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Gar, C. ; Rottenkolber, M. ; Sacco, V. ; Moschko, S. ; Banning, F. ; Hesse, N.* ; Popp, D.* ; Hübener, C.* ; Seissler, J. ; Lechner, A.

Patterns of plasma glucagon dynamics do not match metabolic phenotypes in young women.

J. Clin. Endocrinol. Metab. 103, 972-982 (2017)
Verlagsversion Postprint Forschungsdaten DOI PMC
Open Access Green
Context: The role of hyperglucagonemia in type 2 diabetes is still debated.Objective: We analyzed glucagon dynamics during oral glucose tolerance tests (oGTTs) in young women with one out of three metabolic phenotypes: healthy control (normoglycemic after a normoglycemic pregnancy), normoglycemic high-risk (normoglycemic after a pregnancy complicated by gestational diabetes), and prediabetes/screening-diagnosed type 2 diabetes. We asked if glucagon patterns were homogeneous within the metabolic phenotypes.Design and Setting: Five-point oGTT, sandwich enzyme-linked immunosorbent assay for glucagon, and functional data analysis with unsupervised clustering.Participants: Cross-sectional analysis of 285 women from the monocenter observational study Prediction, Prevention, and Subclassification of gestational and type 2 Diabetes, recruited between November 2011 and May 2016.Results: We found four patterns of glucagon dynamics that did not match the metabolic phenotypes. Elevated fasting glucagon and delayed glucagon suppression was overrepresented with prediabetes/diabetes, but this was only detected in 21% of this group. It also occurred in 8% of the control group.Conclusions: We conclude that hyperglucagonemia may contribute to type 2 diabetes in a subgroup of affected individuals but that it is not a sine qua non for the disease. This should be considered in future pathophysiological studies and when testing pharmacotherapies addressing glucagon signaling.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Glucose-tolerance; Diabetes-mellitus; Fasting Hyperglucagonemia; Insulin Sensitivity; Body-composition; Cell-function; Oral Glucose; Suppression; Hyperglycemia; Secretion
ISSN (print) / ISBN 0021-972X
e-ISSN 1945-7197
Quellenangaben Band: 103, Heft: 3, Seiten: 972-982 Artikelnummer: , Supplement: ,
Verlag Endocrine Society
Verlagsort Bethesda, Md.
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed