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Insulin increases the release of proinflammatory mediators
Susan I Brundage1, Natalie N Kirilcuk, Jason C Lam
1Division of Trauma, Emergency and Critical Care Surgery, Department of Surgery, Stanford University Medical Center, Stanford, California 94305, USA. sbrundage@stanford.edu
The Journal of Trauma
|August 13, 2008
Summary
Insulin does not directly reduce inflammation in activated macrophages. Instead, this study found that insulin significantly increased levels of the proinflammatory cytokine TNF-alpha protein in these cells.
Area of Science:
- Immunology
- Endocrinology
- Critical Care Medicine
Background:
- Strict glucose control with insulin in intensive care units is linked to reduced mortality.
- The direct effects of insulin on inflammation, independent of glucose control, remain debated.
- This study investigates insulin's influence on activated macrophages, distinct from its role in glucose regulation.
Purpose of the Study:
- To determine the direct effect of insulin on activated macrophages.
- To test the hypothesis that insulin directly reduces the inflammatory cascade.
Main Methods:
- Human monocytic THP-1 cells were stimulated with lipopolysaccharide (LPS).
- Cells were treated with insulin for 1 and 24 hours.
- Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels were measured at the protein and gene expression levels.
Main Results:
- Insulin treatment significantly increased TNF-alpha protein production in LPS-stimulated macrophages at both 1 and 24 hours.
- No significant difference in TNF-alpha and IL-6 gene expression was observed between insulin-treated and untreated cells.
- Insulin did not suppress, but rather enhanced, the protein output of a key inflammatory cytokine.
Conclusions:
- Insulin does not possess direct anti-inflammatory properties in this experimental model.
- Insulin administration to activated macrophages increases the release of pro-inflammatory cytokine proteins.
- Findings challenge the notion of insulin as a direct anti-inflammatory agent in this context.
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