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Journal of the American College of Nutrition, Vol. 22, No. 5, 415-420 (2003)
Published by the American College of Nutrition

Original Research

Anti-TNF-{alpha} Antibody Normalizes Serum Leptin in IL-2 Deficient Mice

Lisa M. Gaetke, PhD, RD, Helieh S. Oz, DVM, PhD, Robert C. Frederich, MD, PhD and Craig J. McClain, MD, FACN

Department of Nutrition and Food Science, University of Kentucky, and the Lexington Veterans Administration Medical Center, Lexington (L. M. G.)
Department of Internal Medicine University of Louisville, Louisville (H. S. O., C. J. M.), Kentucky
Department of Internal Medicine, Bristol-Myers Squibb, Lawrenceville Campus, Princeton, New Jersey (R. C. F.)

Address reprint requests to: Lisa Gaetke, Ph.D., R.D., Department of Nutrition and Food Science, University of Kentucky, 218 Funkhouser Building, Lexington, KY 40506-0054. E-mail: lgaetke{at}uky.edu

Objective: A recent study reports that the interleukin-2 deficient (IL-2-/-) mouse model of autoimmune and inflammatory bowel disease (IBD) with elevated pro-inflammatory cytokine production has elevated leptin concentrations during food deprivation. The objective of this study was to examine whether increased tumor necrosis factor-{alpha} (TNF-{alpha}), a pro-inflammatory cytokine, contributes to the abnormally elevated leptin in IL-2-/- mice.

Methods: Eight week old, IL-2-/- and wild-type control (IL-2+/+), male mice were fed regular laboratory mouse food for two weeks. At the end of the study, blood was collected in the fed state, IL-2-/- and IL-2+/+ mice were injected with either anti-TNF-{alpha} monoclonal antibody or normal saline, and blood was collected in the starved state.

Results: The IL-2-/- mice consumed less food and lost weight. Administration of anti-TNF-{alpha} antibody markedly reduced serum leptin concentrations in IL-2-/- and control mice after food deprivation. Serum leptin in the IL-2-/- mice not receiving anti-TNF-{alpha} antibody increased significantly in the starved state. Serum concentrations of TNF-{alpha} were higher in IL-2-/- mice compared to controls in both the fed and starved state.

Conclusions: These results suggest that elevated TNF-{alpha} may be one mechanism for the sustained elevated leptin observed in IL-2-/- mice during food deprivation.

Key words: leptin, IL-2 deficient mice, tumor necrosis factor-{alpha} (TNF-{alpha}), inflammatory bowel disease (IBD)

Abbreviations: IBD, inflammatory bowel disease • IFN-{gamma}, interferon-{gamma} • IL, interleukin • IL-2-/-, interleukin-2 deficient • LIF, leukemia inhibitory factor • LPS, lipopolysaccharide • TNF-{alpha}, tumor necrosis factor-{alpha}






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