# KATP deficiency in hyperinsulinism and diabetes

> **NIH NIH R01** · WASHINGTON UNIVERSITY · 2024 · $485,754

## 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.

## Key facts

- **NIH application ID:** 10880683
- **Project number:** 5R01DK133838-02
- **Recipient organization:** WASHINGTON UNIVERSITY
- **Principal Investigator:** Colin G Nichols
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $485,754
- **Award type:** 5
- **Project period:** 2023-07-03 → 2028-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10880683

## Citation

> US National Institutes of Health, RePORTER application 10880683, KATP deficiency in hyperinsulinism and diabetes (5R01DK133838-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10880683. Licensed CC0.

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