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Adiponectin Deficiency Does Not Affect the Inflammatory Response to Endotoxin or Concanavalin A in Mice

Department of Human Nutrition (M.P., J.A.S., G.F.), University of Illinois at Chicago, Chicago, Illinois 60612; and Department of Molecular and Cellular Biology (L.C.), Baylor College of Medicine, Houston, Texas 77030

Address all correspondence and requests for reprints to: Giamila Fantuzzi, Department of Human Nutrition, University of Illinois at Chicago, 1919 West Taylor Street, MC 517, Chicago, Illinois 60612. E-mail: giamila{at}uic.edu.

Adiponectin (APN) is an adipocyte-derived protein that regulates insulin sensitivity and displays antiinflammatory activities in a variety of experimental models. The present study aimed at investigating the effect of APN deficiency on the inflammatory response to endotoxin (lipopolysaccharide, LPS) and Concanavalin A (ConA) in vivo in mice. Administration of a high dose of LPS (100 µg/mouse) induced production of comparable amounts of IL-6, TNF, and interferon- in wild-type (WT) and APN knockout (KO) mice. Furthermore, LPS-induced hypoglycemia, anorexia, and body weight loss did not differ between WT and APN KO mice. Administration of a low dose of LPS (100 or 10 ng/g) in association with D-galactosamine induced equivalent mortality rates, hepatotoxicity, and serum IL-6 in WT and APN KO mice. Finally, ConA-induced cytokine production and hepatotoxicity were not significantly different between WT and APN KO mice. These data indicate that—despite its well-described role as an antiinflammatory molecule—endogenous APN does not play a critical role in modulating the inflammatory responses to LPS and ConA in mice.

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