Early Metabolic Derangements in Daughters of Women with Polycystic Ovary Syndrome

Sir-Petermann, Teresa; Maliqueo, Manuel; Codner, Ethel; Echiburú, Bárbara; Crisosto, Nicolás; Pérez, Virginia; Pérez-Bravo, Francisco; Cassorla, Fernando

doi:10.1210/jc.2007-1036

Cited by 131 publications

(94 citation statements)

References 50 publications

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“…Androgen excess is considered to be the key feature of PCOS; however, only 80-85% of women with PCOS have clinical hyperandrogenism (Azziz et al 2009). Some metabolic abnormalities have been shown in children and adolescents with PCOS before the onset of hyperandrogenism (Sir-Petermann et al 2007). In our study, evidence of hyperandrogenism was not apparent in PNA rats during early puberty, possibly because androgen levels were low during pubertal development and difficult to be evaluated in adolescent (Rosenfield 2007).…”

Section: Discussionmentioning

confidence: 99%

Prenatal androgen excess programs metabolic derangements in pubertal female rats

Yan¹,

Dai²,

Wang³

et al. 2013

Journal of Endocrinology

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Owing to the heterogeneity in the clinical symptoms of polycystic ovary syndrome (PCOS), the early pathophysiological mechanisms of PCOS remain unclear. Clinical, experimental, and genetic evidence supports an interaction between genetic susceptibility and the influence of maternal environment in the pathogenesis of PCOS. To determine whether prenatal androgen exposure induced PCOS-related metabolic derangements during pubertal development, we administrated 5a-dihydrotestosterone (DHT) in pregnant rats and observed their female offspring from postnatal 4 to 8 weeks. The prenatally androgenized (PNA) rats exhibited more numerous total follicles, cystic follicles, and atretic follicles than the controls. Fasting glucose, insulin, leptin levels, and homeostatic model assessment for insulin resistance were elevated in the PNA rats at the age of 5-8 weeks. Following intraperitoneal glucose tolerance tests, glucose and insulin levels did not differ between two groups; however, the PNA rats showed significantly higher 30-and 60-min glucose levels than the controls after insulin stimulation during 5-8 weeks. In addition, prenatal DHT treatment significantly decreased insulin-stimulated phosphorylation of AKT in the skeletal muscles of 6-week-old PNA rats. The abundance of IR substrate 1 (IRS1) and IRS2 was decreased in the skeletal muscles and liver after stimulation with insulin in the PNA group, whereas phosphorylation of insulin-signaling proteins was unaltered in the adipose tissue. These findings validate the contribution of prenatal androgen excess to metabolic derangements in pubertal female rats, and the impaired insulin signaling through IRS and AKT may result in the peripheral insulin resistance during pubertal development. Key Words" Fetal origin of adult disease " polycystic ovary syndrome " prenatal androgen exposure " insulin resistance " insulin signaling

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Section: Discussionmentioning

confidence: 99%

Prenatal androgen excess programs metabolic derangements in pubertal female rats

Yan¹,

Dai²,

Wang³

et al. 2013

Journal of Endocrinology

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“…In this regard, it is well documented that metabolic deregulation in daughters of women with polycystic ovary syndrome, occurs early during pubertal development in concert with low serum SHBG levels (Sir-Petermann et al, 2007). It remains to be determined whether a low SHBG in these children is predictive for the risk of developing metabolic disorders.…”

Section: Discussionmentioning

confidence: 99%

Sex hormone-binding globulin gene expression in the liver: Drugs and the metabolic syndrome

Pugeat

Nader

Hogeveen

et al. 2010

Molecular and Cellular Endocrinology

105

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. decrease SHBG expression by inducing lipogenesis, which reduces hepatic HNF-4α levels, a transcription factor that play a critical role in controlling the SHBG promoter. Interestingly, diminishing hepatic lipogenesis and free fatty acid liver biosynthesis also appear to be associated with the positive effects of thyroid hormones and PPARγ antagonists on SHBG expression. This mechanism provides a biological explanation for why SHBG is a sensitive biomarker of insulin resistance and the metabolic syndrome, and why low plasma SHBG levels are a risk factor for developing hyperglycemia and type 2 diabetes, especially in women. These important advances in our knowledge of the regulation of SHBG expression in the liver open new approaches for identifying and preventing metabolic disorder associated diseases early in life.

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“…Otra observación interesante que hemos podido establecer es que las alteraciones metabólicas preceden al hiperandrogenismo en las hijas de madres con SOP y que los rasgos bioquímicos del SOP debutan en etapa Tanner IV del desarrollo puberal con aumento de la testosterona y una hiperrespuesta de LH al test de análogo de GnRH 6 . Desde el punto de vista metabólico, las hijas de madres con SOP muestran bajas concentraciones de adiponectina (proteína sensibilizante a la insulina que se origina en el adipocito); y un aumento de las concentraciones de insulina y triglicéridos 5 , mientras que los hijos presentan sobrepeso desde la infancia y desarrollan RI a medida que se hacen más adultos 32 . Estos datos, en conjunto, sugieren que los hijos e hijas de madres con SOP constituyen un grupo de alto riesgo para desarrollar alteraciones metabólicas y reproductivas a lo largo de la vida.…”

Section: ¿Cómo Infl Uye El Embarazo Sobre El Sop?unclassified

“…Se ha propuesto que este trastorno acompañaría a la mujer durante toda la vida, pudiendo manifestarse desde etapas muy tempranas del desarrollo sexual hasta la senectud [3][4][5][6] . El SOP se caracteriza por presentar una morfología ovárica típica con múltiples folículos en crecimiento, aumento del estroma ovárico e hipersecreción de andrógenos, lo que sugiere que las alteraciones de la esteroidogénesis y de la foliculogénesis serían eventos centrales de este síndrome.…”

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Síndrome de ovario poliquístico y embarazo

et al. 2012

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Polycystic ovary syndrome (PCOS) is a common endocrine metabolic dysfunction closely associated with insulin resistance and obesity, which predisposes to pregnancy complications and prenatal programming of the offspring. The aim of this review is to report our experience in PCOS patients, caracterizada por oligo-ovulación e hiperandrogenismo, lo que compromete la función reproductiva de la mujer. Su etiología es incierta y se encuentra en estrecha asociación a la resistencia insulínica (RI), la que juega un papel preponderante en su fi siopatología y en las consecuencias metabólicas a largo plazo, entre las que destacan el desarrollo precoz de síndrome metabólico, diabetes tipo 2 y enfermedad cardiovascular 2 .Las manifestaciones clínicas del SOP son heterogéneas y varían de acuerdo a la edad de la paciente. Se ha propuesto que este trastorno acompañaría a la mujer durante toda la vida, pudiendo manifestarse desde etapas muy tempranas del desarrollo sexual hasta la senectud [3][4][5][6] . El SOP se caracteriza por presentar una morfología ovárica típica con múltiples folículos en crecimiento, aumento del estroma ovárico e hipersecreción de andrógenos, lo que sugiere que las alteraciones de la esteroidogénesis y de la foliculogénesis serían eventos centrales de este

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Early Metabolic Derangements in Daughters of Women with Polycystic Ovary Syndrome

Abstract: Some of the metabolic features of PCOS are present in daughters of PCOS women before the onset of hyperandrogenism. Adiponectin appears to be one of the early markers of metabolic derangement in these girls.

Cited by 131 publications

References 50 publications

Prenatal androgen excess programs metabolic derangements in pubertal female rats

Prenatal androgen excess programs metabolic derangements in pubertal female rats

Sex hormone-binding globulin gene expression in the liver: Drugs and the metabolic syndrome

Síndrome de ovario poliquístico y embarazo

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