1. Leptin deficiency, not obesity, protects mice from Con A-induced hepatitis
- Author
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Kelly C. Lear-Kaul, Britta Siegmund, Raffaella Faggioni, and Giamila Fantuzzi
- Subjects
Hepatitis ,education.field_of_study ,medicine.medical_specialty ,Leptin Deficiency ,Leptin ,Lymphocyte ,Immunology ,Population ,Biology ,medicine.disease ,Gold thioglucose ,medicine.anatomical_structure ,Endocrinology ,Internal medicine ,medicine ,Immunology and Allergy ,Tumor necrosis factor alpha ,Interferon gamma ,education ,medicine.drug - Abstract
Leptin-deficient ob/ob mice are protected from Con A-induced hepatitis. However, it is unclear whether leptin deficiency or obesity itself is responsible for this protection. To address this question, wild-type (WT) obese mice with high serum leptin levels were generated by injection of gold thioglucose (WT GTG). Both Con A-injected WT and WT GTG mice developed hepatitis, whereas no hepatic damage was observed in ob/ob mice. Moreover, TNF-alpha and IFN-gamma levels as well as expression of the activation marker CD69 were elevated in liver mononuclear cells of WT and WT GTG mice, but not in ob/ob mice following administration of Con A. The liver of WT and WT GTG mice had the same percentage of NK T cells, a lymphocyte population involved in Con A-induced hepatitis. This population decreased equally in both WT and WT GTG mice after Con A injection. In contrast, the liver of ob/ob mice contained 50% less NK T cells compared to WT and WT GTG mice. Furthermore, no decrease in NK T cells was observed in Con A-injected ob/ob mice. We conclude that leptin-deficiency, not obesity, is responsible for protection from Con A-induced hepatitis.
- Published
- 2002
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