Association of genetic variants of insulin degrading enzyme with metabolic features in women with polycystic ovary syndrome
Objective
To evaluate the influence of the four single nucleotide polymorphisms of the insulin-degrading enzyme (IDE) gene on metabolic features in women with polycystic ovary syndrome (PCOS) in a Chinese population.
Design
Prospective, case-control study.
Setting
University-based hospital.
Patient(s)
Three hundred fifteen patients with PCOS and 327 healthy controls.
Intervention(s)
Peripheral venous puncture, ultrasonography, oral glucose tolerance test (OGTT).
Main Outcome Measure(s)
Genotype analysis of four single nucleotide polymorphisms in the IDE gene, hormonal and metabolic phenotypes.
Result(s)
No significant differences in genotypes of these polymorphisms were found between PCOS patients and healthy controls. But the frequency of the C allele of rs2209972 was significantly higher in the PCOS group than that in the control group. The single nucleotide polymorphisms rs4646953, rs1887922, and rs1544210 had no impact on clinical and biochemical characteristics of women with PCOS. There were significant differences in body mass index (BMI) and insulin level in the rs2209972 genotype of women with PCOS. The women with PCOS with the CC genotype of rs2209972 had statistically significantly higher fasting insulin level and homeostasis model assessment for insulin resistance than the women with PCOS with the TT genotype.
Conclusion(s)
The single nucleotide polymorphism rs2209972 in the human IDE gene is associated with metabolic features of PCOS women in a Chinese population.
Key Words: Polycystic ovary syndrome, insulin resistance, single nucleotide polymorphism, insulin-degrading enzyme, gene
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Supported by the National Basic Research Program of China (973 Program-2006CB944004) and the National High-Technology Research and Development Program of China (863 Program-2006AA02Z4A4).
PII: S0015-0282(07)01359-3
doi:10.1016/j.fertnstert.2007.06.016
© 2008 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.

