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Diabetes mellitus and genetically programmed defects in β-cell function

Author

Listed:
  • Graeme I. Bell

    (Medicine and Human Genetics, The University of Chicago)

  • Kenneth S. Polonsky

    (Washington University School of Medicine)

Abstract

The pathways that control insulin secretion and regulate pancreatic β-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 β-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 β-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.

Suggested Citation

  • Graeme I. Bell & Kenneth S. Polonsky, 2001. "Diabetes mellitus and genetically programmed defects in β-cell function," Nature, Nature, vol. 414(6865), pages 788-791, December.
  • Handle: RePEc:nat:nature:v:414:y:2001:i:6865:d:10.1038_414788a
    DOI: 10.1038/414788a
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    Cited by:

    1. Ling Qiu & Risu Na & Rong Xu & Siyang Wang & Hongguang Sheng & Wanling Wu & Yi Qu, 2014. "Quantitative Assessment of the Effect of KCNJ11 Gene Polymorphism on the Risk of Type 2 Diabetes," PLOS ONE, Public Library of Science, vol. 9(4), pages 1-9, April.
    2. Radwan H Ahmed & Hasniza Zaman Huri & Zaid Al-Hamodi & Sameer D Salem & Sekaran Muniandy, 2015. "Serum Levels of Soluble CD26/Dipeptidyl Peptidase-IV in Type 2 Diabetes Mellitus and Its Association with Metabolic Syndrome and Therapy with Antidiabetic Agents in Malaysian Subjects," PLOS ONE, Public Library of Science, vol. 10(10), pages 1-12, October.

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