Tissue Lipids and Insulin Resistance
NCT00483210 · Status: WITHDRAWN · Phase: NA · Type: INTERVENTIONAL
Last updated 2015-03-04
Summary
Resistance to the hypoglycemic action of insulin develops within 7 days of bedrest in young, healthy volunteers. We propose that the same event occurs in elderly individuals confined to bed, that alterations in lipid metabolism are, at least in part, responsible for the insulin resistance associated with bedrest, and that the accumulation of intracellular triglyceride (TG) in liver and muscle will play a role in impairing insulin action. Further, we propose that the PPARα (Peroxisome Proliferator-Activated Receptor Alpha) agonist fenofibrate will increase tissue fatty acid disposal by activating mitochondrial oxidative capacity, thereby improving insulin sensitivity.
We will investigate a series of specific hypotheses designed to examine the role of altered lipid metabolism in the development of insulin-resistance associated with bedrest. Further, since inactivity is likely a principal factor in the development of insulin resistance in the elderly, the response to the inactivity imposed by bedrest represents an acceleration of the normal development of insulin resistance in elderly individuals. Therefore, the results of this study will also be pertinent to the understanding of the mechanisms responsible for the natural development of insulin resistance in free-living elderly.
Conditions
- Tissue Lipid Metabolism
Interventions
- DRUG
-
Fenofibrate
Sponsors & Collaborators
-
National Institutes of Health (NIH)
collaborator NIH -
University of Arkansas
lead OTHER
Principal Investigators
-
Robert Wolfe, PhD · University of Arkansas
Study Design
- Allocation
- RANDOMIZED
- Purpose
- TREATMENT
- Masking
- NONE
- Model
- PARALLEL
Eligibility
- Min Age
- 60 Years
- Max Age
- 85 Years
- Sex
- ALL
- Healthy Volunteers
- Yes
Timeline & Regulatory
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