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RECRUITING
NCT06830096
NA

Role of KATP Channel Loss in Type 2 Diabetes

Sponsor: Washington University School of Medicine

View on ClinicalTrials.gov

Summary

Insulin is a hormone that is made by β-cells in the pancreas and when released into the bloodstream helps control blood sugar levels. Insulin release is regulated by electrical activity in the β-cell which is generated by the ATP-sensitive potassium (KATP) channel. While reduced KATP activity is associated with increased insulin secretion, animals lacking KATP exhibit reduced secretion. This crossover from hypersecretion to undersecretion with KATP loss mirrors insulin secretion during type 2 diabetes. Intriguingly, evidence from cell and animal models suggest that chronically stimulated β-cells can lose KATP revealing a possible role for KATP loss in the failure of insulin secretion and poor control of blood sugar observed in type 2 diabetes. This study will therefore examine insulin responses following ingestion of a single dose of a sulfonylurea called glipizide that inhibits KATP channels in people with and without type 2 diabetes. The goal is to determine whether KATP channel activity is reduced during type 2 diabetes progression.

Official title: Hyperglycemia Induced Hyperexcitability: A Novel Role for KATP in the Progression of Type 2 Diabetes

Key Details

Gender

All

Age Range

18 Years - 65 Years

Study Type

INTERVENTIONAL

Enrollment

40

Start Date

2025-03-07

Completion Date

2026-07-01

Last Updated

2025-07-04

Healthy Volunteers

Yes

Interventions

DRUG

10 mg glipizide ingestion

A single dose of 10 mg glipizide will be ingested

Locations (1)

Washington University in St. Louis

St Louis, Missouri, United States