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© 2002 The American Society for Nutritional Sciences J. Nutr. 132:893-896, 2002

Biochemical and Molecular Actions of Nutrients
Research Communication

The Leptin Defense against Wasting Is Abolished in the IL-2–Deficient Mouse Model of Inflammatory Bowel Disease1 ,2

Lisa M. Gaetke*3, Helieh S. Oz*,4, Willem J. S. de Villiers*, Gary W. Varilek*,5 and Robert C. Frederich{dagger}

Departments of Nutrition and Food Science and * Internal Medicine, University of Kentucky and the Lexington Veterans Administration Medical Center, Lexington, KY 40506 and {dagger} Bristol-Myers Squibb, Lawrenceville Campus, Princeton, NJ

3To whom correspondence should be addressed. E-mail: lgaetke{at}uky.edu.

Anorexia is a major complication of inflammatory bowel disease (IBD). We postulated that chronic intestinal inflammation with increased proinflammatory cytokines elevates serum leptin concentration, thereby contributing to anorexia. This hypothesis was studied in interleukin-2–deficient (IL-2-/-) mice, a model of IBD with elevated proinflammatory cytokine production. IL-2-/-, wild-type pair-fed and wild-type control male mice (8 wk old) were fed regular laboratory mouse food for 2 wk. The IL-2-/- and pair-fed groups consumed less food and lost weight. Serum leptin concentrations in the IL-2-/- mice in the fed state were lower than controls, but not different from pair-fed mice, and paradoxically increased in the starved state to levels significantly higher than both starved control and pair-fed groups. This result did not change when serum leptin was adjusted for amount of body fat. These data show abnormal leptin responses in IL-2-/- mice with increased leptin concentrations disproportionate to fat mass and prevention of the normal decline in leptin with food restriction.

KEY WORDS: • leptin • IL-2–deficient mice • inflammatory bowel disease • inflammation




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