Sex Difference In the Effect of Fetal Exposure to Maternal Diabetes on Insulin Secretion
Autor: | Raphaël Porcher, Charbel Abi Khalil, Jean-Pierre Riveline, Michel Marre, Gilberto Velho, Philippe Boudou, Simeon-Pierre Choukem, Eric Ravussin, Franck Mauvais-Jarvis, Etienne Larger, Ronan Roussel, Jean-François Gautier, Samy Hadjadj, Lila Sabrina Fetita, Fidaa Ibrahim |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Diabetes Pancreatic and Gastrointestinal Hormones β-cell function Arginine Offspring sex difference Endocrinology Diabetes and Metabolism 030209 endocrinology & metabolism Stimulation 03 medical and health sciences 0302 clinical medicine Internal medicine medicine glucose homeostasis Glucose homeostasis 10. No inequality Type 1 diabetes Pregnancy fetal programing business.industry Brief Report medicine.disease Gestational diabetes Sexual dimorphism 030104 developmental biology Endocrinology pregnancy gestational diabetes business |
Zdroj: | Journal of the Endocrine Society |
ISSN: | 2472-1972 |
DOI: | 10.1210/js.2017-00482 |
Popis: | We previously showed that fetal exposure to maternal type 1 diabetes (T1D) is associated with altered glucose-stimulated insulin secretion in adult offspring. Here, we investigated whether this β-cell defect displays a sex dimorphism. Twenty-nine adult nondiabetic offspring of T1D mothers (ODMs) were compared with 29 nondiabetic offspring of T1D fathers. We measured early insulin secretion in response to oral glucose and insulin secretion rate in response to intravenous glucose ramping. Insulin sensitivity and body composition were assessed by a euglycemic, hyperinsulinemic clamp and dual-energy X-ray absorptiometry, respectively. In response to oral glucose, male and female ODMs displayed a reduced insulin secretion. In contrast, in response to graded intravenous glucose infusion, only female ODMs (not males) exhibited decreased insulin secretion. There was no defect in response to combined intravenous arginine and glucose, suggesting that male and female ODMs exhibit a functional β-cell defect rather than a reduced β-cell mass. In conclusion, fetal exposure to maternal diabetes predisposes to β-cell dysfunction in adult male and female offspring. This β-cell defect is characterized by a sexual dimorphism following intravenous glucose stimulation. Insulin secretion was evaluated in adults who have been exposed in utero to maternal T1D. Only women (not men) exhibited decreased insulin secretion in response to intravenous glucose. |
Databáze: | OpenAIRE |
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