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This version published online on January 27, 2005
Endocrinology, doi:10.1210/en.2004-1572
A more recent version of this article appeared on May 1, 2005
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*Hepatitis

Submitted on December 3, 2004
Accepted on January 21, 2005

Regulation of T-cell mediated hepatic inflammation by adiponectin and leptin

Joseph A. Sennello, Raja Fayad, Alison M. Morris, Robert H. Eckel, Esra Asilmaz, Jason Montez, Jeffrey M. Friedman, Charles A. Dinarello, and Giamila Fantuzzi*

Division of Infectious Diseases and Endocrinology, Metabolism and Diabetes, University of Colorado Health Sciences Center, Denver, CO; Rockefeller University, New York, NY, Howard Hughes Medical Institute

* To whom correspondence should be addressed. E-mail: giamila{at}uic.edu.

ConA-induced hepatotoxicity was compared in lipodystrophic aP2-nSREBP-1c transgenic mice (LD mice) lacking adipose tissue, obese leptin-deficient ob/ob mice and lean wild-type (WT) mice. Serum leptin and adiponectin were low in LD mice, whereas ob/ob mice had undetectable leptin but high adiponectin. Protection from hepatotoxicity was observed in ob/ob, but not in LD mice, despite low cytokine levels and reduced T cell activation and hepatic NK T cells in both groups. Administration of adiponectin protected LD mice from hepatotoxicity without altering cytokine levels. In contrast, administration of leptin heightened disease susceptibility by restoring cytokine production. Neutralization of TNF{alpha} protected LD mice from liver damage. Increased in vivo susceptibility to the hepatotoxic effect of TNF{alpha} was observed in LD mice. In vitro, adiponectin protected primary hepatocytes from TNF{alpha}-induced death, whereas leptin had no protective effect. In conclusion, whereas leptin increases susceptibility to hepatotoxicity by regulating cytokine production and T cell activation, adiponectin protects hepatocytes from TNF{alpha}-induced death.
Key words: tumor necrosis factor • adipose tissue • inflammation • cytokines • lymphocytes




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