Diabetes mellitus and genetically programmed defects in β-cell function

被引:374
作者
Bell, GI
Polonsky, KS
机构
[1] Univ Chicago, Howard Hughes Med Inst, Chicago, IL 60637 USA
[2] Univ Chicago, Dept Biochem & Mol Biol, Chicago, IL 60637 USA
[3] Univ Chicago, Dept Med & Human Genet, Chicago, IL 60637 USA
[4] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA
[5] Washington Univ, Sch Med, Dept Cell Biol & Physiol, St Louis, MO 63110 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1038/414788a
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The pathways that control insulin secretion and regulate pancreatic beta -cell mass are crucial in the development of diabetes mellitus. Maturity-onset diabetes of the young comprises a number of single-gene disorders affecting pancreatic beta -cell function, and the consequences of mutations in these genes are so serious that diabetes develops in childhood or adolescence. A genetic basis for the more common form of type 2 diabetes, which affects 10-20% of adults in many developed countries, is less clear cut. It is also characterized by abnormal beta -cell function, but other tissues are involved as well. However, in both forms identification of causative and susceptibility genes are providing new insight into the control of insulin action and secretion, as well as suggesting new treatments for diabetes.
引用
收藏
页码:788 / 791
页数:4
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