Although the cause of PCOS is unknown, abnormalities related to insulin actions are common.
Insulin is a hormone secreted by the pancreas in response to a rising blood sugar level, such as occurs after a meal. In PCOS, due to a decreased sensitivity to insulin action (“insulin resistance”), a higher output of insulin (“hyperinsulinemia”) is required to control normal tissue and blood sugar levels. Eventually, even increased insulin output fails to maintain normal blood sugar levels, which results in impaired glucose tolerance. If this is not corrected, Type 2 diabetes develops. Insulin can also augment the production of androgens in the ovary.
Other theories on the cause of PCOS have pointed to a genetic or environmental basis. Abnormal enzyme functions involved in hormone production in the ovary and/or the adrenal gland have also been proposed. Irrespective of the root cause, obesity perpetuates the physiologic and hormonal features of this condition.
In PCOS, the inter-relationship between obesity, altered insulin sensitivity, and unbalanced hormones secreted by the ovary is complex, and its nature is still not completely understood. As well as increased obesity around the abdomen, there are also increased numbers of fat cells surrounding the internal organs (“visceral fat”). Important metabolic communications between these cells are influenced by hormones including insulin. Defective insulin actions can lead to the unfavorable metabolic and hormone profiles seen in women with PCOS. Visceral fat can also convert androstenedione, a weak androgen, to testosterone, a strong androgen. This leads to a “catch-22” situation: the abnormal metabolic and hormonal disturbances exaggerate obesity, which in turn, aggravates the abnormal metabolic and hormonal functions.