T cell–mediated hepatic inflammation modulates adiponectin levels in mice: role of tumor necrosis factor α

• Published in: Metabolism, clinical and experimental clinical and experimental, 2006-04, Vol.55 (4), p.555-559
• Main Authors: Morris, Alison M., Sennello, Joseph A., Fayad, Raja A., Eckel, Robert H., Dinarello, Charles A., Fantuzzi, Giamila
• Format: Article
• Language: English
• Subjects: Adiponectin - blood; Adiponectin - genetics; Adipose Tissue - metabolism; Animals; Biological and medical sciences; Concanavalin A; Hepatitis - blood; Hepatitis - etiology; Hepatitis - metabolism; Hepatitis - pathology; Leptin - blood; Medical sciences; Metabolic diseases; Mice; Mice, Inbred C57BL; Mitogens; Receptors, Adiponectin; Receptors, Cell Surface - metabolism; RNA, Messenger - metabolism; T-Lymphocytes; Tumor Necrosis Factor-alpha - antagonists & inhibitors; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 0026-0495; 1532-8600
• DOI: 10.1016/j.metabol.2005.11.008

Experimental T cell–mediated hepatitis induced by concanavalin A (ConA) results in the initiation of an inflammatory response and the production of cytokines. Adiponectin is an adipocytokine produced by adipose tissue that is involved in the reciprocal regulation of other cytokines, including tumor necrosis factor α (TNF- α). Concanavalin A administration to C57BL/6J mice reduced circulating levels of adiponectin, whereas leptin was markedly increased. Adiponectin messenger RNA expression in adipose tissue was also decreased; however, the expression of both the adiponectin receptors remained unchanged. Neutralization of TNF- α reduced ConA-induced liver damage, and this was associated with restored circulating levels of adiponectin. These findings indicate that inflammation-induced TNF- α is a critical mediator of adipose-tissue-derived adiponectin in vivo.