Both genes and the environment contribute to PCOS. Obesity, exacerbated by poor dietary choices and physical inactivity, worsens PCOS in susceptible individuals. The role of other environmental modifiers such as infectious agents or toxins are speculative. Phenotype confusion has characterized genetic studies of PCOS. Although several loci have been proposed as PCOS genes including CYP11A, the insulin gene, the follistatin gene, and a region near the insulin receptor, the evidence supporting linkage is not overwhelming. The strongest case can be made for the region near the insulin receptor gene (but not involving this gene), as it has been identified in two separate studies, and perhaps most importantly has not yet been refuted by larger studies. However, the responsible gene at chromosome 19p13.3 remains to be identified. To date, no gene has been identified that causes or contributes substantially to the development of a PCOS phenotype.
Polycystic ovary syndrome (PCOS) is probably the most common endocrinopathy of reproductive age. PCOS represents a disorder that not only enhances the risk for type 2 diabetes (T2D) but is also associated with an increased number of cardiovascular risk factors known to facilitate atherogenesis. On the other hand, inflammation is thought to play an important role in the progression and development of complications of atherosclerosis. Evidence of low-grade chronic inflammation in PCOS is indicated by the presence of elevated C-reactive protein (CRP) levels, inflammatory cytokines (i.e., IL-6 and IL-18), and increased leucocyte count. CRP, a nonspecific marker of inflammation, has been proven to be one of the strongest predictors of the risk of cardiovascular events in patients with or without cardiovascular disease. The levels of the adhesion molecules (AM), sIVAM-1, sVCAM-1, and sE-selectin in serum reflect low-grade chronic inflammation of the endothelium and independently predict coronary heart disease (CHD) and T2D. In a recent study in a large number of PCOS women we demonstrated elevated levels of sIVAM-1 and sE-selectin and we further substantiated the existence of a low-grade chronic inflammatory process in PCOS. However, it remains to be assessed with long-term studies whether the early presence of markers of chronic inflammation in young women with this syndrome has clinical significance.
ing Agency (WADA), underline the need for a very active anti-Doping campaign 2 . This review presents a brief account of current data on GH physiology and our understanding of GH abuse in sports. Recent work has opened up a new and exciting area of endocrinology in parallel with the efforts being made to expunge doping from sports.
This study was performed to determine whether phenotypically healthy sisters of women with polycystic ovary syndrome (PCOS) have evidence of insulin resistance. We studied 54 women: 17 with PCOS, 17 sisters of these probands and 20 control women with similar age, body mass index (BMI) and waist-to-hip ratio (WHR). The PCOS sisters had neither clinical nor laboratory evidence of hyperandrogenism. However, estimated insulin resistance indices indicated decreased insulin sensitivity in PCOS sisters compared with the controls. No difference of insulin resistance indices was detected between the PCOS and their sisters. This finding provides additional evidence that there is a hereditary trait regarding insulin resistance in the PCOS families.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.