Obesity and PCOS

Polycystic ovary syndrome (PCOS) is characterized by anovulation, hyperandrogenism
and polycystic ovaries.  Approximately 50% of women with PCOS have insulin
resistance and obesity.  

Hyperandrogenism contributes to abdominal fat deposition and excess hair growth as
demonstrated by long-term high dose testosterone treatment in female-to-male
transsexuals.  Accumulation of abdominal/visceral fat is a common clinical finding in
patients with PCOS.

Abdominal fat predisposes to insulin resistance, dyslipidemia and hypertension.  This
is known as the metabolic syndrome which leads to increased long-term risk of
diabetes mellitus and cardiovascular disease.  Among women with PCOS, 40% have
impaired glucose tolerance and 10% develop Type 2 diabetes by their fourth decade.
There is evidence of disturbed appetite regulation in patients with PCOS, which,
together with the characteristic endocrine/metabolic abnormalities, may explain why
these women have to struggle to maintain normal bodyweight.

Many women with PCOS suffer from a craving for sweets, a reduced feeling of satiety
and a tendency toward binge-eating.  Women with PCOS are known to have reduced
meal-related secretion of the gastrointestinal 'satiety peptide', cholecystokinin.  
Furthermore, patients with PCOS display dysregulation of ghrelin, a hormone
secreted from the gastric mucosa, which stimulates hunger and food intake.
The reported prevalence of obesity in women with PCOS has varied greatly
depending on population and ethnicity, but it could be approximately 50%. The
prevalence of obesity among US women with PCOS has increased from 51% in 1987
to 74% in 2002, paralleling the corresponding increase of obesity in the US
population.

Weight gain often precedes the development of PCOS and, conversely, weight loss is
associated with resolution of symptoms.  Weight gain may induce a vicious circle of
endocrine/ metabolic abnormalities and aggravating clinical symptoms.

Increased bodyweight will result in insulin resistance and compensatory
hyperinsulinemia. Insulin acts directly in the ovary to stimulate the biosynthesis of
testosterone. Furthermore, insulin inhibits SHBG production in the liver, which will
result in increased levels of free testosterone. High levels of testosterone may, in
turn, induce abdominal fat accumulation and insulin resistance. In this way, the
vicious circle resulting from weight gain may continue and worsen the reproductive
and metabolic symptoms of PCOS.
Weight gain induces a vicious circle of endocrine/metabolic abnormalities and aggravating clinical symptoms. Increased bodyweight will result in insulin resistance and compensatory hyperinsulinemia. Insulin stimulates ovarian biosynthesis of testosterone and inhibits SHBG production in the liver, which will result in increased levels of free testosterone. High levels of testosterone may in turn induce abdominal fat accumulation and insulin resistance. SHBG = Sex hormone-binding globulin.
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