ABSTRACT
Glucose and other metabolizable sugars which elicit insulin release from the β-cell of the pancreatic islet induce repetitive oscillations in the β-cell transmembrane potential. Upon each phasic depolarization are superimposed rapid fluctuations in potential, i.e. ‘action potentials’ or ‘spikes’ which occur as bursts of electrical activity; the duration and frequency of each burst is a function of glucose concentration. These established electrophysiological features of glucose-islet cell interaction are described in detail together with a consideration of their possible molecular and ionic basis. Based on these observations, a dynamic mathematical computer model of the β-cell membrane electrical behaviour is presented which utilizes the Goldman equation extended to include divalent ions. The model illustrates how the ionic mechanisms deduced from experimental observations can account for the electrical patterns produced by the β-cells in the presence of D-glucose; it also allows systematic changes to be made in a number of state variables in order to assess their relative importance and possible contribution to the integrated processes actually observed. Finally, distinction is made between aspects of the model which are well supported by experimental results and those areas which require further analysis.
It should, however, be noted that in some cells (see Brehm & Eckert, 1978) Ca,+ entry lead directly to an inactivation of Ca2+ channels which precedes and is independent of any delayed outward K+ current.
