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Metabolic deviation of mouse liver by RhIL1-alpha or RhTNF/cachectin.

Metabolic deviation of mouse liver by RhIL1-alpha or RhTNF/cachectin. Research Abstract Details 

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  • Metabolic deviation of mouse liver by RhIL1-alpha or RhTNF/cachectin. Abstract Text:

    k imamuraK Imamura,z wangZ Wang,k murayama-odaK Murayama-Oda,h k kimH K Kim,t tanakaT Tanaka,

    In this work deviation of liver metabolism by cytokines, especially recombinant human interleukin 1-alpha (rhIL1-alpha), was investigated. Administration of rhIL1-alpha or recombinant human tumor necrosis factor (rhTNF/cachectin) to normal mice resulted in rapid, dose-dependent induction of high liver ornithine decarboxylase (ODC) activity. The effects of these cytokines on liver ODC were not indirect effects mediated by eicosanoids. The induction of liver ODC by rhIL1-alpha was at least partly a direct effect on hepatocytes, and was due to increase in de novo synthesis of the enzyme protein after increase in ODC mRNA. No specific protein was required for increase in the level of ODC-mRNA. On IL1 treatment, actinomycin D caused superinduction of liver ODC, which was at least partly due to increased stability of the ODC enzyme, because actinomycin D doubled the apparent half-life (from 50 to 95 min). Daily administration of 2 x 10(3) U of rhIL1-alpha to mice for 3 days also caused decrease in the level of the differentiated type of pyruvate kinase isozyme (PK-L) and marked increase in that of the prototype isozyme (PK-M2) in the liver, but did not cause significant change in the isozyme patterns of the kidney, thymus, and spleen. RhIL1-alpha also induced hypertrophy of the spleen. These results indicate that rhIL1-alpha causes metabolic deviation of the liver similar to that in tumor-bearing hosts.

    Metabolic deviation of mouse liver by RhIL1-alpha or RhTNF/cachectin. Publishing Authors By Initials

    k imamuraK Imamura,z wangZ Wang,k murayama-odaK Murayama-Oda,hk kimHK Kim,t tanakaT Tanaka,

    For similar peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research

    PUBMED ID PMID:

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    Metabolic deviation of mouse liver by RhIL1-alpha or RhTNF/cachectin. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of biochemistry

    VOLUME: 109

    Page Numbers: 507-13

    Journal Abbreviation: J. Biochem.

    ISSN: 0021-924X

    DAY: 19

    MONTH: Apr

    YEAR: 1991

    Metabolic deviation of mouse liver by RhIL1-alpha or RhTNF/cachectin. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 376600

    Metabolic deviation of mouse liver by RhIL1-alpha or RhTNF/cachectin. Keywords Mesh Terms:

    KEYWORDS: Tumor Necrosis Factor-alpha

    MESH TERMS: pharmacology

    Chemical & Substance for Abstract: Metabolic deviation of mouse liver by RhIL1-alpha or RhTNF/cachectin. Information

    Substance Name: Ornithine Decarboxylase

    Registry Number: EC 4.1.1.17

    Grant and Affiliation Information for Metabolic deviation of mouse liver by RhIL1-alpha or RhTNF/cachectin.

    AFFILIATION: Department of Nutrition and Physiological Chemistry, Osaka University Medical School.

    Country: JAPAN

    JAPAN Research PublicationJAPAN Research Publication

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    MEDLINETA: J Biochem

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