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Incretin hypersecretion in gestational diabetes mellitus.

J. Clin. Endocrinol. Metab. 107, e2425-e2430 (2022)
Verlagsversion Postprint DOI PMC
Open Access Green
CONTEXT: Incretins are crucial stimulators of insulin secretion following food intake. Data on incretin secretion and action during pregnancy are sparse. OBJECTIVE: The aim of the study was to investigate the incretin response during an oral glucose tolerance test in pregnant women with and without gestational diabetes. DESIGN: We analyzed data from the ongoing observational PREG study (NCT04270578). SETTING: The study was conducted at the University Hospital Tübingen. PARTICIPANTS: We examined 167 women (33 with gestational diabetes mellitus (GDM)) during gestational week 27± 2.2. INTERVENTION: Subjects underwent 5-point oral glucose tolerance tests (OGTT) with a 75 g glucose load.Main outcome measures: We assessed insulin secretion and levels of total GLP-1, GIP, glicentin and glucagon during OGTT. Linear regression was used to analyze the relation of GLP-1 and glucose with insulin secretion and the association of incretin levels on birth outcome. RESULTS: Insulin secretion was significantly lower in women with GDM (p<0.001). Postload GLP-1 and GIP were ~20% higher in women with GDM (all p<0.05) independent of age, BMI and gestational age. GLP-1 increase was associated with insulin secretion only in GDM, but not in NGT. Postprandial GLP-1 levels were negatively associated with birth weight. CONCLUSIONS: The more pronounced GLP-1 increase in women with GDM could be part of a compensatory mechanism counteracting GLP-1 resistance. Higher GLP-1 levels might be protective against fetal overgrowth.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Gdm ; Glp-1 ; Incretins ; Birth Weight; Glucagon-like Peptide-1; Insulin-resistance; Women; Pregnancy; Secretion; Association; Postpartum; Predictor; Hormones; Gut
ISSN (print) / ISBN 0021-972X
e-ISSN 1945-7197
Quellenangaben Band: 107, Heft: 6, Seiten: e2425-e2430 Artikelnummer: , Supplement: ,
Verlag Endocrine Society
Verlagsort Bethesda, Md.
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Förderungen Federal Ministry of Education and Research (BMBF)