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Association study of AMP-activated protein kinase subunit genes in polycystic ovary syndrome

¹ Department of Obstetrics and Gynecology, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA² Department of Obstetrics and Gynecology, the David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA³ Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Room B-131, Los Angeles, California 90048, USA⁴ Department of Medicine, the David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA⁵ Medical Genetics Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA

(Correspondence should be addressed to M O Goodarzi at Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Cedars-Sinai Medical Center; Email: mark.goodarzi{at}cshs.org)

Objective: To examine the genes for AMP-activated protein kinase (AMPK) subunits 2 (PRKAA2) and 3 (PRKAG3) as candidates for polycystic ovary syndrome (PCOS) and its component traits.

Design and methods: A total of 287 white PCOS women were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham and 187 white control subjects were recruited from the surrounding community. Seven PRKAA2 single nucleotide polymorphisms (SNPs) and four PRKAG3 SNPs were genotyped in PCOS cases and controls. Genotyping and association analysis were performed at Cedars-Sinai Medical Center.

Results: Nominal associations of PRKAA2 variants with insulin-related traits and the PRKAG3 Pro71Ala variant with PCOS were not statistically significant after multiple testing correction. Among PCOS patients, there were no associations between variants in AMPK subunit genes and androgenic or reproductive traits.

Conclusions: Variants in genes for AMPK2 and AMPK3 were not associated with PCOS or its component traits. Our evidence does not demonstrate that AMPK is a major genetic risk factor for PCOS.