Transcription Factor 7-Like 2 (TCF7L2) Polymorphism and Hyperglycemia in an Adult Italian Population-Based Cohort

OBJECTIVE — To assess whether TCF7L2 polymorphism has a role in the deterioration of glycemic control. RESEARCH DESIGN ANDMETHODS — Metabolic variables were evaluated at base-line and after 6-year follow-up in 1,480 Caucasian subjects from a population-based cohort. RESULTS — At baseline, T-allele carriers showed significantly lower BMI and homeostasis model assessment for-cell function (HOMA-B) values and higher fasting glycemia and diabetes prevalence. At follow-up, fasting glucose and HOMA-B index were increased and reduced, respectively, in carriers of the T-allele. Incident impaired fasting glucose (IFG) and incident diabetes were 5.7, 10.7, 16.9 % and 1.6, 1.7, 3.0 % in the CC, CT, and TT genotypes, respectively. In a multiple logistic regression model, the association between incident IFG and the T-allele was significant (odds ratio [OR] 2.08 [95 % CI 1.35–3.20] and 3.56 [2.11–5.98] in CT and TT genotypes, respectively). CONCLUSIONS — The T-allele of TCF7L2 rs7903146 polymorphism was independently associated with increasing fasting glucose values toward hyperglycemia in the follow-up. Diabetes Care 33:1233–1235, 2010 Among the variety of TCF7L2 poly-morphisms correlating with type 2diabetes, the single nucleotide polymorphism (SNP) rs7903146 has shown the strongest association with the disease (1). We investigated the associa-tion of the SNP rs7903146 with 1) type 2 diabetes or 2) impaired fasting glucose (IFG) or 3) the metabolic syndrome (MS) in an adult Italian population-based co-hort both cross-sectionally and after 6-year follow-up