Glucose Metabolism DisordersPhase 4NCT00108615
Effects of Insulin Sensitizers in Subjects With Impaired Glucose Tolerance
A Phase 4 study testing Metformin, Pioglitazone and CT scans in people with Glucose Metabolism Disorders and Diabetes, run by US Department of Veterans Affairs at 1 site in United States.
Trial 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. Read more about this study
- Who is it for?
- Ages 35 to 65 yearsHealthy volunteers can take part
- Conditions the study is for
- Glucose Metabolism Disorders, Diabetes
- What is being tested?
- Metformin, Pioglitazone and CT scans
- Type of treatment
- Pill or oral medicine, Surgery or procedure
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 48 participants
- Where
- 1 siteUnited States
- Study dates
- Jan 2004to Dec 2007
- Phase
- Phase 4
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 35 to 65 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- Impaired glucose tolerance
- Body mass index (BMI) of 28-38
Who cannot join
- Heart disease
- Renal disease
- Liver disease
Trial locations and contacts
1 site in 1 country.
United States1 site
Central Arkansas Veterans HCS
Little Rock, Arkansas, 72205
About this study
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.
Read the 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.
- Conditions
- Glucose Metabolism Disorders, Diabetes
- Being tested
- Metformin, Pioglitazone, CT scans, Oral glucose tolerance test
- Medical subject headings
- Glucose Metabolism Disorders, Diabetes Mellitus
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
MetforminDrug
PioglitazoneDrug
MetforminDrug
PioglitazoneDrug
CT scansRadiation
To measure changes in adipose tissue volumes
Oral glucose tolerance testProcedure or surgery
To detect a change in glucose tolerance
| Study group | Role | What they receive |
|---|---|---|
| 1 | Experimental | pioglitazone Receives: Drug: Metformin; Drug: Pioglitazone; Radiation: CT scans; Procedure: Oral glucose tolerance test |
| 2 | Active comparator | metformin Receives: Drug: Metformin; Drug: Pioglitazone; Radiation: CT scans; Procedure: Oral glucose tolerance test |
What is being measured
The primary outcome is the main question the study is designed to answer.
Effects of pioglitazone and metformin on ectopic lipid accumulation
Measured: 4 yr
Secondary outcomes (1)
Effects of pioglitazone and metformin on beta cell responsiveness
Measured: 4 yr
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted18 Apr 2005 (estimated)
- Study startJan 2004
- Primary completionApr 2007
- Study completionDec 2007
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (13)Papers the sponsor has linked to this study.
- Other trials for Glucose Metabolism DisordersStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 4
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Enrolment
- 48 participants (actual)
Sponsor and investigators
- Lead sponsor
- US Department of Veterans Affairs
- Sponsor type
- US federal agency
- Investigators
- Philip A Kern, MD, Principal investigator, Central Arkansas Veterans HCS
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00108615
- Sponsor's protocol ID
- CLIN-013-0S3
- Status last verified
- Apr 2008
- First submitted
- 15 Apr 2005
- Last updated
- 25 Apr 2008
- Results posted
- No
- Data monitoring committee
- Yes
Publications
Rasouli N, Raue U, Miles LM, Lu T, Di Gregorio GB, Elbein SC, Kern PA. Pioglitazone improves insulin sensitivity through reduction in muscle lipid and redistribution of lipid into adipose tissue. Am J Physiol Endocrinol Metab. 2005 May;288(5):E930-4. doi: 10.1152/ajpendo.00522.2004. Epub 2005 Jan 4.
PubMed 15632102Di Gregorio GB, Yao-Borengasser A, Rasouli N, Varma V, Lu T, Miles LM, Ranganathan G, Peterson CA, McGehee RE, Kern PA. Expression of CD68 and macrophage chemoattractant protein-1 genes in human adipose and muscle tissues: association with cytokine expression, insulin resistance, and reduction by pioglitazone. Diabetes. 2005 Aug;54(8):2305-13. doi: 10.2337/diabetes.54.8.2305.
PubMed 16046295Bodles AM, Varma V, Yao-Borengasser A, Phanavanh B, Peterson CA, McGehee RE Jr, Rasouli N, Wabitsch M, Kern PA. Pioglitazone induces apoptosis of macrophages in human adipose tissue. J Lipid Res. 2006 Sep;47(9):2080-8. doi: 10.1194/jlr.M600235-JLR200. Epub 2006 Jun 23.
PubMed 16799131Yue L, Rasouli N, Ranganathan G, Kern PA, Mazzone T. Divergent effects of peroxisome proliferator-activated receptor gamma agonists and tumor necrosis factor alpha on adipocyte ApoE expression. J Biol Chem. 2004 Nov 12;279(46):47626-32. doi: 10.1074/jbc.M408461200. Epub 2004 Aug 31.
PubMed 15339912Rasouli N, Yao-Borengasser A, Miles LM, Elbein SC, Kern PA. Increased plasma adiponectin in response to pioglitazone does not result from increased gene expression. Am J Physiol Endocrinol Metab. 2006 Jan;290(1):E42-E46. doi: 10.1152/ajpendo.00240.2005. Epub 2005 Aug 23.
PubMed 16118250Bodles AM, Banga A, Rasouli N, Ono F, Kern PA, Owens RJ. Pioglitazone increases secretion of high-molecular-weight adiponectin from adipocytes. Am J Physiol Endocrinol Metab. 2006 Nov;291(5):E1100-5. doi: 10.1152/ajpendo.00187.2006. Epub 2006 Jun 27.
PubMed 16803857Ranganathan G, Unal R, Pokrovskaya I, Yao-Borengasser A, Phanavanh B, Lecka-Czernik B, Rasouli N, Kern PA. The lipogenic enzymes DGAT1, FAS, and LPL in adipose tissue: effects of obesity, insulin resistance, and TZD treatment. J Lipid Res. 2006 Nov;47(11):2444-50. doi: 10.1194/jlr.M600248-JLR200. Epub 2006 Aug 7.
PubMed 16894240Rasouli N, Kern PA, Reece EA, Elbein SC. Effects of pioglitazone and metformin on beta-cell function in nondiabetic subjects at high risk for type 2 diabetes. Am J Physiol Endocrinol Metab. 2007 Jan;292(1):E359-65. doi: 10.1152/ajpendo.00221.2006. Epub 2006 Sep 12.
PubMed 16968813Yao-Borengasser A, Rasouli N, Varma V, Miles LM, Phanavanh B, Starks TN, Phan J, Spencer HJ 3rd, McGehee RE Jr, Reue K, Kern PA. Lipin expression is attenuated in adipose tissue of insulin-resistant human subjects and increases with peroxisome proliferator-activated receptor gamma activation. Diabetes. 2006 Oct;55(10):2811-8. doi: 10.2337/db05-1688.
PubMed 17003347Varma V, Yao-Borengasser A, Rasouli N, Bodles AM, Phanavanh B, Lee MJ, Starks T, Kern LM, Spencer HJ 3rd, McGehee RE Jr, Fried SK, Kern PA. Human visfatin expression: relationship to insulin sensitivity, intramyocellular lipids, and inflammation. J Clin Endocrinol Metab. 2007 Feb;92(2):666-72. doi: 10.1210/jc.2006-1303. Epub 2006 Nov 7.
PubMed 17090638Wolins NE, Quaynor BK, Skinner JR, Tzekov A, Croce MA, Gropler MC, Varma V, Yao-Borengasser A, Rasouli N, Kern PA, Finck BN, Bickel PE. OXPAT/PAT-1 is a PPAR-induced lipid droplet protein that promotes fatty acid utilization. Diabetes. 2006 Dec;55(12):3418-28. doi: 10.2337/db06-0399.
PubMed 17130488Yao-Borengasser A, Varma V, Bodles AM, Rasouli N, Phanavanh B, Lee MJ, Starks T, Kern LM, Spencer HJ 3rd, Rashidi AA, McGehee RE Jr, Fried SK, Kern PA. Retinol binding protein 4 expression in humans: relationship to insulin resistance, inflammation, and response to pioglitazone. J Clin Endocrinol Metab. 2007 Jul;92(7):2590-7. doi: 10.1210/jc.2006-0816. Epub 2007 Jun 26.
PubMed 17595259Varma V, Yao-Borengasser A, Bodles AM, Rasouli N, Phanavanh B, Nolen GT, Kern EM, Nagarajan R, Spencer HJ 3rd, Lee MJ, Fried SK, McGehee RE Jr, Peterson CA, Kern PA. Thrombospondin-1 is an adipokine associated with obesity, adipose inflammation, and insulin resistance. Diabetes. 2008 Feb;57(2):432-9. doi: 10.2337/db07-0840. Epub 2007 Dec 5.
PubMed 18057090
Study at a glance
From the registry record, last updated by the sponsor on 25 Apr 2008. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Effects of Insulin Sensitizers in Subjects With Impaired Glucose Tolerance
- ClinicalTrials.gov ID
- NCT00108615
- Acronym / sponsor ID
- CLIN-013-0S3
- Conditions
- Glucose Metabolism Disorders, Diabetes
- Phase
- Phase 4
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 48 participants (actual)
- Lead sponsor
- US Department of Veterans AffairsUS federal agency
- Study start
- Jan 2004
- Primary completion
- Apr 2007 (actual)
- Study completion
- Dec 2007 (actual)
- First posted
- 18 Apr 2005 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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.
Study design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| 1 | Experimental | Drug: Metformin, Drug: Pioglitazone, Radiation: CT scans, Procedure: Oral glucose tolerance testpioglitazone |
| 2 | Active comparator | Drug: Metformin, Drug: Pioglitazone, Radiation: CT scans, Procedure: Oral glucose tolerance testmetformin |
Who may qualify
- Ages
- 35 to 65 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (2 listed)
- Impaired glucose tolerance
- Body mass index (BMI) of 28-38
Key exclusion criteria (3 listed)
- Heart disease
- Renal disease
- Liver disease
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Metformin | Drug | 1 |
| Pioglitazone | Drug | 1 |
| Metformin | Drug | 2 |
| Pioglitazone | Drug | 2 |
| CT scansTo measure changes in adipose tissue volumes | Radiation | 1, 2 |
| Oral glucose tolerance testTo detect a change in glucose tolerance | Procedure or surgery | 1, 2 |
Primary outcome
Effects of pioglitazone and metformin on ectopic lipid accumulation
Time frame: 4 yr
1 secondary outcome
Effects of pioglitazone and metformin on beta cell responsiveness
Time frame: 4 yr
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 25 Apr 2008.
- Results publication: PubMed 15632102Rasouli N, Raue U, Miles LM, Lu T, Di Gregorio GB, Elbein SC, Kern PA. Pioglitazone improves insulin sensitivity through reduction in muscle lipid and redistribution of lipid into adipose tissue. Am J Physiol Endocrinol Metab. 2005 May;288(5):E930-4. doi: 10.1152/ajpendo.00522.2004. Epub 2005 Jan 4.
- Results publication: PubMed 16046295Di Gregorio GB, Yao-Borengasser A, Rasouli N, Varma V, Lu T, Miles LM, Ranganathan G, Peterson CA, McGehee RE, Kern PA. Expression of CD68 and macrophage chemoattractant protein-1 genes in human adipose and muscle tissues: association with cytokine expression, insulin resistance, and reduction by pioglitazone. Diabetes. 2005 Aug;54(8):2305-13. doi: 10.2337/diabetes.54.8.2305.
- Results publication: PubMed 16799131Bodles AM, Varma V, Yao-Borengasser A, Phanavanh B, Peterson CA, McGehee RE Jr, Rasouli N, Wabitsch M, Kern PA. Pioglitazone induces apoptosis of macrophages in human adipose tissue. J Lipid Res. 2006 Sep;47(9):2080-8. doi: 10.1194/jlr.M600235-JLR200. Epub 2006 Jun 23.
- Results publication: PubMed 15339912Yue L, Rasouli N, Ranganathan G, Kern PA, Mazzone T. Divergent effects of peroxisome proliferator-activated receptor gamma agonists and tumor necrosis factor alpha on adipocyte ApoE expression. J Biol Chem. 2004 Nov 12;279(46):47626-32. doi: 10.1074/jbc.M408461200. Epub 2004 Aug 31.
- Results publication: PubMed 16118250Rasouli N, Yao-Borengasser A, Miles LM, Elbein SC, Kern PA. Increased plasma adiponectin in response to pioglitazone does not result from increased gene expression. Am J Physiol Endocrinol Metab. 2006 Jan;290(1):E42-E46. doi: 10.1152/ajpendo.00240.2005. Epub 2005 Aug 23.
- Results publication: PubMed 16803857Bodles AM, Banga A, Rasouli N, Ono F, Kern PA, Owens RJ. Pioglitazone increases secretion of high-molecular-weight adiponectin from adipocytes. Am J Physiol Endocrinol Metab. 2006 Nov;291(5):E1100-5. doi: 10.1152/ajpendo.00187.2006. Epub 2006 Jun 27.
- Results publication: PubMed 16894240Ranganathan G, Unal R, Pokrovskaya I, Yao-Borengasser A, Phanavanh B, Lecka-Czernik B, Rasouli N, Kern PA. The lipogenic enzymes DGAT1, FAS, and LPL in adipose tissue: effects of obesity, insulin resistance, and TZD treatment. J Lipid Res. 2006 Nov;47(11):2444-50. doi: 10.1194/jlr.M600248-JLR200. Epub 2006 Aug 7.
- Results publication: PubMed 16968813Rasouli N, Kern PA, Reece EA, Elbein SC. Effects of pioglitazone and metformin on beta-cell function in nondiabetic subjects at high risk for type 2 diabetes. Am J Physiol Endocrinol Metab. 2007 Jan;292(1):E359-65. doi: 10.1152/ajpendo.00221.2006. Epub 2006 Sep 12.
- Results publication: PubMed 17003347Yao-Borengasser A, Rasouli N, Varma V, Miles LM, Phanavanh B, Starks TN, Phan J, Spencer HJ 3rd, McGehee RE Jr, Reue K, Kern PA. Lipin expression is attenuated in adipose tissue of insulin-resistant human subjects and increases with peroxisome proliferator-activated receptor gamma activation. Diabetes. 2006 Oct;55(10):2811-8. doi: 10.2337/db05-1688.
- Results publication: PubMed 17090638Varma V, Yao-Borengasser A, Rasouli N, Bodles AM, Phanavanh B, Lee MJ, Starks T, Kern LM, Spencer HJ 3rd, McGehee RE Jr, Fried SK, Kern PA. Human visfatin expression: relationship to insulin sensitivity, intramyocellular lipids, and inflammation. J Clin Endocrinol Metab. 2007 Feb;92(2):666-72. doi: 10.1210/jc.2006-1303. Epub 2006 Nov 7.
- Results publication: PubMed 17130488Wolins NE, Quaynor BK, Skinner JR, Tzekov A, Croce MA, Gropler MC, Varma V, Yao-Borengasser A, Rasouli N, Kern PA, Finck BN, Bickel PE. OXPAT/PAT-1 is a PPAR-induced lipid droplet protein that promotes fatty acid utilization. Diabetes. 2006 Dec;55(12):3418-28. doi: 10.2337/db06-0399.
- Results publication: PubMed 17595259Yao-Borengasser A, Varma V, Bodles AM, Rasouli N, Phanavanh B, Lee MJ, Starks T, Kern LM, Spencer HJ 3rd, Rashidi AA, McGehee RE Jr, Fried SK, Kern PA. Retinol binding protein 4 expression in humans: relationship to insulin resistance, inflammation, and response to pioglitazone. J Clin Endocrinol Metab. 2007 Jul;92(7):2590-7. doi: 10.1210/jc.2006-0816. Epub 2007 Jun 26.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Philip A Kern, MD principal investigator
Central Arkansas Veterans HCS
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 4 study testing Metformin, Pioglitazone and CT scans in people with Glucose Metabolism Disorders and Diabetes, run by US Department of Veterans Affairs at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 25 Apr 2008. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 4 studies take place after a treatment is approved, to learn more about its long-term benefits and risks in everyday use.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Effects of pioglitazone and metformin on ectopic lipid accumulation (time frame: 4 yr). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT00108615, which also lists 13 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 25 Apr 2008; AzTrials last refreshed its copy on 8 Nov 2026.