摘要: The initial report by Grant et al. [1] that variants in the TCF7L2 gene are strongly associated with risk of developing type 2 diabetes has now been robustly reproduced many other populations. In fact, this contribute more powerfully to than any identified date (see also [2]). Since population-attributable is substantial, we need understand whether causally related diabetes, and if so, what pathogenetic mechanisms are. phenotype individuals carrying susceptibility seems be slightly at odds typical individual risk, BMI reduced relative non-risk rather increased. Virtually all reports have shown impaired insulin secretion following a glucose tolerance test, although degree sensitivity not stringently defined. Using minimal model analysis an IVGTT non-diabetic at-risk individuals, Damcott [3] found both sensitivity. Additional studies characterising detail sensitive techniques will enhance our understanding functions TCF7L2.