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[多囊卵巢综合征患者脂肪组织中胰岛素受体底物-2的酪氨酸磷酸化及蛋白表达]

[Tyrosine phosphorylation and protein expression of insulin receptor substrate-2 in the adipose tissue from patients with polycystic ovary syndrome].

作者信息

Qiu Hong-yu, Chu Yong-li, Li Min, Sun Yong-yu, Li Hong-fa

机构信息

Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022.

出版信息

Zhonghua Fu Chan Ke Za Zhi. 2005 Feb;40(2):116-9.

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.

摘要

目的

通过测定多囊卵巢综合征(PCOS)患者脂肪组织中胰岛素受体底物-2(IRS-2)的酪氨酸磷酸化及蛋白表达,探讨PCOS胰岛素抵抗的分子机制。

方法

收集PCOS伴胰岛素抵抗患者(n = 19)、PCOS不伴胰岛素抵抗患者(n = 17)及对照组(n = 20)的血清和皮下脂肪组织样本。采用蛋白质印迹法评估脂肪组织中IRS-2的表达。免疫组织化学法检测所有患者脂肪组织中IRS-2的分布。通过免疫沉淀和增强化学发光免疫印迹技术测定IRS-2的酪氨酸磷酸化。

结果

(1)PCOS伴胰岛素抵抗组IRS-2蛋白表达为1.15±0.26,与PCOS不伴胰岛素抵抗组1.13±0.26及对照组1.00±0.25相比,差异无统计学意义(P>0.05);(2)PCOS伴胰岛素抵抗组IRS-2的酪氨酸磷酸化水平为0.77±0.16,显著低于PCOS不伴胰岛素抵抗组0.91±0.25及对照组1.00±0.12(P<0.05)。PCOS不伴胰岛素抵抗组与对照组之间差异无统计学意义(P>0.05)。

结论

PCOS患者IRS-2酪氨酸磷酸化水平降低,导致胰岛素信号通路受损,可能是导致胰岛素抵抗的机制之一。

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