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Hum. Reprod. Advance Access published online on February 13, 2009
Human Reproduction, doi:10.1093/humrep/dep019
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© The Author 2009. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Phosphatidylinositol 3-kinase p85{alpha} regulatory subunit gene Met326Ile polymorphism in women with polycystic ovary syndrome

Jin Ju Kim1,2, Young Min Choi1,3,7, Min A. Hong1, Seung Sik Hwang4, Sang Ho Yoon5, Soo Jin Chae6, Byung Chul Jee1,3, Seung Yup Ku1,3, Jung Gu Kim1 and Shin Yong Moon1,3

1 Department of Obstetrics and Gynecology, Seoul National University College of Medicine, Seoul, Republic of Korea 2 Healthcare System Gangnam Center, Seoul National University College of Medicine, Seoul, Republic of Korea 3 The Institute of Reproductive Medicine and Population, Medical Research Center, Seoul National University College of Medicine, Seoul, Republic of Korea 4 Department of Social and Preventive Medicine, College of Medicine, Inha University, Incheon, Republic of Korea 5 Department of Obstetrics and Gynecology, Dongguk University International Hospital, Goyang, Republic of Korea 6 Maria Fertility Hospital, Seoul, Republic of Korea

7 Correspondence address. Department of Obstetrics and Gynecology, The Institute of Reproductive Medicine and Population, Medical Research Center, Seoul National University College of Medicine, 28 Yungun-dong, Chongno-ku, Seoul 110-744, Republic of Korea. Fax: +82-2-762-3599; E-mail: ymchoi{at}snu.ac.kr

BACKGROUND: Insulin resistance is a core feature of polycystic ovary syndrome (PCOS). Phosphatidylinositol (PI) 3-kinase is an important enzyme in the early insulin signaling cascade and plays a key role in insulin-mediated glucose transport. In its regulatory subunit, p85{alpha}, there is a common amino acid substitution (the Met326Ile polymorphism), and this amino acid may be crucial for the function of the p85{alpha} regulatory subunit and PI3-kinase.

METHODS: Analysis of the Met326Ile polymorphism was carried out on DNA samples from 256 PCOS patients and 283 controls. Clinical and biochemical profiles of participants were also compared.

RESULTS: The genotype distribution of the Met326Ile polymorphism in the PCOS group was not different from that of the controls (Met326Met/Met326Ile/Ile326Ile rates were 73.4%/23.4%/3.2% and 70.3%/26.1%/3.6% for the PCOS and control groups, respectively, P = 0.72). The PCOS group was divided into two subgroups according to the presence of the variant 326Ile allele. Compared with those carrying at least one variant 326Ile allele, carriers with the Met326Met genotype had higher serum 17-hydroxyprogesterone (17-OHP) {1.1 [95% confidence interval (CI) 1.1–1.3] ng/ml in those with the Met326Met genotype versus 0.8 (95% CI 0.7–1.0) ng/ml in those with Ile326Ile and Met326Ile genotypes, P = 0.0073} and free testosterone levels [1.2 (95% CI 1.1–1.4) pg/ml for Met326Met genotype versus 0.9 (95% CI 0.6–1.3) pg/ml for Ile326Ile and Met326Ile genotypes, P = 0.038].

CONCLUSIONS: Our results suggest that the PI3-kinase gene Met326Ile polymorphism may not be a major determinant for the development of PCOS, but it may modulate the concentrations of serum 17-OHP or free testosterone in PCOS patients.

Key words: polycystic ovary syndrome/phosphatidylinositol 3-kinase/Met326Ile polymorphism/hyperinsulinemia

Submitted on August 20, 2008; resubmitted on January 7, 2009; accepted on January 16, 2009.


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