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Hum. Reprod. Advance Access published online on January 5, 2006
Human Reproduction, doi:10.1093/humrep/dei452
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© The Author 2005. 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
Received June 2, 2005
Revised November 15, 2005
Accepted November 21, 2005

Article

Controversial role of inhibin {alpha}-subunit gene in the aetiology of premature ovarian failure

Victoria Sundblad 1 *, Violeta A. Chiauzzi 1, Luz Andreone 2, Stella Campo 2, Eduardo H. Charreau 3, and Liliana Dain 4

1 Instituto de Biología y Medicina Experimental (IBYME-CONICET) , Buenos Aires, Argentina
2 Centro de Investigaciones Endocrinológicas (CEDIE), Hospital de Niños R. Gutiérrez, Buenos Aires, Argentina
3 Instituto de Biología y Medicina Experimental (IBYME-CONICET) , Buenos Aires, Argentina; Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina
4 Instituto de Biología y Medicina Experimental (IBYME-CONICET) , Buenos Aires, Argentina; Centro Nacional de Genética Médica (ANLIS), Buenos Aires, Argentina, Buenos Aires, Argentina

* To whom correspondence should be addressed.
Victoria Sundblad, E-mail: sundblad{at}dna.uba.ar


  Abstract

BACKGROUND: Premature ovarian failure (POF) is characterized by hypergonadotropic amenorrhoea before the age of 40. Inhibin {alpha}-subunit (INH3) gene is proposed as a candidate gene due to its role in negative feedback control of FSH. METHODS: Polymorphism -16C>T of INH{alpha} gene was studied in 61 POF patients and 82 controls above 40 years old (C > 40). Substitution 769G>A was studied in 59 POF patients, 76 C > 40 and 73 controls below 40 years old (C < 40). RESULTS: No significant difference in risk of POF development for -16T allele was found when comparing idiopathic POF (I-POF) with C > 40 (Odds ratio = 1.46; 95% confidence interval = 0.63-3.19). Implication of -16C>T polymorphism in serum inhibin levels was analysed in 46 controls, and no significant differences (P > 0.05) were found between CC and CT + TT genotype groups when comparing either mid-follicular phase Pro-{alpha}C and inhibin B values or mid-luteal phase Pro{alpha}3C and inhibin A values. Heterozygosity for substitution 769G>A was found in 1 of 59 POF woman, 2 of 76 C > 40 and 6 of 73 C < 40. Presence of this substitution in a relevant number of control subjects is herein described for the first time. CONCLUSION: Our results indicate that -16C>T and 769G>A variants in INH3 gene may not be associated to POF disease.

Keywords: inhibin {alpha}-subunit gene/inhibin levels/premature ovarian failure.
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