In addition, ovariectomized ARKO hosts with wild-type ovary transplants displayed normal estrous cycles and corpora lutea, despite DHT treatment, implying extraovarian and not intraovarian AR actions are key loci of androgen action in generating the PCOS phenotype.
Our findings support the hypothesis that the PCOS phenotype may result from either elevated androgen levels or an enhanced sensitivity to androgens caused by a more active androgen receptor.
There is a negative association between AMH, AMHR-II expression and BMI, and a positive association between AR expression and BMI in the GC of PCOS and non-PCOS women.
Long SHBG(TAAAA)n alleles (>8 repeats) were at greater frequency in PCOS than normal women (P = 0.001), whereas short AR(CAG)n alleles (<or=20 repeats) tended to be more frequent in PCOS women than controls.
The rs6152G/AAR gene polymorphism has been reported to be associated with male pattern baldness (MPB), which is a common characteristic of males in PCOS families.
At the other extreme, androgen excess leads to disordered follicle development and anovulatory infertility known as polycystic ovary syndrome (PCOS), with studies suggesting that theca cell AR may mediate many of these negative effects.
Polycystic ovary syndrome (PCOS) patients suffer from hyperandrogenemia and infertility and have elevated endometrial androgen receptor (AR) expression.
Moreover, our <i>in vivo</i> study showed that while endometrial ERβ expression was no different between non-PCOS and PCOS patients regardless of whether or not hyperplasia was present, ERα and AR protein expression was gradually increased in women with PCOS following the onset of endometrial hyperplasia.
In conclusion, shorter alleles of the (CAG)n in exon 1 of the AR gene enhanced the susceptibility to PCOS, either by upregulating AR activity or by causing hyperandrogenism.
In stroma, protein expression of estrogen receptor alpha, Bcl-2, and Bax was higher in PCOSE than in NE; epithelial cells had a greater expression of androgen receptor in the nucleus and a lower expression in the cytoplasm of PCOSE.
These results suggest that testosterone treatment of myotubes increases the aromatase and androgen receptor gene expression without affecting insulin sensitivity and if testosterone is implicated in muscular insulin resistance in PCOS, this is by and indirect mechanism.
we examined the influence of the androgen receptor gene (AR) CAG microsatellite (AR-CAG) repeat polymorphism and X-chromosome inactivation (XCI) pattern on ovarian reserve markers (follicle stimulating hormone (FSH) and antral follicle count on menstrual cycle day 3-5) and disease etiology in patients with polycystic ovarian syndrome (PCOS) or premature ovarian failure (POF).
Preferential expression of longer CAG repeat alleles was also observed in PCOS and correlated with increased serum T. We conclude that the AR (CAG)n gene locus and/or its differential methylation patterns influence the disease process leading to PCOS.
The mRNA and expression levels of FKBP52 and AR in the PCOS model rats were significantly increased, when compared with levels in the other rats (P<0.05).