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Laboratory of Animal Physiology and Endocrinology (S.E.R., P.R.), Faculty of Veterinary Medicine, University of Concepción, Chillán 3801061, Chile; and Laboratory of Endocrinology and Metabolism West Division (M.M., B.E., T.S.-P.) and Institute of Maternal and Child Research (R.S., R.R., E.C., F.C.), School of Medicine, University of Chile, Santiago 8360160, Chile
Address all correspondence and requests for reprints to: Prof. T. Sir-Petermann, Laboratory of Endocrinology, Department of Medicine West Division, School of Medicine, Las Palmeras 299, Interior Quinta Normal, Casilla 33052, Correo 33, Santiago, Chile. E-mail: tsir{at}med.uchile.cl.
Context: Polycystic ovary syndrome (PCOS) is a common endocrine-metabolic disorder with strong familial aggregation. It has been demonstrated that parents and brothers of PCOS women exhibit insulin resistance and related metabolic defects. However, metabolic phenotypes in sons of PCOS women have not been described.
Objective: Our objective was to assess the metabolic profiles in sons of women with PCOS during different stages of life: early infancy, childhood, and adulthood.
Design: Eighty sons of women with PCOS (PCOSS) and 56 sons of control women without hyperandrogenism (CS), matched for age, were studied. In early infancy, glucose and insulin were determined in the basal sample. In children and adults, a 2-h oral glucose tolerance test was performed with measurements of glucose and insulin. Adiponectin, leptin, C-reactive protein, SHBG, and serum lipids were determined in the basal sample during the three periods.
Results: During early infancy, PCOSS showed higher weight (P = 0.038) and weight SD score (P = 0.031) than CS. During childhood, weight (P = 0.003), body mass index (BMI) (P < 0.001), BMI SD score (P < 0.001), waist circumference (P = 0.001), total cholesterol (P = 0.007), and low-density lipoprotein cholesterol (P = 0.022) were higher in PCOSS compared with CS, but after adjusting for BMI, these differences were nonsignificant. During adulthood, PCOSS exhibited higher weight (P = 0.022), BMI (P = 0.046), and waist circumference (P = 0.028) than CS. Fasting insulin (P = 0.030), homeostasis model assessment for insulin resistance (P = 0.034), total cholesterol (P = 0.043), low-density lipoprotein cholesterol (P = 0.034), and 2-h insulin (P = 0.006) were also significantly higher and insulin sensitivity index composite significantly lower in PCOSS than in CS (P = 0.003). After adjusting for BMI, only 2-h insulin and insulin sensitivity index composite remained significantly different.
Conclusions: This study indicates that sons of PCOS women exhibit higher body weight from early infancy. In addition, insulin resistance became evident as the subjects got older, which may place them at risk for the development of type 2 diabetes and cardiovascular disease.
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