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NOBEL PRIZE 2026

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NIHNATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASESR01

KATP deficiency in hyperinsulinism and diabetes

Active
Institution
Washington University, MO
Principal investigator
Colin G Nichols
Funding
$455K
Duration
2023–2028
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Abstract

Project Summary The long-term goals of this joint project are to understand the mechanisms, role and significance of electrical control of insulin secretion in hyperinsulinism and diabetes. Previous efforts demonstrated the central role of the KATP channel in electrical activity of the pancreatic beta-cell and revealed how defective channel activity can have profound effects on insulin secretion, and cause hyperinsulinism and neonatal diabetes. This understanding now underlies the use of KATP channel activators and inhibitors, respectively, as first line therapies. However, a paradoxical, essentially unexplained, crossover to glucose-insufficiency, or outright diabetes, is seen in both animals and humans with hyperinsulinism. In Type 2 diabetes, a parallel crossover from initial hypersecretion to secretory failure, may reflect a similar progression. Proposed studies will utilize novel inducible KATP channel knockdown models and models of type 2 diabetes to comprehensively probe the mechanistic basis of this reversal, and thereby improve understanding and management of HI and other forms of long-term -cell secretory failure.

Research team

  • Colin G NicholsPI
  • Maria Sara RemediPI

LOADING MOONBASE SCORE

R01NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASESBasic Mechanisms of Diabetes and Metabolism Study Section[BMDM]channeldiabetessecretioninsulinsecretoryinsulin secretioncrossovertype diabetes

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