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Herzberg-Schäfer, S.* ; Heni, M.* ; Stefan, N. ; Häring, H.-U. ; Fritsche, A.

Impairment of GLP1-induced insulin secretion: Role of genetic background, insulin resistance and hyperglycaemia.

Diabetes Obes. Metab. 14, S3, 85-90 (2012)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
One major risk factor of type 2 diabetes is the impairment of glucose-induced insulin secretion which is mediated by the individual genetic background and environmental factors. In addition to impairment of glucose-induced insulin secretion, impaired glucagon-like peptide (GLP)1-induced insulin secretion has been identified to be present in subjects with diabetes and impaired glucose tolerance, but little is known about its fundamental mechanisms. The state of GLP1 resistance is probably an important mechanism explaining the reduced incretin effect observed in type 2 diabetes. In this review, we address methods that can be used for the measurement of insulin secretion in response to GLP1 in humans, and studies showing that specific diabetes risk genes are associated with resistance of the secretory function of the beta-cell in response to GLP1 administration. Furthermore, we discuss other factors that are associated with impaired GLP1-induced insulin secretion, for example, insulin resistance. Finally, we provide evidence that hyperglycaemia per se, the genetic background and their interaction result in the development of GLP1 resistance of the beta-cell. We speculate that the response or the non-response to therapy with GLP1 analogues and/or dipeptidyl peptidase-4 (DPP-IV) inhibitors is critically dependent on GLP1 resistance.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Korrespondenzautor
Schlagwörter Glp1 ; Hyperglycaemia ; Insulin Secretion ; Risk Genes; Glucagon-like Peptide-1 ; Relative Physical Inactivity ; Type-2 Diabetes-mellitus ; Blood-glucose Improves ; Beta-cell Function ; High-calorie Diet ; Healthy-subjects ; Incretin ; Glp-1 ; Polymorphism
ISSN (print) / ISBN 1462-8902
e-ISSN 1463-1326
Zeitschrift Diabetes, Obesity and Metabolism
Quellenangaben Band: 14, Heft: , Seiten: 85-90, Artikelnummer: , Supplement: S3
Verlag Wiley
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes Research and Metabolic Diseases (IDM)