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Role of KATP Channel Loss in Type 2 Diabetes

NCT06830096 · Status: RECRUITING · Phase: NA · Type: INTERVENTIONAL · Enrollment: 40

Last updated 2025-07-04

No results posted yet for this study

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.

Conditions

  • Obesity and Type 2 Diabetes

Interventions

DRUG

10 mg glipizide ingestion

A single dose of 10 mg glipizide will be ingested

Sponsors & Collaborators

  • National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

    collaborator NIH

  • Washington University School of Medicine

    lead OTHER

Study Design

Allocation
NON_RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
NONE
Model
PARALLEL

Eligibility

Min Age
18 Years
Max Age
65 Years
Sex
ALL
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2025-03-07
Primary Completion
2026-03-31
Completion
2026-07-01

Countries

  • United States

Study Locations

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT06830096 on ClinicalTrials.gov