Hong-yu Qiu1, Yong-li Chu, Min Li, Yong-yu Sun, Hong-fa Li. 1. Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022.
Abstract
OBJECTIVE: To explore molecular mechanisms of insulin resistance of polycystic ovary syndrome (PCOS) by determining the tyrosine phosphorylation and protein expression of insulin receptor substrate-2 (IRS-2) in adipose tissue from patients with PCOS. METHODS: Serum and subcutaneous adipose tissue samples from patients with PCOS with insulin resistance (n = 19), PCOS without insulin resistance (n = 17) and controls (n = 20) were collected. The expression of IRS-2 in adipose tissue was assessed by Western blot. Immunohistochemistry was used to detect the distribution of IRS-2 in adipose tissues of all patients. The tyrosine phosphorylation of IRS-2 was measured by immunoprecipitation and enhanced chemiluminescent immunoblotting technique. RESULTS: (1) There was no significant difference of the protein expression of IRS-2 in PCOS with insulin resistance 1.15 +/- 0.26 compared to those in PCOS without insulin resistance 1.13 +/- 0.26 and control group 1.00 +/- 0.25 (P > 0.05); (2) The tyrosine phosphorylation of IRS-2 was significantly decreased in PCOS with insulin resistance 0.77 +/- 0.16 compared to that of PCOS without insulin resistance 0.91 +/- 0.25 and control groups 1.00 +/- 0.12 (P < 0.05). There was no significant difference between PCOS without insulin resistance and control groups (P > 0.05). CONCLUSIONS: The decrease of tyrosine phosphorylation of IRS-2 in PCOS patients, which induces impairment of the insulin signal pathway, may be one of the mechanisms leading to insulin resistance.
OBJECTIVE: To explore molecular mechanisms of insulin resistance of polycystic ovary syndrome (PCOS) by determining the tyrosine phosphorylation and protein expression of insulin receptor substrate-2 (IRS-2) in adipose tissue from patients with PCOS. METHODS: Serum and subcutaneous adipose tissue samples from patients with PCOS with insulin resistance (n = 19), PCOS without insulin resistance (n = 17) and controls (n = 20) were collected. The expression of IRS-2 in adipose tissue was assessed by Western blot. Immunohistochemistry was used to detect the distribution of IRS-2 in adipose tissues of all patients. The tyrosine phosphorylation of IRS-2 was measured by immunoprecipitation and enhanced chemiluminescent immunoblotting technique. RESULTS: (1) There was no significant difference of the protein expression of IRS-2 in PCOS with insulin resistance 1.15 +/- 0.26 compared to those in PCOS without insulin resistance 1.13 +/- 0.26 and control group 1.00 +/- 0.25 (P > 0.05); (2) The tyrosine phosphorylation of IRS-2 was significantly decreased in PCOS with insulin resistance 0.77 +/- 0.16 compared to that of PCOS without insulin resistance 0.91 +/- 0.25 and control groups 1.00 +/- 0.12 (P < 0.05). There was no significant difference between PCOS without insulin resistance and control groups (P > 0.05). CONCLUSIONS: The decrease of tyrosine phosphorylation of IRS-2 in PCOSpatients, which induces impairment of the insulin signal pathway, may be one of the mechanisms leading to insulin resistance.
Authors: Emmanuella Doh; Armand Mbanya; Jean Dupont Kemfang-Ngowa; Sama Dohbit; Mycilline Tchana-Sinou; Pascal Foumane; Olivier Trésor Donfack; Anderson S Doh; Jean Claude Mbanya; Eugene Sobngwi Journal: Int J Endocrinol Date: 2016-09-08 Impact factor: 3.257