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Interleukin-1, anorexia, and dietary fatty acids
C A Dinarello1, S Endres, S N Meydani
1Department of Medicine, Tufts University, Boston, Massachusetts.
Annals of the New York Academy of Sciences
|January 1, 1990
Summary
Interleukin-1 (IL-1) reduces food intake, a response mitigated by N-3 fatty acids. These fatty acids also decrease IL-1 production, suggesting a therapeutic role in managing anorexia associated with diseases like cancer.
Area of Science:
- Biomedical Science
- Nutrition Science
- Immunology
Background:
- Interleukin-1 (IL-1) and other cytokines are implicated in pathological processes, including cachexia in cancer and chronic infections.
- Cachexia, characterized by reduced food intake and weight loss, is a significant complication in various diseases.
Purpose of the Study:
- To investigate the role of IL-1 in reducing food intake and its modulation by N-3 fatty acids.
- To explore the mechanisms by which N-3 fatty acids affect IL-1 production and its anorexic effects.
Main Methods:
- Administration of recombinant IL-1 beta or IL-1 alpha to experimental animals to assess effects on food intake and weight gain.
- Utilizing cyclooxygenase inhibitors to investigate the IL-1 anorexic pathway.
- Supplementing animal diets with N-3 fatty acids and analyzing cyclooxygenase and lipoxygenase metabolite production.
- Measuring IL-1 production in leukocytes from human subjects taking N-3 fatty acid supplements.
Main Results:
- IL-1 significantly reduced food intake and slowed weight gain in meal-fed rats.
- The anorexic effect of IL-1 was attenuated by cyclooxygenase inhibitors and N-3 fatty acid supplementation.
- N-3 fatty acids reduced IL-1 production in human leukocytes, potentially via the lipoxygenase pathway.
Conclusions:
- IL-1-induced anorexia involves cyclooxygenase metabolites, such as PGE2.
- N-3 fatty acids may alleviate anorexia by reducing both the sensitivity to IL-1 and IL-1 synthesis.
- N-3 fatty acid supplementation shows promise for managing anorexia in disease states.