Generating new candidate genes for neonatal diabetes: functional and genetic studies of insulin secretion in type 2 diabetes.
Although the molecular lesions underlying a substantial proportion of all cases of permanent and neonatal diabetes have now been defined, in as many as 30% of cases the defect is unknown. Three complementary approaches may help to define further disease-causing changes: (1) the molecular dissection of the insulin secretory process itself using cellular, physiological and imaging techniques; (2) measurements of the level of expression of beta-cell genes in islets from rodents or humans with type 2 diabetes (T2D) by oligonucleotide micro-array or proteomic analysis, and (3) population-wide whole-genome association studies of T2D. Here, I survey recent published data in this context.
Rutter
Guy A
GA
Department of Cell Biology, Division of Medicine, Imperial College London, London , UK.
D003924:Diabetes Mellitus, Type 2 / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology*; D005786:Gene Expression Regulation; D015894:Genome, Human; D006801:Humans; D007231:Infant, Newborn; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis; D020641:Polymorphism, Single Nucleotide; D011494:Protein Kinases / Q000235:genetics*
D007328:Insulin; D011494:Protein Kinases