, Volume 50, Issue 1, pp 214-216
Date: 09 Nov 2006

No major contribution of TCF7L2 sequence variants to maturity onset of diabetes of the young (MODY) or neonatal diabetes mellitus in French white subjects

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To the Editor: Maturity onset diabetes of the young (MODY), and permanent and transient neonatal diabetes mellitus (NDM), are the most prevalent monogenic forms of diabetes. Dominant activating mutations in the KCNJ11 gene [1, 2], which encodes the inwardly rectifying Kir6.2 subunit of the ATP-sensitive potassium (KATP) channel expressed at the surface of the pancreatic beta cell, or in the ABCC8 gene [3], which encodes the SUR1 regulatory subunit of the channel, account for more than 30% of cases of NDM in the French population. So far, genes involved in the aetiology of MODY include glucokinase (GCK) [4] (also occasionally responsible for permanent NDM) and at least five beta cell-expressed transcription factors [5]. Common DNA polymorphisms in most of these genes have also been repeatedly associated with beta cell dysfunction and with type 2 diabetes in a polygenic context [6]. Recently, intronic single nucleotide polymorphisms (SNPs) of the transcription factor 7-like 2 (TCF7L2) ge