Abstract
BackgroundWe and others have observed that young girls predisposed to polycystic ovary syndrome (PCOS) display defective insulin sensitivity, beta-cell function and non-esterified fatty acids (NEFA) suppressibility during early pubertal years, compared to controls. Our objective is to assess whether these differences in glucose and NEFA metabolisms persist after 5 years in late/post-puberty.MethodsWe conducted a prospective cohort study between 2007 and 2015 with 4–6 years of follow-up in an academic institution research center. We compared 8 daughters and sisters of PCOS women (PCOSr) to 8 age-matched girls unrelated to PCOS (±1.5 years). Girls were assessed initially at 8–14 years old and re-assessed after a median follow-up of 5.4 years, at 13–21 years old. Our main measures were a frequently sampled intravenous glucose tolerance test (FSivGTT)-derived insulin sensitivity (IS) and beta-cell function (disposition index, DIFSivGTT); and indices of NEFA suppression during FSivGTT (logn-linear slope of NEFA and T50 of NEFA suppression).ResultsAt follow-up, both PCOSr and controls had similar results: IS = 3.2 vs 3.4 (p = 0.88), DIFSivGTT = 1926 vs 1380 (p = 0.44), logn-linear slope = −0.032 vs −0.032 (p = 0.88) and T50NEFA = 18.1 vs 20.8 min (p = 0.57). IS, DIFSivGTT and NEFA suppressibility were stable in PCOSr after 5 years, but decreased significantly in controls (all p < 0.05).ConclusionsImpaired metabolism observed during early puberty in girls predisposed to PCOS remains stable after 5 years whereas control girls deteriorated their metabolic parameters. Therefore, both groups become comparable in late/post-puberty. Early puberty may thus represent a window during which metabolic alterations are transiently apparent in girls at risk of PCOS.
Highlights
We and others have observed that young girls predisposed to polycystic ovary syndrome (PCOS) display defective insulin sensitivity, beta-cell function and non-esterified fatty acids (NEFA) suppressibility during early pubertal years, compared to controls
From the 9 girls having a first-degree relative diagnosed with PCOS and the 10 girls unrelated to PCOS recruited at baseline, we were able to reassess 7 girls from the PCOS relative group and 8 girls from the control group
Two PCOSr and one control girls withdrew between baseline and follow-up, and one control girl was lost to follow-up
Summary
We and others have observed that young girls predisposed to polycystic ovary syndrome (PCOS) display defective insulin sensitivity, beta-cell function and non-esterified fatty acids (NEFA) suppressibility during early pubertal years, compared to controls. Polycystic ovary syndrome (PCOS) is a common disorder, affecting 6–12% of women of reproductive age [1, 2]. It is defined as clinical and/or biochemical hyperandrogenism with ovarian dysfunction such as oligo-anovulation and/or polycystic ovaries, excluding any other androgen excess disorder [3]. Twenty to 40% of daughters and sisters of women with PCOS will develop the syndrome [6]. Daughters or sisters of women diagnosed with PCOS develop abnormalities in glucose metabolism
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