Abstract
Polycystic ovary syndrome (PCOS) is a common endocrine, metabolic and heterogeneous disorder in women of reproductive age, the exact etiology of which remains unknown. To unravel the molecular mechanisms underlying the hyperandrogenic phenotype of PCOS, prenatally androgenized (PNA) mice were used to mimic this phenotype in women with PCOS. Using microarray analysis, 1188 differentially expressed genes, including 671 upregulated and 517 downregulated genes, were identified in ovaries from PNA mice. Five differentially expressed genes (Aldh1a7, Bhmt, Mtr, Nrcam, Ptprg) were validated, and decreased MTR expression was shown in ovaries of PNA mice. In addition, results from qRT-PCR showed decreased MTR expression in granulosa cells (GCs) from women with the hyperandrogenic phenotype of PCOS. Serum levels of S-adenosyl methionine (SAM), the downstream product of MTR, were also decreased in PNA mice and women with the hyperandrogenic phenotype of PCOS. Our study provides evidence that the hyperandrogenic phenotype of PCOS is linked to abnormal folate one-carbon metabolism.
Highlights
Polycystic ovary syndrome (PCOS) is one of the most common endocrine and metabolic disorders, affecting about 5%-15% of women of reproductive age [1]
Previous studies have been conducted on many candidate genes for PCOS, principally related to reproductive hormones, insulin resistance, and chronic inflammation, including follicle-stimulating hormone receptor (FSHR) [3], insulin receptor (INSR) [4], and tumor necrosis factor (TNF) [5]
Prenatal androgenization of the ICR mouse with DHT can replicate most of the common clinical features of PCOS, especially the hyperandrogenic phenotype of PCOS
Summary
Polycystic ovary syndrome (PCOS) is one of the most common endocrine and metabolic disorders, affecting about 5%-15% of women of reproductive age [1]. Symptoms of PCOS include amenorrhea or oligomenorrhea, hyperandrogenism, and polycystic ovarian morphology. PCOS shows evidence of a genetic predisposition among patients, but the exact etiology remains unknown [2]. Previous studies have been conducted on many candidate genes for PCOS, principally related to reproductive hormones, insulin resistance, and chronic inflammation, including follicle-stimulating hormone receptor (FSHR) [3], insulin receptor (INSR) [4], and tumor necrosis factor (TNF) [5].
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