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Fasting‐induced dissociation of cationic and secretory events in pancreatic islets
Author(s) -
Carpinelli A. R.,
Mathias P. C. F.,
LeclercqMeyer V.,
Malaisse W. J.
Publication year - 1986
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.290040208
Subject(s) - medicine , endocrinology , pancreatic islets , chemistry , islet , insulin , intracellular , biology , biochemistry
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 86 Rb and 45 Ca outflow from pre‐labelled islets. Likewise, fasting only causes a modest decrease of the secondary rise in 45 Ca outflow evoked by D ‐glucose in islets perifused at normal Ca 2+ 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 86 Rb outflow) nor the sequestration of Ca 2+ by intracellular organelles and/or direct inhibition of Ca 2+ outward transport (decrease in 45 Ca outflow) represent the sole determinant(s) of the subsequent gating of Ca 2+ channels (secondary rise in 45 Ca efflux).