科研之友
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摘要
Recent genomewide association studies revealed that many genes with weak or moderate effects contribute to the risk of type 2 diabetes. The risk genes that are known so far explain 5%-10% of the genetic predisposition. Although the combination of genotype data shows that individuals with many risk alleles have a higher diabetes risk than individuals with fewer risk alleles, and genetic tests lead to a statistically significant improvement of prediction models based on simple anthropometric and clinical data only, this difference is currently not clinically relevant. The novel genetic data substantiate the hypothesis that a genetically programmed beta-cell dysfunction interacts with insulin resistance, caused by environmental and lifestyle factors, in the development of type 2 diabetes. Initial studies indicate that the genetic risk can be modified by lifestyle intervention and that gene variants can have an impact on the therapeutic efficacy of certain drugs. A better understanding of the genetics will result in a deeper insight into the molecular pathogenesis of type 2 diabetes and in the development of novel therapeutic approaches.
- 出版日期2010-5
