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The Role of Interleukin-6 in Lipopolysaccharide-Induced Weight Loss, Hypoglycemia and Fibrinogen Production, in Vivo
ARMED FORCES RADIOBIOLOGY RESEARCH INST BETHESDA MD
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It was recently shown that interleukin IL-6 is an important mediator involved in the Colon C-26 model of experimental cancer cachexia. In this study, we wished to determine whether IL-6 is also involved in several metabolic changes associated with lipopolysaccharide LPS challenge. Administration of a relatively high amount of LPS to mice induced a transient weight loss, hypoglycemia, Hypertriglyceridemia and an increase in the hepatic acute phase reactant, fibrinogen. pretreatement of mice with the rat anti-murine IL-6 antibody 20F3, but not with a control antibody, resulted in a significant improvement of LPS-induced hypoglycemia and weight loss as well as a significant decrease of plasma fibrinogen. Anti- IL-6 antibody had no effect on LPS-induced hypertriglyceridemia. On the other hand, the pretreatment of mice with anti- murine TNF TN3.19 antibody was able to completely inhibit elevation of triglycerides and modestly improve LPS-induced weight loss although it had no effect on hypoglycemia and fibrinogen production. Taken together, these results suggest that IL-6 plays a role in some of the metabolic changes associated with both an acute i.e. LPS challenge and chronic C-26 cachexia inflammatory conditions
APPROVED FOR PUBLIC RELEASE