Polycystic Ovary Syndrome (PCOS)

Clinical Trials

Below is a list of Polycystic Ovary Syndrome (PCOS) clinical trials from the clinical trials database at Mayo Clinic.

This list includes only trials about which Mayo researchers choose to publish information. Mayo Clinic may be conducting other trials which are not in this database. Mayo's clinical trials include experimental treatments, often unavailable elsewhere, which frequently lead to improved patient care for people worldwide. Patients should ask their doctor at Mayo about clinical trials appropriate for their situation.

Assessment of Inflammation, Metabolism and Mental Status in Normal Reproductive-Age Women Before and After Male Hormone Therapy
Polycystic Ovary Syndrome (PCOS) is characterized by hyperandrogenism, chronic anovulation and polycystic ovarian morphology. Insulin resistance is a common finding in the disorder, and low grade chronic inflammation is currently considered to be a contributor to insulin resistance. Women with PCOS exhibit increased mononuclear cell (MNC) sensitivity characterized by upregulation of the inflammation pathway during physiological hyperglycemia that is independent of obesity, and highly correlated with circulating androgens. The cause of this increased sensitivity is unknown. The proposed research is a double-blind randomized placebo-controlled study of 16 lean reproductive age women without PCOS. Eight subjects receiving oral DHEA for 5 days will be compared to 8 controls receiving placebo. The primary hypothesis is that oral androgen administration to increase circulating androgens to levels present in women with PCOS, will upregulate the inflammation pathway in MNC during hyperglycemia. The primary specific aim is to examine the inflammation pathway in MNC during hyperglycemia in response to the high dose oral DHEA treatment. The approach involves evaluation of the inflammatory response of MNC during an oral glucose challenge before and after DHEA administration by measuring ROS generation, expression of protein markers of the inflammation pathway, activated nuclear factor kB (NFkB) and cytokine release from cultured MNC. It is our expectation that we will demonstrate a pronounced inflammatory response following DHEA administration. These results will be significant because they will determine whether excess circulating androgen as observed in PCOS, is a promoter of inflammation and thus, is responsible for the preactivation of MNC that can increase their sensitivity to hyperglycemia. This in turn will serve as a guide for designing future studies that examine androgen-induced MNC preactivation in PCOS at the molecular level.
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