Hyperinsulinemia and elevated IGF-I levels appear to play a pathogenetic role in polycystic ovarian disease.
Supports hyperinsulinemia and IGF-I in PCOD pathogenesis; leaves open causality and therapeutic implications.
Concentrations of growth factors were examined in 28 patients with clinical and endocrinologic signs of polycystic ovarian disease (PCOD). Elevated levels of total insulin-like growth factor I (IGF-I) and decreased levels of the human growth hormone (HGH) were found. Studies of carbohydrate metabolism and of insulin receptors on erythrocytes indicated insulin resistance in all PCOD patients. Elevated insulin and IGF-I levels seem to play a pathogenetic role in PCOD by influencing the development and steroid production of ovarian follicles. Interactions between insulin and IGF-I could be shown at different levels. A positive correlation between elevated insulin and IGF-I concentrations was demonstrated in patients with different classes of gestational diabetes. Hyperinsulinemia seems to be the trigger mechanism and therefore the key to the pathogenetic loop of polycystic ovarian disease.
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Urdl et al. (1991) studied this question.
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