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mediates leptin induction during inflammation
1 Metabolism Section, Veterans Affairs Medical Center, University of California, San Francisco, California 94121; and 2 Division of Infectious Diseases, University of Colorado Health Sciences Center, Denver, Colorado 80262
Interleukins
(IL) are key mediators of the host response to infection and
inflammation. Leptin is secreted by adipose tissue and plays an
important role in the control of food intake. Administration of
lipopolysaccharide (LPS), tumor necrosis factor (TNF), or IL-1 acutely
increases leptin mRNA and protein levels. To investigate the role of
IL-1
and IL-6 in leptin expression during inflammation, we used
IL-1-deficient (
/) and IL-6 / mice. Mice
were injected intraperitoneally with LPS or subcutaneously with
turpentine, as models of systemic or local inflammation, respectively.
In IL-1 +/+ mice, both LPS and turpentine increased leptin mRNA and
circulating leptin. In contrast, neither LPS nor turpentine increased
leptin levels in IL-1 / mice. In IL-6 +/+ or IL-6 / mice, turpentine increased leptin protein to comparable
levels. We conclude that IL-1 is essential for leptin induction by
both LPS and turpentine in mice, but IL-6 is not.
Ob protein; interleukin-6; interleukin-1; turpentine; endotoxin; lipopolysaccharide; knockout mice
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