GLUCOSE-6-PHOSPHATE AND CA2+ SEQUESTRATION ARE MUTUALLY ENHANCED IN MICROSOMES FROM LIVER, BRAIN, AND HEART

Citation
Py. Chen et al., GLUCOSE-6-PHOSPHATE AND CA2+ SEQUESTRATION ARE MUTUALLY ENHANCED IN MICROSOMES FROM LIVER, BRAIN, AND HEART, Diabetes, 47(6), 1998, pp. 874-881
Citations number
44
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00121797
Volume
47
Issue
6
Year of publication
1998
Pages
874 - 881
Database
ISI
SICI code
0012-1797(1998)47:6<874:GACSAM>2.0.ZU;2-A
Abstract
Microsomes prepared from three rat tissues were examined for their abi lity to import glucose-6-phosphate (G-6-P). Microsomes from liver, whi ch possess a high level of glucose-6-phosphatase activity, mere compar ed with those from cerebral cortex and cardiac muscle, which are not i nvolved in the export of glucose and in which glucose-6-phosphatase ac tivity is relatively low In all three, a selective permeability to G-6 -P was detected by light scattering. However, the sugar-phosphate spec ificity of the transport process differed. G-6-P was able to enhance A TP-dependent Ca2+ sequestration in all three types of microsomes, In a ddition, enzymatic detection of G-6-P after the rapid filtration of mi crosomes determined that, in the absence of Ca2+ and ATP, a level of i ntramicrosomal G-6-P approaching a passive equilibrium with the extram icrosomal G-6-P concentration was rapidly achieved in all three tissue s. However under conditions in which Ca2+ was being actively accumulat ed, the intramicrosomal levels of G-6-P exceeded the equilibrium value by three-to fourfold. This enhanced sequestration was not observed in the presence of Ca2+ or ATP alone or in the presence of a Ca2+ ionoph ore or an inhibitor of the microsomal Ca2+ ATPase. These data are cons istent with a selective import pathway into the endoplasmic/sarcoplasm ic reticulum for G-6-P independent of glucose-g-phosphatase activity. In addition, they suggest an alternate explanation for the enhanced se questration of Ca2+ by the endoplasmic/sarcoplasmic reticulum of intac t cells seen when extracellular glucose is increased.