Ignite Creation Date:
2024-05-05 @ 4:54 PM
Last Modification Date:
2024-10-26 @ 9:25 AM
Study NCT ID:
NCT00330967
Status:
COMPLETED
Last Update Posted:
2015-04-03
First Post:
2006-05-26
Brief Title:
Mechanisms of Insulin Resistance in Humans
Sponsor:
US Department of Veterans Affairs
Organization:
VA Office of Research and Development
Study Overview
Official Title:
Mechanisms of Insulin Resistance in Humans
Status:
COMPLETED
Status Verified Date:
2015-03
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
The Objectives of the study are to 1compare the inflammatory response and insulin resistance in skeletal muscles during a systemic infusion of lipid with that during a local infusion of lipid into the femoral artery which would cause minimal or no systemic hyperlipidemia but local plasma free fatty acid FFA concentrations similar to those during the systemic lipid infusion and 2 determine the inflammatory response and insulin resistance in skeletal muscle during an infusion of lipid into the femoral artery as described above after NF-KB inhibition by high dose salicylate treatment in humans
Detailed Description:
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 BNF-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 NF-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
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None