Differences in the Involvement of Prostanoids from Kupffer Cells in the Mediation of Anaphylatoxin C5a-, Zymosan-, and Lipopolysaccharide-Dependent Hepatic Glucose Output and Flow Reduction
| Autor: | Otto Götze, G. Schlaf, Sabine Pestel, Kurt Jungermann, Henrike L. Schieferdecker |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Lipopolysaccharides
Male medicine.medical_specialty Lipopolysaccharide Kupffer Cells Thromboxane Indomethacin Prostaglandin Complement C5a Pathology and Forensic Medicine chemistry.chemical_compound Internal medicine Escherichia coli medicine Animals Anaphylatoxin Rats Wistar Molecular Biology Cells Cultured Phenylacetates Sulfonamides Kupffer cell Zymosan Hemodynamics Thromboxanes Prostanoid hemic and immune systems Cell Biology Metabolism respiratory system musculoskeletal system Rats Perfusion Glucose medicine.anatomical_structure Endocrinology Liver chemistry Biochemistry Hepatocytes Prostaglandins cardiovascular system lipids (amino acids peptides and proteins) |
| Zdroj: | Laboratory Investigation. 83:1733-1741 |
| ISSN: | 0023-6837 |
| DOI: | 10.1097/01.lab.0000101727.89483.37 |
| Popis: | Various inflammatory stimuli such as anaphylatoxin C5a, zymosan, and lipopolysaccharides (LPSs) have been reported both to enhance glucose output in the perfused rat liver and to induce prostanoid (ie, prostaglandin and thromboxane) release from Kupffer cells, the resident liver macrophages. Because prostanoids can enhance glucose output from hepatocytes, it was the aim of this study to compare the possible roles of prostanoids released after C5a, zymosan, and LPS in the mediation of hepatic glucose output. In perfused livers both C5a and zymosan immediately enhanced glucose output, reduced flow, and induced prostanoid overflow into the hepatic vein, but with different quantities and kinetics. Only the C5a-induced but not the zymosan-induced effects were abrogated by inhibitors of prostanoid signaling as the prostanoid synthesis inhibitor indomethacin and the thromboxane receptor antagonist daltroban. In contrast to C5a and zymosan, LPS had no effect on glucose output, flow rate, or prostanoid overflow. In isolated Kupffer cells, C5a and zymosan induced maximal release of prostaglandins D(2) and E(2) and of thromboxane A(2) within a period of 0 to 2 minutes and 5 to 15 minutes, respectively. In pulse-chase experiments, maximal prostanoid release was already observed after 2 minutes of continuous stimulation with C5a, but only after 10 to 15 minutes of continuous stimulation with zymosan. LPS-dependent prostanoid release was not seen before 1 hour. Thus, even though C5a, zymosan, and LPS induced prostanoid release from Kupffer cells, only C5a quickly regulated hepatic glucose metabolism in a prostanoid-dependent manner (due to the kinetics and quantities of prostanoids released). |
| Databáze: | OpenAIRE |
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