N1-methylnicotinamide as a possible modulator of cardiovascular risk markers in polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a multifactorial disease, which is resulted from the three common features, hyperandrogenism (HA), ovulatory dysfunction (OD), and polycystic ovarian morphology (PCOM). The environmental inducers (like diet, lifestyle, chemicals, drugs, and ageing) and cardiometabolic risk factors (such as insulin resistance, metabolic syndrome, and obesity) are involved in pathogenesis of PCOS. The growing body of evidence has been shown that there exist endothelial cell dysfunction (ECD) in women with PCOS independent of age, weight and metabolic abnormalities. It has been shown that a broad spectrum of cardiovascular risk markers are involved in ECD- induced cardiovascular disease. It is well described that there are no worldwide treatments for PCOS and all of pharmacological treatments are off -label without any approval. MNAM is one of potential therapeutic factor, which produced by nicotinamide N-methyltransferase (NNMT) via consumption of S-adenosyl methionine (SAM) and nicotinamide. Only one study has shown higher expression of its producer enzyme, NNMT, in the cumulus cells of women with PCOS. Therefore, we reviewed beneficial effects of MNAM on modulation of cardiometabolic risk factors, which are associated to PCOS and try to describe possible mode of action of MNAM in the regulation of these markers.

Copyright © 2019 Elsevier Inc. All rights reserved.