[Tyrosine phosphorylation and protein expression of insulin receptor substrate-1 in the patients with polycystic ovary syndrome].
OBJECTIVE
To investigate the tyrosine phosphorylation and protein expression of insulin receptor substrate-1 in adipose tissue from patients with polycystic ovary syndrome, and explore molecular mechanisms of insulin resistance of PCOS.


METHODS
Samples from patients with PCOS with insulin resistance (group A, n = 19), PCOS without insulin resistance (group B, n = 10) and controls group (n = 15) were collected. Serum luteinizing hormone (LH), follicle stimulating hormone (FSH) and testosterone (T) were measured by chemiluminescence assay. Fasting insulin (FIN) was measured by radioimmunoassay. Fasting plasma glucose (FPG) was measured by oxidase assay. Insulin resistance index was calculated using homeostasis model assessment (HOMA) to analyze the relationship between these markers and insulin resistance. The amount of insulin receptor substrate-1 in adipose tissue was assessed by western blot. The tyrosine phosphorylation of IRS-1 was measured by immunoprecipitation.


RESULTS
(1) The levels of serum LH (15.8 +/- 2.8) U/L, LH/FSH 2.8 +/- 0.6, T (4.3 +/- 0.9) nmol/L, FIN (25.2 +/- 3.8) mU/L and HOMA IR (1.56 +/- 0.25) in group A were significantly higher than those of group B (13.9 +/- 1.9) U/L, 2.3 +/- 0.4, (3.6 +/- 0.4) nmol/L, (13.4 +/- 3.8) mU/L, 0.87 +/- 0.28 and control group (7.3 +/- 2.1) U/L, 1.3 +/- 0.3, (0.9 +/- 0.2) nmol/L, (9.5 +/- 2.6) mU/L, 0.50 +/- 0.30 (all P < 0.05); (2) The protein expression and tyrosine phosphorylation of IRS-1 in group A (690 +/- 19 and 528 +/- 72 respectively) were significantly lower than those in group B (892 +/- 31, 801 +/- 64) and control group (988 +/- 29, 1139 +/- 124) (P < 0.05, and P < 0.01 respectively). (3) Insulin resistance index in group A and group B were negatively related with protein expression and tyrosine phosphorylation (r = -0.52, P < 0.05; r = -0.61, P < 0.01 and r = -0.60, P < 0.05; r = -0.63, P < 0.05).


CONCLUSIONS
The signal transduction malfunction because of protein expression and tyrosine phosphorylation changes of IRS-1 in adipose tissue from polycystic ovary syndrome patients may be one of the mechanisms leading to insulin resistance.
Chu
Yong-li
YL
Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Sun
Yong-yu
YY
Qiu
Hong-yu
HY
Li
Hong-fa
HF
D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D015153:Blotting, Western; D005215:Fasting; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006801:Humans; D007328:Insulin / Q000097:blood; D055504:Insulin Receptor Substrate Proteins; D007333:Insulin Resistance; D007986:Luteinizing Hormone / Q000097:blood; D010750:Phosphoproteins / Q000096:biosynthesis*; D010766:Phosphorylation; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D014443:Tyrosine / Q000378:metabolism*
D001786:Blood Glucose; C526292:IRS1 protein, human; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D010750:Phosphoproteins; D014443:Tyrosine; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone