Risk loci for type 2 diabetes - quo vadis?
Reduced insulin sensitivity plays a role in the early pathogenesis of type 2 diabetes, and defects in insulin secretion by pancreatic beta-cells are instrumental in hyperglycemic progression. There is strong evidence that genetic factors play an important role in both of these components. Several of the single nucleotide polymorphisms (SNPs) of genes associated with an increased risk of type 2 diabetes are hypothesized to influence beta-cell function. The aim of the present study was to describe the function of the latter genes, to analyze the implications of the SNP positions within or near these genes, and to evaluate the suggested primary role of pancreatic beta-cells in the etiology of type 2 diabetes.
Weijers
Rob N M
RN
Teaching Hospital OLVG, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands. robw01@xs4all.nl
D000818:Animals; D027682:Cation Transport Proteins / Q000378:metabolism; D050756:Cyclin-Dependent Kinase Inhibitor Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000235:genetics* / Q000378:metabolism*; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism; D006801:Humans; D050417:Insulin-Secreting Cells / Q000378:metabolism / Q000473:pathology; D020641:Polymorphism, Single Nucleotide / Q000235:genetics; D051820:TCF Transcription Factors / Q000235:genetics / Q000378:metabolism; D058118:Transcription Factor 7-Like 2 Protein
D027682:Cation Transport Proteins; D050756:Cyclin-Dependent Kinase Inhibitor Proteins; D018398:Homeodomain Proteins; D051820:TCF Transcription Factors; C544894:TCF7L2 protein, human; D058118:Transcription Factor 7-Like 2 Protein