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. 2007 Apr;22(4):1003-10.
doi: 10.1093/humrep/del466. Epub 2007 Jan 4.

Amelioration of insulin resistance in women with PCOS via reduced insulin receptor substrate-1 Ser312 phosphorylation following laparoscopic ovarian electrocautery

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Amelioration of insulin resistance in women with PCOS via reduced insulin receptor substrate-1 Ser312 phosphorylation following laparoscopic ovarian electrocautery

Kok-Min Seow et al. Hum Reprod. 2007 Apr.

Abstract

Background: Increased Ser(312) phosphorylation of insulin receptor substrate (IRS)-1 is one possible molecular mechanism of insulin resistance in polycystic ovary syndrome (PCOS). We investigated whether laparoscopic ovarian electrocautery (LOE) improved insulin sensitivity in women with PCOS and examined the underlying molecular mechanism of LOE.

Methods: Adipose tissue and blood samples from 12 women with PCOS before, and 3 months after, LOE were analysed.

Results: Before LOE, women with PCOS were found to have significantly higher 2 h glucose, fasting and 2 h insulin levels, homeostasis model insulin resistance index and lower fasting glucose-to-insulin ratio (G(0)/I(0)) than healthy, lean, age-matched controls. Serum levels of glucose and insulin were significantly decreased, and G(0)/I(0) ratio was significantly increased 3 months after LOE. Levels of activated extracellular signal-regulated kinase 1/2 in PCOS women were higher than in controls, but were significantly decreased after LOE. Levels of insulin receptor, glucose transporter-4 and phosphatidylinositol 3-kinase were lower in PCOS patients before LOE than in controls and increased after LOE. Levels of Ser(312)-phosphorylated IRS-1 in PCOS women before LOE were higher than in controls and decreased significantly after LOE, whereas IRS-1 tyrosine phosphorylation in PCOS women before LOE was lower than in controls and increased significantly after LOE.

Conclusion: Over the short observation period of this study, our results demonstrated that LOE effectively ameliorated insulin resistance in women with PCOS via decreased IRS-1 Ser(312) phosphorylation.

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