| Polycystic ovary syndrome (PCOS) is the most common, but perhaps least understood endocrine disorder of women. It affects 5% to 10% of women of reproductive age. It is characterized by anovulation menstrual irregularity (oligomenorrhea, or amenorrhea), signs of hyperandrogenia, enlarged ovaries with multiple subcapsular cysts 8 to 10mm in size under transvaginal ultrasound scan. Recently there are many clinic and experiment phenomenon, which can't be explained by the abnormality of single gonad-axis: 1. Most of patients with PCOS have abnormality in glycometabolism, mainly as insulin resistance (IR) and hyperinsulinemia (HI). Women with PCOS have an approximately seven-fold increased risk of developing type 2 diabetes mellitus (DM), compared to that of unaffected women; 2.In PCOS patients from different ethnic groups, prevalence of insulin resistance is fairly uniform, compared to the clinic behave of PCOS; 3. In puberty patients with PCOS, IR and HI are earlier than anovulation and hyperandrogenia; 4. In animal modals, LH and HCG lead to polycystic ovary, but not feature biochemical abnormalwithout insulin; 5. Insulin sensitizing agents have shown to also decrease ovarian androgen secretion in PCOS patients and finally to improve their rate of ovulation.Insulin resistance was a common feature in patients with PCOS, and may play a direct role in the development of PCOS, exacerbating and underlying metabolic abnormality.Insulin resistance is a common pathologic state in which target cells fail to respond to ordinary levels of circulating insulin, followed by compensatory HI. The IR in patients with PCOS will exacerbating the HA and anovulation, increasing the risk of developing type 2 DM, hypertension, arteriosclerosis, vascular disease, and carcinoma of endometrium, et al.Recent studies show that the insulin receptor may play a master role in the IR in PCOS. The insulin receptor is a heterotetrameric glycoprotein containing two α - and two β -subunits linked by disulfide bonds. The α -subunit contains the ligand binding domain; the membrane-spanning β -subunit has an intracytoplasmic portion that possesses intrinsic tyrosine kinase activity. Binding in the a -subunit of insulin activates the receptor's kinase and leads to rapid autophosphorylation of specific tyrosine residues on the β -subunit. Insulin binding initiates signal transduction by activating of β -subunit. So, the activation of β -subunit of insulin receptor is a key step in the pathways ultimately resulting in stimulation of insulin-mediated metabolism functions. Its abnormality may induce the IR in PCOS.The abnormality of β -subunit of insulin receptor including: The abnormality in the amount and in the autophosphorylate function. Previous study demonstrated a reduction in INSR binding in RBC in patients with PCOS, but it was about whole receptor, not designate to β -subunit. Previous studies showed that polymorphisms in the INSR gene that induce mild changes in insulin receptor function may contribute to the development of PCOS,especially in the tyro sine domain of INSR, which is critical to the function of the gene. There are nine absolutely conservative amino acid sequences in domain, which determined the tyrosine kinase activity. INSR gene exon 17 encodes three of them, -Tyr965-, -Tyr972-, and 1003-1030 ATP combinding region. The polymorphisms in these region will influence the autophosphorylate function of β -subunit . A recent study found an association between a single nucleotide polymorphism at exon 17 and PCOS patients. In country, study of this gene has been preceded in cardiovascular and endocrine fields, but it's still blank about this gene study in patients with PCOS.In this study, the expression of β -subunit of insulin receptor binding in RBC membrane of patients with PCOS will be detected by Western Blot, and the polymorphophism of INSR gene exon 17 of patients with PCOS will be detected by PCR-SSCP and sequence. The aim of the study is to investigate the mechanisms by which IR occur in the patien...
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