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Sponsored by: |
Department of Veterans Affairs |
Information provided by: | Department of Veterans Affairs |
ClinicalTrials.gov Identifier: | NCT00330967 |
The objectives of the study are to:
Condition | Intervention |
Inflammation Insulin Resistance |
Drug: 20% Intralipid Drug: Salicylate |
ChemIDplus related topics: | Insulin Dextrose Lipids |
Study Type: | Observational |
Study Design: | Other, Prospective |
Official Title: | Mechanisms of Insulin Resistance in Humans |
Blood samples, muscle biopsies
Estimated Enrollment: | 32 |
Study Start Date: | April 2006 |
Estimated Study Completion Date: | February 2009 |
Estimated Primary Completion Date: | December 2008 (Final data collection date for primary outcome measure) |
Groups/Cohorts | Assigned Interventions |
1
healthy subjects
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Drug: 20% Intralipid
lipid infusion
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2
healthy subjects different from group 1
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Drug: 20% Intralipid
lipid infusion
Drug: Salicylate
treatment with anti-inflammatory agent
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Insulin resistance in skeletal muscle is a characteristic abnormality in obesity and the metabolic syndrome and a major factor responsible for the development of type 2 diabetes. Although the mechanisms responsible for muscle insulin resistance are largely unclear, lipid oversupply is an important factor. Among numerous potential mechanisms whereby lipid oversupply may cause muscle insulin resistance, current evidence points towards inflammation as being critical. Recent studies in animals, however, indicate that the inflammatory response in skeletal muscles may require the presence of circulating pro-inflammatory factors suggesting that the inflammation induced insulin resistance in skeletal muscles may be a secondary event. More specifically, activation of Nuclear Factor-Kappa B(NF-kB), and inflammatory master switch that drives the production of numerous pro-inflammatory cytokines in fat and liver, has been implicated in causing insulin resistance in skeletal muscles by increasing circulating pro-inflammatory cytokines. In contrast, animal studies have found that activation of NP-KB directly in skeletal muscles has no or little effect on its insulin sensitivity but does produce other abnormalities such as increased proteasome activity. The study shall therefore be undertaken to determine to what extent lipid-induced inflammation and insulin resistance in skeletal muscles requires the presence of circulating proinflammatory factors in humans.
Ages Eligible for Study: | 21 Years to 65 Years |
Genders Eligible for Study: | Both |
Accepts Healthy Volunteers: | Yes |
Sampling Method: | Non-Probability Sample |
healthy subjects
Inclusion Criteria:
Exclusion Criteria:
Contact: Rosemarie Vedda, PA-C | (602) 277-5551 ext 6183 | rosemarie.vedda@va.gov |
United States, Arizona | |||||
Carl T. Hayden VA Medical Center | Recruiting | ||||
Phoenix, Arizona, United States, 85012 | |||||
Contact: Rosemarie Vedda, PA-C 602-277-5551 ext 6183 rosemarie.vedda@va.gov | |||||
Principal Investigator: Christian Meyer, MD |
Principal Investigator: | Christian Meyer, MD | Carl T. Hayden VA Medical Center |
Responsible Party: | Department of Veterans Affairs ( Meyer, Christian - Principal Investigator ) |
Study ID Numbers: | ENDA-029-05F |
First Received: | May 26, 2006 |
Last Updated: | May 5, 2008 |
ClinicalTrials.gov Identifier: | NCT00330967 |
Health Authority: | United States: Federal Government |
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