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Regulatory factor linked to late-onset diabetes?

Author

Listed:
  • Sanjoy Dutta

    (Joslin Diabetes Center)

  • Susan Bonner-Weir

    (Joslin Diabetes Center)

  • Marc Montminy

    (Joslin Diabetes Center)

  • Christopher Wright

    (Vanderbilt University School of Medicine)

Abstract

Maintenance of glucose balance in mammals depends on the production of insulin by the β-cells of the pancreas, in response to raised concentrations of blood glucose. In humans suffering from non-insulindependent diabetes (NIDDM), β-cell failure follows chronic resistance to insulin-stimulated glucose uptake and causes the development of hyperglycaemia1. NIDDM shows a polygenic inheritance pattern in most cases2: defined genetic defects that have little effect on their own, in combination induce diabetes by epistatic interactions3. Here we show that mice heterozygous for the gene pdx-1, which encodes a transcription factor for the insulin gene and regulates pancreatic development, have impaired glucose tolerance. This pancreatic nuclear regulatory factor is required for glucose homeostasis even when the pancreas is morphologically normal.

Suggested Citation

  • Sanjoy Dutta & Susan Bonner-Weir & Marc Montminy & Christopher Wright, 1998. "Regulatory factor linked to late-onset diabetes?," Nature, Nature, vol. 392(6676), pages 560-560, April.
    • Handle: RePEc:nat:nature:v:392:y:1998:i:6676:d:10.1038_33311
    DOI: 10.1038/33311
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