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Resistin messenger-RNA expression is increased by proinflammatory cytokines in vitro
S Kaser1, A Kaser, A Sandhofer
1Department of Medicine, University Hospital Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria.
Abstract:
Resistin is a recently discovered polypeptide that induces insulin resistance in rodents. While in rodents resistin is predominantly expressed in adipocytes, in humans peripheral blood mononuclear cells (PBMC) seem to a be a major source of resistin. In the present study, we show that in human PBMC resistin mRNA expression-determined by fluorescence-based real-time polymerase chain reaction-is strongly increased by the proinflammatory cytokines interleukin (IL)-1, IL-6, tumor necrosis factor alpha (TNF-alpha), and also by lipopolysaccharides (LPS), respectively, while no effect was found by interferon-gamma (IFN-gamma) or leptin. Our results suggest that in humans resistin may be a link in the well-known association between inflammation and insulin resistance.
Insights
Resistin, a protein linked to insulin resistance, is increased by inflammatory signals in human immune cells. This suggests inflammation may drive insulin resistance in humans via resistin.
Area of Science:
- Endocrinology
- Immunology
- Molecular Biology
Background:
- Resistin is a polypeptide hormone known to induce insulin resistance in rodents.
- In rodents, resistin is primarily produced by fat cells (adipocytes).
- In humans, peripheral blood mononuclear cells (PBMC) are identified as a significant source of resistin.
Purpose of the Study:
- To investigate the regulation of resistin mRNA expression in human PBMC.
- To determine the effect of proinflammatory cytokines and other factors on resistin expression in human PBMC.
Main Methods:
- Human PBMC were treated with various cytokines and lipopolysaccharides (LPS).
- Resistin mRNA expression was quantified using fluorescence-based real-time polymerase chain reaction (PCR).
Main Results:
- Proinflammatory cytokines, including interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-alpha), significantly increased resistin mRNA expression in human PBMC.
- Lipopolysaccharides (LPS) also markedly elevated resistin mRNA levels.
- Interferon-gamma (IFN-gamma) and leptin did not affect resistin mRNA expression.
Conclusions:
- Human PBMC are a key site for resistin production and its expression is upregulated by inflammatory stimuli.
- Resistin may act as a molecular link between inflammation and the development of insulin resistance in humans.