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This Article Full Text Full Text (PDF) All Versions of this Article: 294/2/E371    most recent 00507.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Krogh-Madsen, R. Articles by Pedersen, B. K. PubMed PubMed Citation Articles by Krogh-Madsen, R. Articles by Pedersen, B. K.

Effect of short-term intralipid infusion on the immune response during low-dose endotoxemia in humans

¹Centre of Inflammation and Metabolism, Department of Infectious Diseases and Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen, Faculty of Health Sciences; ²Intensive Care Unit, Rigshospitalet, Copenhagen; and ³Department of Diabetes and Endocrinology M, Aarhus University Hospital and Institute of Pharmacology, University of Aarhus, Aarhus, Denmark

Submitted 3 August 2007 ; accepted in final form 30 November 2007

Novel anti-inflammatory effects of insulin have recently been described, and insulin therapy to maintain euglycemia suppresses the plasma levels of free fatty acids (FFA) and increases the survival of critically ill patients. We aimed to explore the effect of short-term high levels of plasma FFA on the inflammatory response to a low dose of endotoxin. Fourteen healthy male volunteers underwent the following two trials in a randomized crossover design: 1) continuous infusion of 20% Intralipid [0.7 ml·kg^–1·h^–1 (1.54 g/kg)] for 11 h, and 2) infusion of isotonic saline for 11 h (control). In each trial, heparin was given to activate lipoprotein lipase, and an intravenous bolus of endotoxin (0.1 ng/kg) was given after 6 h of Intralipid/saline infusion. Blood samples and muscle and fat biopsies were obtained before the Intralipid/saline infusion and before as well as after infusion of an endotoxin bolus. Plasma levels of FFA, triglycerides, and glycerol were markedly increased during the Intralipid infusion. Endotoxin exposure induced an increase in plasma levels of TNF-, IL-6, and neutrophils and further stimulated gene expression of TNF- and IL-6 in both skeletal muscle and adipose tissue. The systemic inflammatory response to endotoxin was significantly pronounced during Intralipid infusion. Short-term hyperlipidemia enhances the inflammatory response to endotoxin, and skeletal muscle and adipose tissue are capable of producing essential inflammatory mediators after endotoxin stimulation.

free fatty acids; lipopolysaccharide; inflammation

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