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Effects of Insulin Sensitizers in Subjects With Impaired Glucose Tolerance

Phase 4
Completed
Conditions
Glucose Metabolism Disorders
Diabetes
Interventions
Radiation: CT scans
Procedure: Oral glucose tolerance test
Registration Number
NCT00108615
Lead Sponsor
US Department of Veterans Affairs
Brief Summary

Subjects with impaired glucose tolerance will be randomized to receive pioglitazone or metformin for 10 weeks. Measurements of insulin sensitivity, body composition, glucose tolerance, and muscle lipid accumulation will be performed. Adipose tissue and muscle biopsies are performed. The goal of the study is to determine whether the lipotoxiciy of impaired glucose tolerance is ameliorated by pioglitazone.

Detailed Description

The progression to type 2 diabetes represents an evolution, which results from a vicious cycle where both glucotoxicity and lipotoxicity act to reduce insulin secretion and insulin action. Lipotoxicity is a new concept, which refers to overaccumulation of lipids in non-adipose tissue reflecting increased free fatty acid delivery. Increased fat content of skeletal muscle and islet cell is associated with insulin resistance and impaired pancreatic -cell function respectively in animal models. Whether lipotoxicity is the link between obesity and diabetes, in humans, and whether reducing intracellular fat content will improve insulin secretion and sensitivity in humans is not known. In this study, we will focus on obese subjects with impaired glucose tolerance (IGT) who have not yet developed glucose toxicity. We will examine insulin secretion, insulin action, hepatic glucose production, and muscle lipid metabolism in response to two insulin sensitizers with two different modes of action. We propose that thiazolidinediones will improve cell function by reversing lipotoxicity as reflective in reduced muscle lipid accumulation.

Hypothesis 1. In subjects with impaired glucose tolerance, who are insulin resistant and also have an insulin secretory defect, thiazolidinediones, but not biguanides, improve cell function.

Hypothesis 2. In subjects with impaired glucose tolerance, thiazolidinediones, but not biguanides, decrease the accumulation of fat in non-adipose tissues including muscle, pancreas, liver and myocardium.

Specific Aim 1. Fifty subjects with impaired glucose tolerance will be recruited and randomized to pioglitazone or metformin treatment

Specific Aim 2. cell function will be evaluated by measuring changes in acute insulin response to glucose and non-glucose secretagogues in subjects with IGT and it will be compared in response to treatment with pioglitazone versus metformin.

Specific Aim 3. The muscle fat content will be evaluated as the surrogate measure for lipotoxicity and overaccumulation of fat in non-adipose tissue. From the muscle biopsy specimens, we will measure the amount of intramyocellular triglyceride before and after treatment with pioglitazone versus metformin.

Specific Aim 4. Adipose tissue cytokine expression is associated with changes in muscle lipid accumulation.

Recruitment & Eligibility

Status
COMPLETED
Sex
All
Target Recruitment
48
Inclusion Criteria
  • Impaired glucose tolerance
  • Body mass index (BMI) of 28-38
Exclusion Criteria
  • Heart disease
  • Renal disease
  • Liver disease

Study & Design

Study Type
INTERVENTIONAL
Study Design
PARALLEL
Arm && Interventions
GroupInterventionDescription
2CT scansmetformin
1CT scanspioglitazone
1Oral glucose tolerance testpioglitazone
2Oral glucose tolerance testmetformin
1Pioglitazonepioglitazone
1Metforminpioglitazone
2Metforminmetformin
2Pioglitazonemetformin
Primary Outcome Measures
NameTimeMethod
Effects of pioglitazone and metformin on ectopic lipid accumulation4 yr
Secondary Outcome Measures
NameTimeMethod
Effects of pioglitazone and metformin on beta cell responsiveness4 yr

Trial Locations

Locations (1)

Central Arkansas Veterans HCS

🇺🇸

Little Rock, Arkansas, United States

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