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Pregnancy glucagon-like peptide 1 predicts insulin but not glucose concentrations

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posted on 2024-07-04, 13:41 authored by Danielle L Jones, Clive J Petry, Keith Burling, Peter Barker, Elizabeth H Turner, Laura C Kusinski, Claire L Meek

Aims Incretin hormones glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP) cause increased insulin secretion in non-pregnant adults, but their role in pregnancy, where there are additional metabolically-active hormones from the placenta, is less clear. The aim of the present study was to assess if fasting and post-load incretin concentrations were predictive of pregnancy insulin and glucose concentrations. Methods Pregnant women (n = 394) with one or more risk factors for gestational diabetes were recruited at 28 weeks for a 75 g oral glucose tolerance test (OGTT). Glucose, insulin, GLP-1 and GIP were measured in the fasting state and 120 min after glucose ingestion. Results Fasting plasma GLP-1 concentrations were associated with plasma insulin (standardised β’ 0.393 (0.289–0.498), p = 1.3 × 10–12; n = 306), but not with glucose concentrations (p = 0.3). The association with insulin was still evident when adjusting for BMI (β’ 0.271 (0.180–0.362), p = 1.1 × 10–8; n = 297). Likewise, at 120 min the OGTT GLP-1 concentrations were associated with plasma insulin concentrations (β’ 0.216 (0.100–0.331), p = 2.7 × 10–4; n = 306) even after adjusting for BMI (β’ 0.178 (0.061–0.294), p = 2.9 × 10–3; n = 296), but not with glucose (p = 0.9). GIP concentrations were not associated with insulin or glucose concentrations at either time point (all p > 0.2). In pregnancy plasma GLP-1, but not GIP, concentrations appear to be predictive of circulating insulin concentrations, independently of associations with BMIs. Conclusions These results suggest that the relationship between insulin and incretins is preserved in pregnancy, but that other factors, such as placental hormones or counter-regulatory hormones, may be more important determinants of glycaemia and gestational diabetes aetiology.

Funding

Diabetes UK Harry Keen Intermediate Clinical Fellowship (DUK-HKF 17/0005712)

European Foundation for the Study of Diabetes—Novo Nordisk Foundation Future Leader’s Award (NNF19SA058974

European Foundation for the Study of Diabetes—Sanofi grant

National Institute of Health Research Cambridge Biomedical Research Centre (BRC)

History

Citation

Acta Diabetol 60, 1635–1642 (2023)

Author affiliation

College of Life Sciences Population Health Sciences

Version

  • VoR (Version of Record)

Published in

Acta Diabetologica

Volume

60

Issue

12

Pagination

1635 - 1642

Publisher

Springer Science and Business Media LLC

issn

0940-5429

eissn

1432-5233

Acceptance date

2023-06-16

Copyright date

2023

Available date

2024-07-04

Spatial coverage

Germany

Language

en

Deposited by

Professor Claire Meek

Deposit date

2024-07-03

Rights Retention Statement

  • No

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