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Betamethasone-exposed preterm birth does not impair insulin action in adult sheep

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Version 2 2024-06-05, 02:04
Version 1 2019-01-16, 15:32
journal contribution
posted on 2024-06-05, 02:04 authored by R De Matteo, DJ Hodgson, T Bianco-Miotto, V Nguyen, Julie OwensJulie Owens, R Harding, BJ Allison, G Polglase, MJ Black, KL Gatford
Preterm birth is associated with increased risk of type 2 diabetes (T2D) in adulthood; however, the underlying mechanisms are poorly understood. We therefore investigated the effect of preterm birth at ~0.9 of term after antenatal maternal betamethasone on insulin sensitivity, secretion and key determinants in adulthood, in a clinically relevant animal model. Glucose tolerance and insulin secretion (intravenous glucose tolerance test) and whole-body insulin sensitivity (hyperinsulinaemic euglycaemic clamp) were measured and tissue collected in young adult sheep (14 months old) after epostane-induced preterm (9M, 7F) or term delivery (11M, 6F). Glucose tolerance and disposition, insulin secretion, β-cell mass and insulin sensitivity did not differ between term and preterm sheep. HepaticPRKAG2expression was greater in preterm than in term males (P = 0.028), but did not differ between preterm and term females. In skeletal muscle,SLC2A4(P = 0.019),PRKAA2(P = 0.021) andPRKAG2(P = 0.049) expression was greater in preterm than in term overall and in males, whileINSR(P = 0.047) andAKT2(P = 0.043) expression was greater in preterm than in term males only. HepaticPRKAG2expression correlated positively with whole-body insulin sensitivity in males only. Thus, preterm birth at 0.9 of term after betamethasone does not impair insulin sensitivity or secretion in adult sheep, and has sex-specific effects on gene expression of the insulin signalling pathway. Hence, the increased risk of T2D in preterm humans may be due to factors that initiate preterm delivery or in early neonatal exposures, rather than preterm birthper se.

History

Journal

Journal of Endocrinology

Volume

232

Pagination

175-187

Location

England

Open access

  • Yes

ISSN

0022-0795

eISSN

1479-6805

Language

English

Publication classification

C1.1 Refereed article in a scholarly journal

Copyright notice

2017 Society for Endocrinology

Issue

2

Publisher

BIOSCIENTIFICA LTD