| First Author | Pini M | Year | 2006 |
| Journal | Endocrinology | Volume | 147 |
| Issue | 11 | Pages | 5019-22 |
| PubMed ID | 16901963 | Mgi Jnum | J:129728 |
| Mgi Id | MGI:3770074 | Doi | 10.1210/en.2006-0855 |
| Citation | Pini M, et al. (2006) Adiponectin deficiency does not affect the inflammatory response to endotoxin or concanavalin a in mice. Endocrinology 147(11):5019-22 |
| abstractText | 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 microg/mouse) induced production of comparable amounts of IL-6, TNFalpha, and interferon-gamma 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. |
