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Role of KATP Channel Loss in Type 2 Diabetes

Washington University School of Medicine · with National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) · NCT06830096

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Opens the official ClinicalTrials.gov record, with the study team’s contacts. Bored Studies doesn’t enroll anyone.

Key facts

Compensation
Not posted. Ask the study team before screening.
Who can join
Ages 18–65 · All sexes
Healthy volunteers
Accepted
Study type
Interventional · Not applicable
Target enrollment
40
US sites recruiting
1
Study start
March 7, 2025
Record last updated
August 10, 2026

Status re-checked against ClinicalTrials.gov within the last 12 hours.

What the study is about

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.

Being studied: 10 mg glipizide ingestion

Conditions: Obesity and Type 2 Diabetes

Eligibility criteria

Copied from the official record. The study team makes the final decision at screening.

Show full criteria

Inclusion Criteria

  • Lean-normoglycemic group (n=10): BMI ≥18.5 and \<25.0 kg/m², fasting plasma glucose concentration \<95 mg/dl, 2-hr oral glucose tolerance test plasma glucose concentration ≤140-mg/dl, and hemoglobin A1C (HbA1C) ≤5.6%.
  • Obesity-normoglycemic group (n=10): BMI ≥30 and \<50 kg/m², fasting plasma glucose concentration \<95 mg/dl, 2-hr oral glucose tolerance test plasma glucose concentration ≤140 mg/dl, and hemoglobin A1C (HbA1C) ≤5.6%.
  • Obesity-impaired fasting glucose group (n=10): BMI ≥30 and \<50 kg/m², fasting plasma glucose concentration 100-125 mg/dl, and 2-hr oral glucose tolerance test plasma glucose concentration \<200 mg/dl.
  • Obesity-type 2 diabetes group (n=10): BMI ≥30 and \<50 kg/m²; HbA1C 6.5-9.5%, fasting plasma glucose ≥126 mg/dl, 2-hr oral glucose tolerance test plasma glucose concentration ≥200 mg/dl and/or medical history of T2DM and currently using anti-diabetic medications.

Exclusion Criteria

  • Diabetes therapy with insulin at >0.5 units/kg/day.
  • Any change in diabetes medication in previous 3 months.
  • Unstable weight (>2% change during the last 2 months before entering the study).
  • Evidence of significant organ system dysfunction or disease other than obesity and T2D.
  • Regular use of tobacco products.
  • Excessive consumption of alcohol (≥3 drinks/day for men and ≥2 drinks/day for women).
  • Use of medications that are known to affect the study outcome measures (e.g., steroids, non-statin lipid-lowering medications) or increase the risk of study procedures (e.g., anticoagulants) and that cannot be temporarily discontinued for this study.
  • Anemia (Hemoglobin \<10.0 g/dL).
  • Pregnant or breastfeeding.
  • Unable or unwilling to follow the study protocol or for any reason the research team believes the volunteer is not an appropriate candidate for this study, including non-compliance with screening appointments or previous medical visits.

Recruiting US locations

  • Washington University in St. Louis

    St Louis, MO 63110

    Site contact: Kyle Timmons · 314-362-8699 · timmons@wustl.edu

Study contacts (from the official record)

  • Kyle Timmons · 314-273-1879 · nutritionresearch@wustl.edu
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Role of KATP Channel Loss in Type 2 Diabetes (NCT06830096) | Bored Studies