Insulin resistance (IR) is a complication of obesity and a possible mechanism for its deleterious effects. This retrospective analysis examines the theory that molecules implicated in mediating IR may also enhance the insulin secretory response during IR. Interleukin-6 (IL-6) has been identified as a mediator of IR and possible beta cell compensatory factor. A pharmacological model was developed to test the dual role of IL-6. Participants were treated with nicotinic acid, titrated up to a two gram dose over two weeks, to induce IR. Multiple blood draws enabled measurement of development of IR, evaluated using the homeostatic model assessment (HOMA), IL-6, fasting plasma insulin and glucose. Despite increases in HOMA and insulin in all subjects, there was no significant change in IL-6 concentrations. It is concluded that despite successful induction of IR using this pharmacological model, IL-6 did not contribute to the generation of IR or the insulin compensatory response.
|School:||California State University, Long Beach|
|School Location:||United States -- California|
|Source:||MAI 50/05M, Masters Abstracts International|
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