Molecular Mechanisms of Type 2 Diabetes Mellitus
Public ClinicalTrials.gov record NCT00816218. Field values are reproduced from the official study page; the official ClinicalTrials.gov record remains the source of truth for eligibility, enrollment, and contact information.
Data is sourced from official ClinicalTrials.gov public API records. Always review the official ClinicalTrials.gov record for the latest information.
Official title
Molecular Mechanisms of Endothelial Dysfunction in Type 2 Diabetes Mellitus
Brief summary
Reproduced verbatim from the official ClinicalTrials.gov record. Not medical advice.
This project is designed to evaluate the molecular mechanisms involved in the early development of endothelial dysfunction in type 2 diabetic patients. The investigators intend to correlate increases in insulin signaling pathway activity following pioglitazone therapy with improvements in nitric oxide synthase expression in skeletal muscle. In addition, the investigators will evaluate vascular responses and in vivo nitric oxide release during administration of acetylcholine and nitroprusside in patients with type 2 diabetes. Enhanced knowledge of the molecular mechanisms responsible for endothelial dysfunction, an early abnormality in the pathogenesis of atherosclerosis, is critical before novel therapies to arrest or delay the appearance of cardiovascular complications in diabetes can be developed. The investigators intend to recruit fifty type 2 diabetic patients treated with diet alone or diet plus sulfonylureas or meglitinides and add Pioglitazone (45 mg), an insulin sensitizer, for 6 months. In addition to assessment of clinical and metabolic parameters, insulin sensitivity and brachial artery and skin microcirculatory responses to acetylcholine and nitroprusside in combination with simultaneous determination of nitric oxide release will be documented before, 3 and 6 months after Pioglitazone therapy is initiated. Circulating levels of markers of endothelial damage (VCAM, ICAM, selectins), inflammation (C-reactive protein and interleukins), increased coagulability (PAI-1) as well as lipids and apolipoproteins will measured during the study. Skeletal muscle biopsies will be performed during the euglycemic insulin clamp before and 6 months after therapy for measurements of NO synthase activity and key elements of the insulin signal transduction pathway involved in the regulation of glucose metabolism (IRS-1, PI-3 kinase, PI-3 kinase associated with IRS-1 and the mitogenesis MAP-kinase. Type 2 diabetes confers a substantial increase in the risk of cardiovascular disease. This is believed to be due, in part, to endothelial dysfunction, which correlates closely with impaired vascular responsiveness. Our study will clarify further the extent to which resistance to insulin action and impaired nitric oxide release from endothelial cells are interrelated. We also expect to demonstrate that insulin sensitizers (pioglitazone) can help to restore normal endothelial function, and ultimately prevent/delay the appearance of vascular disease in patients with type 2 diabetes.
Study identification
- NCT ID
- NCT00816218
- Recruitment status
- Completed
- Study type
- Interventional
- Phase
- Phase 4
- Enrollment
- 39 participants
Conditions and interventions
Conditions
Eligibility (public fields only)
- Age range
- 18 Years to 65 Years
- Sex
- All
- Healthy volunteers
- Healthy volunteers not accepted
This page does not interpret eligibility. Detailed inclusion and exclusion criteria are on the official ClinicalTrials.gov record.
Study timeline
- Start date
- Feb 28, 2003
- Primary completion
- Jun 30, 2006
- Completion
- Oct 31, 2008
- Last update posted
- May 30, 2012
2003 – 2008
United States locations
- U.S. sites
- 1
- U.S. states
- 1
- U.S. cities
- 1
| Facility | City | State | ZIP | Site status |
|---|---|---|---|---|
| The University of Texas Health Science Center at San Antonio | San Antonio | Texas | 78229 | — |
Site contact phone numbers, emails, and investigator names are intentionally not displayed here. Open the official ClinicalTrials.gov record for site contact information.
About this trial record page
- What this page shows
- Public field values for ClinicalTrials.gov record NCT00816218, including study identification, conditions, interventions, eligibility (age, sex, healthy volunteer), timeline, and U.S. site list.
- What this page does not do
- No medical advice, eligibility judgments, treatment recommendations, study quality scoring, or AI-generated medical summaries. No site contact phone numbers, emails, or investigator names.
- Where the data comes from
- Sourced from the official ClinicalTrials.gov public API. The official record is the source of truth.
- Last refresh
- Last update posted May 30, 2012 · Synced Sep 2, 2026
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Open the official record
The complete protocol, eligibility criteria, and contact information for NCT00816218 live on ClinicalTrials.gov.