Type 2 diabetes affects over 300 million people worldwide. A total of 42 ESR1 single nucleotide polymorphisms (SNPs) were genotyped in 380 African-American type 2 diabetic case subjects with end-stage renal disease (ESRD) and 276 African-American control subjects. In recent years, there has been a surge in the number of genetic studies of T2D in attempts to identify some of the underlying risk factors. We have summarized what we have learned so far about the genes that affect T2D risk and their functions. No significant association with type 2 diabetes was found at any of the polymorphic loci. Egeberg, J. Previous studies have identified over 80 areas in the genome that are associated with type 2 diabetes.
However, these studies focused on the role of common DNA differences that appear frequently in the population, and they generally stopped short of identifying exactly which DNA sequence changes, or which specific genes, were responsible for this risk. 3). Most importantly, however, the addition of a known TCF7L2 genotype in a validated model for predicting prevalent diabetes was not able to improve the performance of the risk score: area under ROC curve in both models equal to 0.776, ie the inclusion of TCF7L2 genotype is not better than the utilization of only clinical characteristics to predict diabetes risk in our population. Using various models of the mouse FTO gene, we discovered that reduced function of the gene led to lean mice, whereas overexpression resulted in overeating and obesity. Future strategies to develop a personalized prevention or treatment approach should take into account a patient’s genetic profile as well as environmental risk factors, the researchers suggested. This variant was one of 18, each found by other researchers to have a mild association with type-2 diabetes risk, that the Butte team incorporated into its analysis. We designate the promoter at 72.11 Mb as P1 and the promoter at 72.14 Mb as P2.
This finding means that future efforts to develop a personalized approach to treatment and prevention will need to be tailored toward an individual’s broader genetic profile, non-genetic risk factors and clinical features. In the study, a group of mice was treated with a lipid metabolism-altering drug and DNA microarray technology was used for mRNA expression profiling of various tissues. Approximately 38% of siblings and one-third of children of people with type 2 diabetes will develop diabetes or abnormal glucose metabolism at some point. One such variant – in the TM6SF2 gene – has been shown to alter the amount of fat stored in the liver, which in turn results in an increase in the risk of type 2 diabetes. These studies suggest that we reconsider our current thinking of the pathogenesis of type 2 diabetes; three different concepts seem to emerge (A). “This study highlights both the challenges we face, and the opportunities that exist, in resolving the complex processes underlying a disease such as type 2 diabetes. In this study, we have been able to highlight, with unprecedented precision, a number of genes directly involved in the development of type 2 diabetes.
Disclaimer: AAAS and EurekAlert! More alternative measures of adiposity need to be considered in future studies. With this in-depth analysis we have obtained a more complete picture of the number and characteristics of the genetic variants that influence type 2 diabetes risk,” added joint senior author Michael Boehnke, Richard G Cornell Distinguished University Professor of Biostatistics, Director, Center for Statistical Genetics, University of Michigan School of Public Health. “Our study tells us that genetic risk for type 2 diabetes reflects hundreds or even thousands of different genetic variants, most of them shared across populations. The search for T2D associated genes and variants continues, with many scientists questioning where the ‘missing heritability’ lies. Neurogenin3, NeuroD1, MafA and Pdx1 , .