Free Fatty Acid Induced Insulin Resistance (FFAIR)
Recruitment status was Recruiting
This study aims to explore time-dependent effects of lipid infusion an intramyocellular lipid metabolites and the induction of impaired insulin signaling.
|Study Design:||Time Perspective: Prospective|
|Official Title:||Assessment of the Time Course of Lipid Induced Insulin Resistance|
- intramyocellular lipid metabolites [ Time Frame: after 4 hours lipid infusion ] [ Designated as safety issue: No ]Muscle biopsies are taken before, after 2.5 and 4 hours of lipid infusion
- insulin resistance of glucose uptake and mitochondrial function [ Time Frame: after 4 hours lipid infusion ] [ Designated as safety issue: No ]Mitochondrial function will bes assessed from muscle biopsy samples taken after 4 hours, insulin sensitivity will be assessed from hyperinsulinemic-euglycemic clamps following 4 hours lipid infusion
Biospecimen Retention: Samples With DNA
|Study Start Date:||March 2010|
|Estimated Study Completion Date:||April 2011|
|Estimated Primary Completion Date:||April 2011 (Final data collection date for primary outcome measure)|
healthy lean humans before and after lipid infusion
Dietary Supplement: Lipovenös lipid infusion
Lipid enriched infusions will be applied for 2-6 hours.
Other Name: soy oil
Increased availability of free fatty acids impairs glucose disposal in young healthy humans. Patients with type 2 diabetes have reduced whole body glucose disposal, increased ectopic lipid deposition in skeletal muscle and the liver and impaired mitochondrial function. Recent studies suggest that lipid metabolites such as diacylglycerol (DAG), ceramides and long-chain acyl-coA represent the active mediators inducing insulin resistance. Possible targets are DAG-sensitive Proteinkinase C (PKC θ, PKC ε) which inhibit the insulin signaling cascade and ceramides which interfere with the insulin signaling cascade at Proteinkinase B/AKT. Prior studies raised controvesial evidence, thus, it is yet unclear, whether DAG or ceramides are the primary agents inducig lipid-induced insulin resistance. Therefore, the current study aims to explore the time course of the appearance of intramyocellular lipid compunds during lipid infusion in parallel assessing markers of impaired insulin action.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01229059
|Contact: Michael Roden, MD||00492113382 ext email@example.com|
|German Diabetes Center||Recruiting|
|Duesseldorf, NRW, Germany, 40225|
|Contact: Michael Roden, MD 00492113382 ext 201 firstname.lastname@example.org|
|Principal Investigator: Michael Roden, MD|
|Principal Investigator:||Michael Roden, Prof||German Diabetes Center|