Potential associations of AMH and follistatin levels with PCOS-related parameters were compared between the subgroups as well as longitudinally before and in the first trimester of pregnancy.
CRY decreased inhibin B and follistatin mRNA and protein expression but upregulated activin A mRNA and protein expression in the ovarian tissue of rats with PCOS (<i>P</i> < 0.05).
Our results reveal that manifestation of PCOS-like phenotype following prenatal exposure to excess androgen is associated with irregularity in expression of the FST gene during the estrus cycle.
We conclude that FST is not a susceptibility locus for PCOS; however, the SNP rs3797297 from FST gene was associated with androgenic markers for PCOS and may be of importance in the hyperandrogenaemia of the disease.
We conclude that FST is not a susceptibility locus for PCOS; however, the SNP rs3797297 from FST gene was associated with androgenic markers for PCOS and may be of importance in the hyperandrogenaemia of the disease.
Genes for adrenal biosynthetic enzymes, insulin receptors, leptin and leptin receptors, follistatin, activin and inhibins are attractive candidates for polycystic ovarian disease.
In both types of follicles, follistatin and alpha-, beta a-, and beta b-subunit cytoplasmic staining were observed in granulosa cells, as were their corresponding messages, with the exception of the undetectable follistatin mRNA signal in the PCOS follicles.