suck pdf from google scholar
unlimited free pdf from europmc23207144    free
PDF from PMC    free
html from PMC    free
PDF vom PMID23207144  :  Publisher
PDF vom PMID23207144
suck pdf from library genesis
English Wikipedia

Nephropedia Template TP (

Twit Text


  • DeepDyve
  • Pubget Overpricing


  • lüll
  • Leptin is key to peroxynitrite-mediated oxidative stress and Kupffer cell activation in experimental non-alcoholic steatohepatitis
  • Chatterjee S; Ganini D; Tokar EJ; Kumar A; Das S; Corbett J; Kadiiska MB; Waalkes MP; Diehl AM; Mason RP
  • J Hepatol 2013[Apr]; 58 (4): 778-84
  • BACKGROUND & AIMS: Progression from steatosis to steatohepatitic lesions is hypothesized to require a second hit. These lesions have been associated with increased oxidative stress, often ascribed to high levels of leptin and other proinflammatory mediators. Here we have examined the role of leptin in inducing oxidative stress and Kupffer cell activation in CCl4-mediated steatohepatitic lesions of obese mice. METHODS: Male C57BL/6 mice fed with a high-fat diet (60%kcal) at 16 weeks were administered CCl(4) to induce steatohepatitic lesions. Approaches included use of immuno-spin trapping for measuring free radical stress, gene-deficient mice for leptin, p47 phox, iNOS and adoptive transfer of leptin primed macrophages in vivo. RESULTS: Diet-induced obese (DIO) mice, treated with CCl4 increased serum leptin levels. Oxidative stress was significantly elevated in the DIO mouse liver, but not in ob/ob mice, or in DIO mice treated with leptin antibody. In ob/ob mice, leptin supplementation restored markers of free radical generation. Markers of free radical formation were significantly decreased by the peroxynitrite decomposition catalyst FeTPPS, the iNOS inhibitor 1400W, the NADPH oxidase inhibitor apocynin, or in iNOS or p47 phox-deficient mice. These results correlated with the decreased expression of TNF-alpha and MCP-1. Kupffer cell depletion eliminated oxidative stress and inflammation, whereas in macrophage-depleted mice, the adoptive transfer of leptin-primed macrophages significantly restored inflammation. CONCLUSIONS: These results, for the first time, suggest that leptin action in macrophages of the steatotic liver, through induction of iNOS and NADPH oxidase, causes peroxynitrite-mediated oxidative stress thus activating Kupffer cells.
  • |*Oxidative Stress[MESH]
  • |Animals[MESH]
  • |Cytokines/metabolism[MESH]
  • |Disease Models, Animal[MESH]
  • |Fatty Liver/etiology/*metabolism[MESH]
  • |Inflammation Mediators/metabolism[MESH]
  • |Kupffer Cells/*metabolism/pathology[MESH]
  • |Leptin/*metabolism[MESH]
  • |Male[MESH]
  • |Mice[MESH]
  • |Mice, Inbred C57BL[MESH]
  • |NADPH Oxidases/metabolism[MESH]
  • |Nitric Oxide Synthase Type II/metabolism[MESH]
  • |Non-alcoholic Fatty Liver Disease[MESH]
  • |Obesity/complications[MESH]
  • |Peroxynitrous Acid/metabolism[MESH]





  • *{{pmid23207144}}
    *<b>[http://www.kidney.de/mlpefetch.php?search=23207144 Leptin is key to peroxynitrite-mediated oxidative stress and Kupffer cell activation in experimental non-alcoholic steatohepatitis ]</b> J Hepatol 2013; 58(4) ; 778-84 Chatterjee S; Ganini D; Tokar EJ; Kumar A; Das S; Corbett J; Kadiiska MB; Waalkes MP; Diehl AM; Mason RP

        *23207144*

    Nephropedia PMID record

    Deutsche Wikipedia - im Artikel

    Hier den unten stehenden Textblock hineinkopieren

    J Hepatol

    778 4.58 2013