The coupling of metabolic to secretory events in pancreatic islets: effects of 2-cyclohexene-1-one upon GSH content and secretory behaviour |
| |
| Authors: | A Sener S P Dufrane W J Malaisse |
| |
| Affiliation: | 1. School of Economics and Management, Beijing University of Technology, Beijing 100124, China;2. Institute of Automation, Chinese Academy of Sciences, Beijing 100000, China;1. Faculty of Earth and Life Sciences, VU University Amsterdam (VUA), Amsterdam, Netherlands;2. Transmissivity B.V./VanderSat, Space Technology Centre, Noordwijk, Netherlands;3. Centre d''Etudes Spatiales de la Biosphere (CESBIO), Toulouse, France;4. INRA, UMR1391 ISPA, Villenave d''Ornon, France;5. School of Civil and Environmental Engineering, University of New South Wales, Sydney, Australia;6. European Space Research Institute (ESRIN), ESA, Frascati, Italy;7. European Space Research and Technology Centre (ESTEC), ESA, Noordwijk, Netherlands;1. EquiNew Therapy LLC, River Falls, WI;2. Steele and Associates, Vernon, NY |
| |
| Abstract: | The GSH content and GSH/GSSG ratio were decreased in rat pancreatic islets exposed to 2-cyclohexene-1-one (CHX; 1.0 mM), but the drug failed to affect the cytosolic NADH/NAD+ and NADPH/NADP+ ratios. This coincided with inhibition of D-glucose oxidation, whilst the oxidation of L-leucine and L-glutamine was little affected by CHX (1.0 mM). The release of insulin evoked by either D-glucose or 2-ketoisocaproate was inhibited by CHX (1.0 mM), whereas such was not the case for insulin secretion induced by L-leucine, alone or in combination with L-glutamine. The latter amino acid protected the B-cell against the inhibitory action of CHX upon glucose-stimulated insulin release. CHX severely altered the normal relationship between nutrient oxidation, [45Ca] net uptake and insulin release. Since CHX also inhibited insulin release evoked by non-nutrient secretagogues, it is speculated that GSH may be involved in several cytophysiological processes including the control of glycolysis, intracellular calcium distribution, and responsiveness to this cation of Ca2+-sensitive targets. |
| |
| Keywords: | |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
