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Background: Gestational diabetes mellitus (GDM) affects approximately 10% of successful pregnancies worldwide. Individuals exposed to GDM in utero are at increased risk of developing type II diabetes during childhood and later in life. The hormone cortisol has important roles in metabolism, and cortisol dysregulation is associated with metabolic dysfunction, thus representing a possible mechanistic link between GDM exposure and later diabetes. Methods: We aimed to determine whether adolescents exposed to GDM exhibited dysregulation in diurnal cortisol and the cortisol awakening response. Salivary cortisol was measured in 22 GDM-exposed adolescents (aged 11–14) and 10 controls at 0, 15, 30, and 45 minutes after awakening over 2 consecutive days. Afternoon and night samples were also collected. Data were represented as area under the curve with respect to ground (AUCg) and increase (AUCi) and averaged between days. Findings: The control group had lower AUCg (p = 0.025, ω2= 0.124), representing lower total morning cortisol secretion, but similar AUCi (p = 0.662, ω2= -0.025), indicating that the hormonal response to awakening is comparable. These findings may partially reflect altered pre-awakening cortisol secretion. Interpretation: Given that a dysregulated cortisol profile, including sustained, low cortisol production, is associated with metabolic dysfunction and the development of type II diabetes, we suggest that this may be one mechanism by which exposure to maternal GDM increases the risk of these problems in offspring. Funding Statement: An intramural grant funded this study. MRG was supported by an NHMRC-ARC Dementia Research Development Fellowship. JMVD was supported by a Government of Australia Research Training Program scholarship and a Healthy Development Adelaide/Channel 7 Children’s Research Foundation supplementary scholarship. Declaration of Interests: The authors state they have nothing to declare. Ethics Approval Statement: Ethical Approval for all protocols and procedures was given by the University of Adelaide and Women’s and Children’s Health Network Human Research Ethics Committees (I.D. number: HREC/16/WCHN/50). |
