Analysis of KLF transcription factor family gene variants in type 2 diabetes

doi:10.1186/1471-2350-8-53

BMC Medical Genetics
Volume 8

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Gutiérrez-Aguilar R
Benmezroua Y
Vaillant E
Balkau B
Marre M
Charpentier G
Sladek R
Froguel P
Neve B

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Benmezroua Y
Vaillant E
Balkau B
Marre M
Charpentier G
Sladek R
Froguel P
Neve B
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Research article

Analysis of KLF transcription factor family gene variants in type 2 diabetes

Ruth Gutiérrez-Aguilar¹^,2 , Yamina Benmezroua¹^,2 , Emmanuel Vaillant¹^,2 , Beverley Balkau³^,4 , Michel Marre⁵^,6 , Guillaume Charpentier⁷ , Rob Sladek⁸^,9 , Philippe Froguel¹^,2^,10^,11 and Bernadette Neve¹^,2^,10

¹UMR8090, CNRS, Institute of Biologie/Institute Pasteur de Lille, Lille, France

²Université de Lille 2, Lille, France

³INSERM, U780-IFR69, Villejuif, France

⁴U780-IFR69, Université Paris-Sud, Villejuif, France

⁵U695, INSERM, Xavier Bichat Faculty of Medicine, Université Paris 7, Paris, France

⁶Hospital Bichat – Claude Bernard, Paris, France

⁷Departement of Diabetes, Sud Francilien Hospital, Corbeil-Essonnes, France

⁸Human Genetics and Medicine, Faculty of Medicine, McGill University, Montreal, Canada

⁹Genome, Quebec Innovation Centre, Montreal, Canada

¹⁰Genomic Medicine, Hammersmith Hospital, Imperial College London, UK

¹¹Genomic Medicine, Hammersmith Hospital, Imperial College, Du Cane Road, London W12 0NN, UK

author email corresponding author email

BMC Medical Genetics 2007, 8:53doi:10.1186/1471-2350-8-53


Published:	9 August 2007

Abstract

Background

The Krüppel-like factor (KLF) family consists of transcription factors that can activate or repress different genes implicated in processes such as differentiation, development, and cell cycle progression. Moreover, several of these proteins have been implicated in glucose homeostasis, making them candidate genes for involvement in type 2 diabetes (T2D).

Methods

Variants of nine KLF genes were genotyped in T2D cases and controls and analysed in a two-stage study. The first case-control set included 365 T2D patients with a strong family history of T2D and 363 normoglycemic individuals and the second set, 750 T2D patients and 741 normoglycemic individuals, all of French origin. The SNPs of six KLF genes were genotyped by Taqman^®SNP Genotyping Assays. The other three KLF genes (KLF2, -15 and -16) were screened and the identified frequent variants of these genes were analysed in the case-control studies.

Results

Three of the 28 SNPs showed a trend to be associated with T2D in our first case-control set (P < 0.10). These SNPs, located in the KLF2, KLF4 and KLF5 gene were then analysed in our second replication set, but analysis of this set and the combined analysis of the three variants in all 2,219 individuals did not show an association with T2D in this French population. As the KLF2, -15 and -16 variants were representative for the genetic variability in these genes, we conclude they do not contribute to genetic susceptibility for T2D.

Conclusion

It is unlikely that variants in different members of the KLF gene family play a major role in T2D in the French population.