New Role of Resistin in Lipopolysaccharide-Induced Liver Damage in Mice

• DOI: 10.1124/jpet.108.136721
• Publication Date: 2008-03-14T01:28:37Z
• Authors: Juliane I. Beier; Luping Guo; Claudia von Montfort; J. Phillip Kaiser; Swati Joshi-Barve; Gavin E. Arteel
• Keywords: Resistin; Proinflammatory cytokine

Studies in rodents suggest that the adipocytokine resistin causes insulin resistance via impairing normal signaling. However, humans, may play a more important role inflammation than resistance. Whether contributes to is unclear. Therefore, purpose of present study was determine effect exposure on basal and stimulated [lipopolysaccharide (LPS)] inflammatory response mouse liver vivo. Resistin alone had no major effects hepatic expression insulin-responsive genes, either presence or absence LPS. Although it alone, significantly enhanced necrosis caused by increased proinflammatory e.g., plasminogen activator inhibitor (PAI)-1, activity mitogen-activated protein (MAP) kinase, extracellular signal-regulated kinase 1/2, LPS, but little anti-inflammatory gene expression. also fibrin deposition (an index hemostasis) The increase PAI-1 expression, deposition, damage LPS + almost completely prevented inhibiting coagulation cascade, hirudin, blocking MAP signaling, U0126 [1,4-diamino-2,3-dicyano-1,4-bis(2-aminophenylthio) butadiene], indicating these pathways causal observed resistin. Taken together, augmentation LPS-induced seems involve, at least part, up-regulation mechanisms most likely involving cascade accumulation. These data have roles independent its analogous previous work humans.