An interventional study of Fenofibrate in Tissue Lipid Metabolism, sponsored by University of Arkansas. Withdrawn. Open to participants aged 60 Years to 85 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2015-03-04.
Sponsored by University of Arkansas · Not applicable, Interventional, and Treatment
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.
The accumulation of intracellular lipid reflects a dysregulation of tissue fatty acid metabolism involving abnormal relationships between tissue fatty acid uptake and oxidation. It has been postulated that such dysregulation of lipid metabolism causes insulin resistance as a direct consequence of the accumulated intracellular triglyceride (TG), or that the increased intracellular TG reflects an increase in active products of fatty acids, such as diacylglycerol, that inhibit the insulin signaling pathway. We recently found that both muscle and liver intracellular TG concentrations were elevated in more than one-half of otherwise healthy elderly individuals.
We hypothesize that an increase in tissue lipids in the elderly reflects altered tissue lipid metabolism that puts them at high risk for the development of insulin resistance with bedrest. 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 examine the role of alterations in lipid metabolism in the development of insulin resistance that occurs with bedrest.
Methods: A total of 40 elderly subjects ranging in age from 60-85 will be studied. Subjects will be randomized to one of two groups: 1) 10 days of bedrest or 2) 10 days of bedrest plus fenofibrate. Each of the subjects will complete a 5- day diet stabilization period and have a metabolic infusion study on day 5, followed by 10 days of bedrest and a metabolic study on day 18. This will be followed by a 3 week rehabilitation program. Pre-test and post bedrest measurements include body composition by DEXA, intracellular TG measurements by MRS, strength testing.
The results will provide insight into the mechanisms responsible for the development of insulin resistance with inactivity and strategies for ameliorating this response.
1,960 studies on the registry are indexed under Insulin Resistance; 306 are open to participants now.
Browse Insulin Resistance studies →University of Arkansas is the lead sponsor of 391 studies on the registry; 39 are open to participants now.
Of its 37 completed or terminated interventional studies of FDA-regulated products, 34 (92%) have results posted.
Counted across the registry records on this site, refreshed daily.
Exclusion Criteria:
Any subjects taking Coumadin adn risk factors of DVT as listed:
No study locations are listed for this record.
This study is withdrawn, as verified in Mar 2015. You cannot join it, but the record below documents what was studied.
Get an email when the registry record changes — status, dates, results — or when someone posts here.
Sign in to followQuestions and observations about this study, from anyone following it. Not medical advice, and not a channel to the study team — their contact details are on the registry record.
Sign in to join the discussion. Reading takes no account; posting does. You choose a display name, and a pseudonym is the default.
Nothing here yet. If you are running this trial, taking part in it, or weighing whether to, this is the place to say so.
University of Arkansas