RT Journal Article
SR Electronic
T1 Further Studies on the Metabolism of D-Glucose Anomers in Pancreatic Islets
JF Diabetes
JO Diabetes
FD American Diabetes Association
SP 450
OP 458
DO 10.2337/diab.25.5.450
VO 25
IS 5
A1 Idahl, Lars-Åke
A1 Rahemtulla, Firoz
A1 Sehlin, Janove
A1 Täljedal, Inge-Bert
YR 1976
UL http://diabetes.diabetesjournals.org/content/25/5/450.abstract
AB The α and β anomers of commercially available D-(5-3H) glucose were separated by miniaturized Hudson-Dale procedures based on precipitation with acetic acid. Reflectometric measurements of the reactivity with matrix-bound glucose oxidase showed that the preparations were about 90 per cent pure with respect to anomeric composition. Nonradioactive anomers separated by the same procedures were analyzed by optic polarimetry and gas chromatography. The preparations were about 90 per cent pure with respect to anomeric composition and produced no peaks but D-glucose on trimethylsilylation and chromatography. Microdissected pancreatic islets of noninbred ob/ob-mice exhibited a linear production of 3H2O for three to nine minutes when incubated with 6 mM α-D-(5-3H) glucose, β-D-(5-3H) glucose, or D-(5-3H) glucose in anomeric equilibrium; the three glucose preparations did not differ in their rate of conversion to 3H2O. The rate of 3H2O production increased with glucose concentration (3–21 mM) during incubations for three minutes and, again, there was no evidence for the metabolic activity's being dependent on the anomeric composition of the labeled sugar. When microdissected islets were perifused without glucose and suddenly exposed to 5–6 mM α-D-glucose or β-D-glucose, the concentration of glucose-6-phosphate rose within five minutes and did not differ significantly between experiments with α-D-glucose and β-D-glucose. In the same perifusion experiments, only α-D-glucose caused a pronounced stimulation of insulin secretion, the difference from β-D-glucose being significant. The results indicate that the recognition of glucose as an insulin secretagogue does not only involve metabolism by glucose-6-phosphate. The possible roles of the sorbitol pathway and of hypothetical regulatory sites for the glucose molecule (“receptors”) are briefly discussed.