Author(s): Weaver DC, McDaniel ML, Lacy PE, Weaver DC, McDaniel ML, Lacy PE
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Abstract Alloxan inhibits subsequent glucose-induced insulin release from isolated rat islets of Langerhans maintained in vitro. Several agents (D-glucose, D-mannose, 3-0-methyl-D-glucose, caffeine, and cytochalasin B) when present during the alloxan exposure protect against alloxan inhibition of insulin release. To examine the mechanism of alloxan inhibition, the uptake of [2-14C]alloxan was measured in isolated islets. [2-14C]Alloxan was rapidly accumulated by the islets in a time- and temperature-dependent manner. The radio-activity from islets incubated with [2-14C]alloxan was isolated and shown by thin layer chromatography to comigrate with alloxan and alloxanic acid, an alloxan decomposition product. As no uptake of radioactivity occurred in the presence of medium containing the radioactive decomposition product, it was concluded that alloxan enters the intracellular space of the islet and undergoes a subsequent internal decomposition. Some of the protective agents (3-0-methyl-D-glucose, caffeine, and cytochalasin B) partially inhibited alloxan uptake, whereas others (D-glucose and D-mannose) increased the uptake of alloxan. These and other results suggest that the experimental agents do not provide protection against alloxan inhibition by preventing the entry of alloxan into the intracellular space of the islet. The possibility of D-glucose and alloxan competing for a common binding site on the cell membrane is discussed.
This article was published in Endocrinology
and referenced in Journal of AIDS & Clinical Research