Tissue Lipids and Insulin Resistance

NCT00483210 · Status: WITHDRAWN · Phase: NA · Type: INTERVENTIONAL

Last updated 2015-03-04

No results posted yet for this study

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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Read the full study record

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View NCT00483210 on ClinicalTrials.gov