Leptin deficiency, not obesity, protects mice from Con A-induced hepatitis.

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.

• Authors: Britta Siegmund, Kelly C Lear-Kaul, Raffaella Faggioni, Giamila Fantuzzi
• Journal: European journal of immunology (Eur J Immunol) Vol. 32 Issue 2 Pg. 552-60 (02 2002) ISSN: 0014-2980 [Print] Germany
• PMID: 11828372 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Leptin
• Tumor Necrosis Factor-alpha
• Concanavalin A
• Aurothioglucose
• Interferon-gamma

Topics

• Animals
• Aurothioglucose
• Body Weight
• Chemical and Drug Induced Liver Injury (immunology, pathology, prevention & control)
• Concanavalin A (toxicity)
• Female
• Interferon-gamma (biosynthesis)
• Killer Cells, Natural (immunology)
• Leptin (blood, deficiency)
• Lymphocyte Activation
• Mice
• Mice, Inbred C57BL
• Mice, Obese
• Obesity (genetics, pathology, physiopathology)
• T-Lymphocyte Subsets (immunology)
• Tumor Necrosis Factor-alpha (biosynthesis)