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Wagner, R. ; Hakaste, L.H.* ; Ahlqvist, E.* ; Heni, M. ; Machann, J. ; Schick, F.* ; Van Obberghen, E.* ; Stefan, N. ; Gallwitz, B. ; Tuomi, T.* ; Häring, H.-U. ; Groop, L.* ; Fritsche, A.

Nonsuppressed glucagon after glucose challenge as a potential predictor for glucose tolerance.

Diabetes 66, 1373-1379 (2017)
Publ. Version/Full Text Research data DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
Glucagon levels are classically suppressed after glucose challenge. It is still not clear as to whether a lack of suppression contributes to hyperglycemia and thus to the development of diabetes. We investigated the association of postchallenge change in glucagon during oral glucose tolerance tests (OGTTs), hypothesizing that higher postchallenge glucagon levels are observed in subjects with impaired glucose tolerance (IGT). Glucagon levels were measured during OGTT in a total of 4,194 individuals without diabetes in three large European cohorts. Longitudinal changes in glucagon suppression were investigated in 50 participants undergoing a lifestyle intervention. Only 66-79% of participants showed suppression of glucagon at 120 min (fold change glucagon(120/0) <1) during OGTT, whereas 21-34% presented with increasing glucagon levels (fold change glucagon(120/0) 1). Participants with nonsuppressed glucagon(120) had a lower risk of IGT in all cohorts (odds ratio 0.44-0.53, P < 0.01). They were also leaner and more insulin sensitive and had lower liver fat contents. In the longitudinal study, an increase of fold change glucagon(120/0) was associated with an improvement in insulin sensitivity (P = 0.003). We characterize nonsuppressed glucagon(120) during the OGTT. Lower glucagon suppression after oral glucose administration is associated with a metabolically healthier phenotype, suggesting that it is not an adverse phenomenon.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Insulin-resistance; Fasting Glucagon; Suppression; Secretion
ISSN (print) / ISBN 0012-1797
e-ISSN 1939-327X
Journal Diabetes
Quellenangaben Volume: 66, Issue: 5, Pages: 1373-1379 Article Number: , Supplement: ,
Publisher American Diabetes Association
Publishing Place Alexandria, VA.
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Diabetes Research and Metabolic Diseases (IDM)