Endocrine Abstracts

Prenatal and postnatal environment can regulate gene expression through multiple epigenetic mechanisms, being DNA methylation among the most relevant. Metabolic and reproductive function may be modified by this mechanism. Sons born to women with PCOS show altered markers of metabolic and reproductive function during childhood and adulthood. However, these functions have not been studied during puberty. The aim of the present study was to assess the global methylation pattern a...

Context: Insulin resistance is an important component of polycystic ovary syndrome (PCOS). Local cytokine production in adipose tissue increases local insulin resistance. The effect of testosterone on local adipose tissue cytokine production has not been explored thoroughly.Aim: To evaluate cytokine expression in subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) from PCOS and control women and evaluate the response to testosterone on th...

Polycystic ovary syndrome (PCOS) is an important metabolic and reproductive disorder which confers substantially increased risk for type two diabetes and metabolic syndrome (MS). Our aim is to characterize the metabolic profile, insulin sensitivity (IS) and insulin secretion in control (Cw) and PCOS women (PCOSw) during different stages of reproductive life (S1: 18–35 years old, S2: 36–44 years old, S3: 45–55 years old). A total of 131 Cw and 129 PCOSw were incl...

DNA methylation is an epigenetic mechanism of gene regulation that can be modified during intrauterine and postnatal life. Pregnant women with polycystic ovary syndrome (PCOS) present elevated androgen and insulin levels, which can affect the DNA methylation pattern of their offspring. Then, we studied the global DNA methylation pattern (GDNAm) in daughters and sons born to PCOS women compared to controls. Daughters (99 born to PCOS and 87 born to control women) and sons (74 b...

Our previous study showed that polycystic ovary syndrome (PCOS)-like reproductive and metabolic phenotypes induced by maternal dihydrotestosterone (DHT)-exposure, can be passed on in mice from mothers (F0) to daughters (F1), granddaughters (F2), and even to great-granddaughters (F3). The female transmission is independent of diet-induced obesity and is mediated by transcriptional and mitochondrial perturbations of oocytes accompany. ...