Fasting-induced dissociation of cationic and secretory events in pancreatic islets.
In pancreatic islets removed from 48 h-fasted rats, as distinct from fed animals, the release of insulin evoked by D-glucose is more severely impaired than that evoked by 2-ketoisocaproate. This decreased secretory response to D-glucose contrasts with an unimpaired cationic response to the sugar in terms of the glucose-induced decrease in both 86Rb and 45Ca outflow from pre-labelled islets. Likewise, fasting only causes a modest decrease of the secondary rise in 45Ca outflow evoked by D-glucose in islets perifused at normal Ca2+ concentration. The latter decrease appears more marked, however, if the cationic response to glucose is expressed relative to that evoked by 2-ketoisocaproate in islets removed from rats in the same nutritional state. It is concluded that, in the process of nutrient-stimulated insulin release, neither the decrease in K+ conductance (inhibition of 86Rb outflow) nor the sequestration of Ca2+ by intracellular organelles and/or direct inhibition of Ca2+ outward transport (decrease in 45Ca outflow) represent the sole determinant(s) of the subsequent gating of Ca2+ channels (secondary rise in 45Ca efflux).
D000818:Animals; D002132:Calcium Radioisotopes; D002413:Cations, Divalent / Q000378:metabolism*; D004533:Egtazic Acid / Q000494:pharmacology; D005215:Fasting; D005947:Glucose / Q000494:pharmacology; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D007651:Keto Acids / Q000494:pharmacology; D011868:Radioisotopes; D051381:Rats; D011919:Rats, Inbred Strains; D012413:Rubidium; D013997:Time Factors
D002132:Calcium Radioisotopes; D002413:Cations, Divalent; D007328:Insulin; D007651:Keto Acids; D011868:Radioisotopes; D004533:Egtazic Acid; C013082:alpha-ketoisocaproic acid; D005947:Glucose; D012413:Rubidium