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Maternal Androgen Excess Increases the Risk of Metabolic Syndrome in Female Offspring in Their Later Life: A Long-term Population-based Follow-up Study

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Date 2023 Jul 9
PMID 37422863
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Abstract

Purpose: Hyperandrogenic intrauterine environment may lead to the development of metabolic disorders in offspring in their later life. In this study, we aimed to determine the impact of maternal hyperandrogenism (MHA) on metabolic syndrome (MetS) risk in female offspring in their later life.

Methods: In this cohort study conducted in Tehran, Iran, female offspring with MHA (n = 323) and without MHA (controls) (n = 1125) were selected. Both groups of female offspring were followed from the baseline to the date of the incidence of events, censoring, or end of the study period, whichever came first. We used age-scaled unadjusted and adjusted Cox regression models to assess the hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between MHA and MetS in female offspring. The software package STATA was used for statistical analysis, and the significance level was set at P < 0.05.

Results: We observed a higher risk of MetS (unadjusted HR (95% CI), 1.36 (1.05-1.77)), (P = 0.02) and (adjusted HR (95% CI), 1.34 (1.00-1.80)), (P = 0.05, borderline)), in female offspring with MHA, compared to controls. The results were adjusted for the potential confounders including body mass index (BMI) at baseline, net changes of BMI, physical activity, education status, and birth weight.

Conclusion: Our results suggest that MHA increases the risk of developing MetS in female offspring in their later life. Screening of these female offspring for MetS may be recommended.

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References
1.
Grundy S . Metabolic syndrome scientific statement by the American Heart Association and the National Heart, Lung, and Blood Institute. Arterioscler Thromb Vasc Biol. 2005; 25(11):2243-4. DOI: 10.1161/01.ATV.0000189155.75833.c7. View

2.
Xita N, Tsatsoulis A . Fetal origins of the metabolic syndrome. Ann N Y Acad Sci. 2010; 1205:148-55. DOI: 10.1111/j.1749-6632.2010.05658.x. View

3.
Recabarren S, Sir-Petermann T, Maliqueo M, Lobos A, Rojas-Garcia P . [Prenatal exposure to androgens as a factor of fetal programming]. Rev Med Chil. 2006; 134(1):101-8. DOI: 10.4067/s0034-98872006000100015. View

4.
Hakim C, Padmanabhan V, Vyas A . Gestational Hyperandrogenism in Developmental Programming. Endocrinology. 2016; 158(2):199-212. PMC: 5413081. DOI: 10.1210/en.2016-1801. View

5.
Fowden A, Forhead A . Endocrine mechanisms of intrauterine programming. Reproduction. 2004; 127(5):515-26. DOI: 10.1530/rep.1.00033. View