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Rottenkolber, M.* ; Ferrari, U. ; Holland, L. ; Aertsen, S. ; Kammer, N.N.* ; Hetterich, H.* ; Fugmann, M. ; Banning, F. ; Weise, M. ; Sacco, V. ; Kohn, D.* ; Freibothe, I. ; Hutter, S.* ; Hasbargen, U.* ; Lehmann, R.* ; Grallert, H. ; Parhofer, K.G.* ; Seissler, J. ; Lechner, A.

The diabetes risk phenotype of young women with recent gestational diabetes.

J. Clin. Endocrinol. Metab. 100, E910-E918 (2015)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Context: The pathogenesis of type 2 diabetes (T2D) is still incompletely understood. In-depth phenotyping of young individuals at risk for T2D can contribute to the understanding of this process. Objective: To metabolically characterize women with recent gestational diabetes (GDM), an at-risk cohort for T2D. Study participants: 147 consecutively recruited women 3-16 months after pregnancy, women who had GDM and women after a normoglycemic pregnancy (controls) in a 2:1 ratio Design: Mono-center cross-sectional analysis (PPS-Diab study) Methods: 5-point OGTT with calculation of insulin sensitivity (ISI) and disposition index (DI; validation by euglycemic clamp and IVGTT), anthropometrics, medical and family history, clinical chemistry and biomarkers, statistical modelling, MRI/MRS substudy (body fat distribution, liver and muscle fat; n=66) Results: Compared to control subjects, women post GDM had a reduced DI, higher levels of plasma fetuin-A and a lower ISI. A low ISI was also the major determinant of pathologic glucose tolerance after GDM. The factors most strongly predictive of low insulin sensitivity were high plasma leptin, BMI, triglycerides, and waist circumference. Ectopic lipids showed no BMI-independent associations with having had GDM or low insulin sensitivity in an MRI substudy. Conclusions: We found that beta cell function is already impaired in women with recent GDM, a young at-risk cohort for T2D. Additionally, our data suggest that fetuin-A and leptin signaling may be important early contributors to the pathogenesis of T2D, at this disease stage equally or more relevant than ectopic lipids and low-grade inflammation.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
ISSN (print) / ISBN 0021-972X
e-ISSN 1945-7197
Zeitschrift Journal of Clinical Endocrinology & Metabolism, The
Quellenangaben Band: 100, Heft: 6, Seiten: E910-E918 Artikelnummer: , Supplement: ,
Verlag Endocrine Society
Verlagsort Bethesda, Md.
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) CCG Biomarker for the subclassification of T2DM (KKG-KDB)
CCG Nutrigenomics and Type 2 Diabetes (KKG-KDN)
Institute of Epidemiology II (EPI2)