Glucose has regulatory effects on insulin release also in the virtual absence of extracellular Ca2+.
The glucose effect on insulin release in a Ca(2+)-deficient medium was analyzed in perifusion experiments with aggregates of cells prepared by dispersal of the beta-cell-rich pancreatic islets of ob/ob-mice. Hyperosmolar additions of 20 mM D-glucose or its poorly metabolized transport analogue 3-0-methyl-D-glucose resulted in 50% suppression of the secretory rate. However, after isosmolar additions of the sugars, replacing non-penetrating sucrose, there was a stimulation of insulin release. Whereas D-glucose was less effective than 3-O-methyl-D-glucose in stimulating insulin release after isosmolar addition, the opposite was found for the enhanced secretory response obtained when the sugars were excluded from the perifusion medium. The studies indicate that D-glucose has regulatory actions on insulin release also in the virtual absence of extracellular Ca2+. This effect is not only due to osmolar influences but involves also direct suppression of the secretory activity probably mediated by the metabolism of the sugar.
Berts
A
A
Department of Medical Cell Biology, University of Uppsala, Sweden.
Lund
P E
PE
Dryselius
S
S
Hellman
B
B
D019325:3-O-Methylglucose; D000818:Animals; D002118:Calcium / Q000502:physiology*; D005947:Glucose / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D008757:Methylglucosides / Q000494:pharmacology; D051379:Mice; D008820:Mice, Obese; D010477:Perfusion
D007328:Insulin; D008757:Methylglucosides; D019325:3-O-Methylglucose; D005947:Glucose; D002118:Calcium