Association of shorter CAG repeats with PCOS is consistent with in vitro functional studies demonstrating higher activity of androgen receptors expressed from alleles with fewer CAG repeats, suggesting inherited alteration in androgen sensitivity may contribute to PCOS. In some women, such heightened sensitivity may also result from preferential expression of androgen receptors with shorter alleles. Thus, genetic and epigenetic changes may be involved in the pathogenesis of PCOS.

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This study suggests that selective COX-2 inhibition has a negative, local effect on human ovulation, resulting in delayed follicular rupture, without affecting peripheral hormonal cyclicity.

Not applicable.

Polymorphisms in PPARG implicated in previous studies of metabolic traits do not appear to influence component phenotypes of PCOS, but do affect androgens and insulin resistance in the general population.Objective-To investigate the relationship of the PPARG Pro12Ala and silent exon 6 (His447His) polymorphisms with the clinical features of polycystic ovary syndrome (PCOS).Design-PCOS and control subjects were genotyped for Pro12Ala and His447His; associations between genotype, diagnosis, and hormonal/metabolic parameters were assessed.Setting-Subjects were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham; control subjects were recruited from the surrounding community. Genotyping was performed at Cedars-Sinai Medical Center in Los Angeles.Reprint Request: Mark O. Goodarzi, M.D., Ph.D., Cedars-Sinai Medical Center, Division of Endocrinology, Diabetes and Metabolism, 8700 Beverly Blvd., Los Angeles, CA 90048, email: mark.goodarzi@cshs.org Presented in part at the 87 th Annual Meeting of the Endocrine Society, San Diego, June 4-7, 2005 Supported by:This study was supported in part by the Helping Hand of Los Angeles, and by grants R01-HD29364 and K24-HD01346 from the National Institutes of Health (to RA). Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Result(s)-Pro12Ala and His447His did not influence risk of PCOS or its component phenotypes in PCOS patients. In controls, Pro12Ala did not influence measures of insulin resistance or androgen production; however, carriers of the His447His T allele had significantly decreased free and total testosterone levels and HOMA-IR. Furthermore, haplotypes in controls bearing the His447His T allele were also associated with decreased testosterone. Conflict of Interest NIH Public AccessConclusion(s)-does not appear to be an important modifier gene in PCOS. In controls, however, the His447His T allele may be in linkage disequilibrium with a functional variant that influences insulin resistance and testosterone production. Keywordsperoxisome proliferator activated receptor gamma; polycystic ovary syndrome; single nucleotide polymorphism; testosterone; insulin resistance Polycystic ovary syndrome (PCOS) is a common disorder affecting 6-8% of reproductive aged women (1) and clinically manifests as menstrual irregularities, hyperandrogenism, polycystic ovaries, and often obesity. Several studies demonstrate substantial familial aggregation of PCOS with most showing significantly higher rates of PCOS among first-degree relatives when compared to the general population (2,3). Fifty to s...