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Am J Physiol Regul Integr Comp Physiol 284: R763-R770, 2003; doi:10.1152/ajpregu.00610.2002
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Vol. 284, Issue 3, R763-R770, March 2003

Hyperleptinemia and reduced TNF-alpha secretion cause resistance of db/db mice to endotoxin

Abram M. Madiehe, Tiffany D. Mitchell, and Ruth B. S. Harris

Department of Foods and Nutrition, University of Georgia, Athens, Georgia 30602

Leptin deficiency in ob/ob mice increases susceptibility to endotoxic shock, whereas leptin pretreatment protects them against LPS-induced lethality. Lack of the long-form leptin receptor (Ob-Rb) in db/db mice causes resistance. We tested the effects of LPS in C57BL/6J db3J/db3J (BL/3J) mice, which express only the circulating leptin receptors, compared with C57BL/6J db/db (BL/6J) mice, which express all short-form and circulating isoforms of the leptin receptor. Intraperitoneal injections of LPS significantly decreased rectal temperature and increased leptin, corticosterone, and free TNF-alpha in fed and fasted BL/3J and BL/6J mice. TNF-alpha was increased three- and fourfold in BL/3J and BL/6J, respectively. LPS (100 µg) caused 50% mortality of fasted BL/6J mice but caused no mortality in fasted BL/3J mice. Pretreatment of fasted BL/3J mice with 30 µg leptin prevented the drop in rectal temperature, blunted the increase in corticosterone, but had no effect on TNF-alpha induced by 100 µg LPS. Taken together, these data provide evidence that fasted BL/3J mice are more resistant than BL/6J mice to LPS toxicity, presumably due to the absence of leptin receptors in BL/3J mice. This resistance may be due to high levels of free leptin cross-reacting with other cytokine receptors.

tumor necrosis factor-alpha ; leptin receptor; lipopolysaccharides


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