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Additive Effects of Obesity and TCF7L2 Variants on Risk for Type 2 Diabetes Among Cardiac Patients

¹ Department of Medicine, Université de Montréal and Centre Hospitalier de l'Université de Montréal, Montréal, Canada
² Department of Human Genetics, McGill University, Montréal, Canada
³ Montreal Heart Institute and Department of Medicine, Université de Montréal, Montréal, Canada
⁴ Department of Psychiatry and School of Nursing, McGill University, Montréal, Canada
⁵ Research Center, Montreal Heart Institute, Montréal, Canada
⁶ Department of Psychiatry, Université de Montréal, Montréal, Canada
⁷ Research Center, Centre Hospitalier de l'Université de Montréal, Montréal, Canada
⁸ Weight Control and Diabetes Research Center, Brown Medical School and The Miriam Hospital, Providence, Rhode Island

Address correspondence and reprint requests to Jeanne M. McCaffery, PhD, Weight Control and Diabetes Research Center, 196 Richmond St., Providence, RI 02903. E-mail: jeanne_mccaffery@brown.edu

The first 20% of the full text of this article appears below.

	INTRODUCTION

 
A microsatellite marker, DG10S478, in the transcription factor 7-like 2 (TCF7L2) gene was previously associated with type 2 diabetes in three Caucasian populations (1). This association followed earlier reports by the same group (2) and a separate team (3), which showed suggestive linkage to chromosomal 10q. Grant et al. (1) demonstrated that allele X (a composite of all but the shortest allele) of DG10S478 conferred an increased risk for type 2 diabetes of 45 and 141% among heterozygotes and homozygotes, respectively. Since this report, numerous groups have replicated the association in various populations and extended it to include two intronic single nucleotide polymorphisms (rs12255372 and rs7903146) (4–20). In this study, we investigated the combined effect of obesity and genotype at DG10S478 and rs12255372 in predicting type 2 diabetes risk in a sample of French Canadian cardiac patients.

	RESEARCH DESIGN AND METHODS—

 
Patients of French Canadian descent with established coronary artery disease recruited in two earlier studies, Polymorphisme (n = 484) and the Epidemiological Study of Acute Coronary Syndromes and the Pathophysiology of Emotions (ESCAPE; n = 596) (21), were included. All participants were identified between November 1998 and April 2002 at the Montreal Heart Institute and Hôpital Sacré-Coeur and gave written informed consent. Protocols were approved by the ethics committees at . . . [Full Text of this Article]

Genotyping
Statistical analysis

	RESULTS—

 
Genetic association tests

	CONCLUSIONS—

 

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