Succinic acid monomethyl ester protects rat pancreatic islet secretory potential against interleukin-1β (IL-1β) without affecting glutamate decarboxylase expression or nitric oxide production
| Autor: | Willy Malaisse, Decio L. Eizirik, Licio A. Velloso, Nils Welsh, Audrey Niemann |
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| Jazyk: | angličtina |
| Předmět: |
Male
medicine.medical_specialty Carboxy-lyases Succinate ester Glutamate decarboxylase Biophysics Biology Biochemistry Aconitase Nitric oxide Rats Sprague-Dawley Pancreatic islet chemistry.chemical_compound Islets of Langerhans Diabetes mellitus Biosynthesis Structural Biology Internal medicine Insulin Secretion Genetics medicine Animals Insulin Molecular Biology Aconitate Hydratase Glutamic acid decarboxylase geography geography.geographical_feature_category Glutamate Decarboxylase Pancreatic islets Succinates Cell Biology Islet Interleukin-1β Recombinant Proteins Rats Endocrinology medicine.anatomical_structure Glucose chemistry Succinic acid Interleukin-1 |
| Zdroj: | FEBS Letters. (3):298-302 |
| ISSN: | 0014-5793 |
| DOI: | 10.1016/0014-5793(94)80213-0 |
| Popis: | Rat pancreatic islets exposed to interleukin-1 beta (IL-1 beta) in the presence of succinic acid monomethyl ester (SAM) have a higher insulin release in response to glucose and higher glucose oxidation rates, as compared to islets exposed to IL-1 beta alone. These beneficial effects of SAM were not accompanied by any decrease in IL-1 beta-induced nitric oxide (NO) production nor inhibition of aconitase activity. Moreover, SAM did not increase biosynthesis of glutamate decarboxylase. SAM apparently improves beta-cell function mostly by increasing the capacity of these cells to endure NO exposure and partial blockage of the Krebs cycle. |
| Databáze: | OpenAIRE |
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