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Metabolic profile in sons of women with polycystic ovary syndrome (PCOS)

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2008-01
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Recabarren, Sergio E.
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Metabolic profile in sons of women with polycystic ovary syndrome (PCOS)
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Author
  • Recabarren, Sergio E.;
  • Smith Garcés, Rosita;
  • Ríos, Rafael;
  • Maliqueo Yevilao, Manuel;
  • Echiburú López, Bárbara;
  • Codner Dujovne, Ethel;
  • Cassorla Goluboff, Fernando;
  • Rojas, Pedro;
  • Sir Petermann, Teresa;
Abstract
Context: PCOS is an endocrine–metabolic disorder with 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: 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 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 OGTT 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 than Cs (p=0.038). During childhood, weight, BMI, waist circumference, total cholesterol and LDL-cholesterol were higher in PCOSS (p<0.05), but after adjusting for BMI, these differences were nonsignificant. During adulthood, PCOSS exhibited higher weight, BMI and waist circumference (p<0.05). Fasting insulin, HOMA-IR, total cholesterol, LDL-cholesterol and 2 h insulin were also higher and ISI composite lower in PCOSs than in Cs (p<0.05). After adjusting for BMI, 2 h insulin and ISI composite remained different. Conclusions: The 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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This work was presented in part at the 46th meeting of Paediatric Endocrinology of the European Society for Paediatric Endocrinology (ESPE), Helsinki 2007, and was supported by Fondo Nacional de Desarrollo Científico y Tecnológico Grant 1050915 and by the Alexander von Humboldt foundation.
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URI: https://repositorio.uchile.cl/handle/2250/128188
ISSN: 0021-972X
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Journal of Clinical Endocrinology & Metabolism, Vol. 93, No. 5 1820-1826, 2008
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