Revista Brasileira de Ginecologia e Obstetrícia. 2019;41(3):137-141
Polycystic Ovarian Syndrome (PCOS) is the leading endocrine disorder in women of childbearing age with a prevalence of more than 15% among this group. These women are predisposed to obesity, have a predominance of the abdominal obesity phenotype associated with the hyperandrogenic state, insulin resistance (IR) and compensatory hyperinsulinemia. It is estimated that 80% of women with PCOS have IR, and this scenario worsens in the presence of obesity.
A few authors suggest that there are abnormalities in the energy expenditure of women with PCOS, resulting from a reduction in the resting metabolic rate, especially in those with IR. In PCOS, has been considered a lower postprandial response of gastrointestinal hormones involved in neural control of food intake. Food intake is controlled by complex interrelationships between homeostatic mechanisms that regulate caloric intake through a neuroendocrine system involving central and peripheral signals as well as mechanisms related to eating behavior. The central mechanisms are regulated by learning, memory and the reward system that acts in the mesolimbic circuit present in the central nervous system. Gastrointestinal peripheral signs encompass several hormones that act on hunger (ghrelin) and satiation/satiety (cholecystokinin, YY peptide, oxintomodulin, glucagon like peptide – GLP-1, glucagon and amylin), and play an important role in regulating appetite and caloric intake.
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Polycystic Ovarian Syndrome (PCOS) is the leading endocrine disorder in women of childbearing age with a prevalence of more than 15% among this group. These women are predisposed to obesity, have a predominance of the abdominal obesity phenotype associated with the hyperandrogenic state, insulin resistance (IR) and compensatory hyperinsulinemia. It is estimated that 80% of women with PCOS have IR, and this scenario worsens in the presence of obesity.
A few authors suggest that there are abnormalities in the energy expenditure of women with PCOS, resulting from a reduction in the resting metabolic rate, especially in those with IR. In PCOS, has been considered a lower postprandial response of gastrointestinal hormones involved in neural control of food intake. Food intake is controlled by complex interrelationships between homeostatic mechanisms that regulate caloric intake through a neuroendocrine system involving central and peripheral signals as well as mechanisms related to eating behavior. The central mechanisms are regulated by learning, memory and the reward system that acts in the mesolimbic circuit present in the central nervous system. Gastrointestinal peripheral signs encompass several hormones that act on hunger (ghrelin) and satiation/satiety (cholecystokinin, YY peptide, oxintomodulin, glucagon like peptide - GLP-1, glucagon and amylin), and play an important role in regulating appetite and caloric intake.
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