Zymosan-induced changes in glucose release and fatty acid oxidation in the perfused rat liver
Autor: | Alice M. Derbocio, Renata B. D'Avila, Ana Maria K. Bracht, Silvana Martins Caparroz-Assef, Emy Luiza Ishii-Iwamoto, Jorgete Constantin |
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Rok vydání: | 2000 |
Předmět: |
chemistry.chemical_classification
medicine.medical_specialty Glycogenolysis Health Toxicology and Mutagenesis Zymosan Fatty acid Endogeny Stimulation General Medicine Biology Toxicology Biochemistry chemistry.chemical_compound Endocrinology chemistry Gluconeogenesis Internal medicine Ketogenesis medicine Molecular Medicine Molecular Biology Beta oxidation |
Zdroj: | Journal of Biochemical and Molecular Toxicology. 14:252-261 |
ISSN: | 1099-0461 1095-6670 |
DOI: | 10.1002/1099-0461(2000)14:5<252::aid-jbt4>3.0.co;2-6 |
Popis: | The aim of the present study was to investigate the actions of zymosan on glucose release and fatty acid oxidation in perfused rat livers and to determine if Kupffer cells and Ca2+ ions are implicated in these actions. Zymosan caused stimulation of glycogenolysis in livers from fed rats. In livers from fasted rats zymosan caused gradual inhibition of glucose production and oxygen consumption from lactate plus pyruvate. Ketogenesis, oxygen consumption, and [14C-]-CO2 production were inhibited by zymosan when the [1-14C]-palmitate was supplied exogenously. However, ketogenesis and oxygen consumption from endogenous sources were not inhibited. An interference with substrate-uptake by the liver may be the cause of the changes in gluconeogenesis and oxidation of fatty acids from exogenous sources. The pretreatment of the rats with gadolinium chloride and the removal of Ca2+ ions did not suppress the effects of zymosan on glucose release, a finding that argues against the participation of Kupffer cells or Ca2+ ions in the liver responses. The hepatic metabolic changes caused by zymosan could play a role in the systemic metabolic alterations reported to occur after in vivo zymosan administration. |
Databáze: | OpenAIRE |
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