title: Multiple cytokines and acute inflammation raise mouse leptin levels: potential role in inflammatory anorexia.
abstract: Several inflammatory cytokines, most notably tumor necrosis factor (TNF) and IL-1, induce anorexia and loss of lean body mass, common manifestations of acute and chronic inflammatory conditions. In C57BL/6 female mice, the administration of TNF, IL-1, and, to a lesser extent, leukemia inhibitory factor (LIF), produced a prompt and dose-dependent increase in serum leptin levels and leptin mRNA expression in fat. IL-10, IL-4, ciliary neurotrophic factor, and IL-2, cytokines not known to induce anorexia or decrease food intake, had no effect on leptin gene expression or serum leptin levels. After administration of Escherichia coli lipopolysaccharide (LPS), leptin gene expression and leptin levels were increased. These findings suggest that leptin levels may be one mechanism by which anorexia is induced during acute inflammatory conditions.
authors.affiliation: Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
authors.forename: P
authors.initials: P
authors.lastname: Sarraf
authors.forename: R C
authors.initials: RC
authors.lastname: Frederich
authors.forename: E M
authors.initials: EM
authors.lastname: Turner
authors.forename: G
authors.initials: G
authors.lastname: Ma
authors.forename: N T
authors.initials: NT
authors.lastname: Jaskowiak
authors.forename: D J
authors.initials: DJ
authors.lastname: Rivet
authors.forename: J S
authors.initials: JS
authors.lastname: Flier
authors.forename: B B
authors.initials: BB
authors.lastname: Lowell
authors.forename: D L
authors.initials: DL
authors.lastname: Fraker
authors.forename: H R
authors.initials: HR
authors.lastname: Alexander
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D000818:Animals; D000855:Anorexia; D020934:Ciliary Neurotrophic Factor; D016207:Cytokines / Q000494:pharmacology*; D004926:Escherichia coli; D005260:Female; D006131:Growth Inhibitors / Q000494:pharmacology; D006801:Humans; D007249:Inflammation; D016753:Interleukin-10 / Q000494:pharmacology; D007376:Interleukin-2 / Q000494:pharmacology; D015847:Interleukin-4 / Q000494:pharmacology; D015850:Interleukin-6; D007378:Interleukins / Q000494:pharmacology; D007700:Kinetics; D020738:Leptin; D053605:Leukemia Inhibitory Factor; D008070:Lipopolysaccharides / Q000494:pharmacology; D008222:Lymphokines / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D009419:Nerve Tissue Proteins / Q000494:pharmacology; D014176:Protein Biosynthesis; D011506:Proteins / Q000032:analysis; D012333:RNA, Messenger / Q000096:biosynthesis; D011994:Recombinant Proteins / Q000494:pharmacology; D014158:Transcription, Genetic / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D020934:Ciliary Neurotrophic Factor; D016207:Cytokines; D006131:Growth Inhibitors; D007376:Interleukin-2; D015850:Interleukin-6; D007378:Interleukins; C507837:LIF protein, human; D020738:Leptin; D053605:Leukemia Inhibitory Factor; C507838:Lif protein, mouse; D008070:Lipopolysaccharides; D008222:Lymphokines; D009419:Nerve Tissue Proteins; D011506:Proteins; D012333:RNA, Messenger; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D015847:Interleukin-4