and could be of benefit in patients with a broad range of metabolic disorders.}},
author = {{Dunning, B E and Foley, J E and Ahrén, Bo}},
issn = {{1432-0428}},
keywords = {{IGT; dipeptidyl peptidase IV; diabetes treatment; DPP-4; GLP-1; glucagon-like peptide-1; glucagon; incretin; impaired glucose tolerance}},
language = {{eng}},
number = {{9}},
pages = {{1700--1713}},
publisher = {{Springer}},
series = {{Diabetologia}},
title = {{Alpha cell function in health and disease: influence of glucagon-like peptide-1}},
url = {{http://dx.doi.org/10.1007/s00125-005-1878-0}},
doi = {{10.1007/s00125-005-1878-0}},
volume = {{48}},
year = {{2005}},
}