Glucose-induced oscillatory insulin secretion in perifused rat
pancreatic islets and clonal [beta]-cells (hit).
Cunningham, Barbara A., Jude T. Deeney, Cheryl R. Bliss, Barbara E.
Corkey, and Keith Tornheim.
Diabetes and Metabolism Unit, Evans Department of Medicine, and
Department of Biochemistry, Boston University School of Medicine,
Boston, Massachusetts 02118
APStracts 3:0126E, 1996.
Normal insulin secretion is oscillatory in vivo and from groups of
perifused islets. Stimulation of rat islets with different glucose
concentrations gave insulin oscillations of similar period (5-8 min)
but increasing amplitude. It has been assumed that oscillatory
secretion is due to oscillations in intracellular free Ca2+, as seen
in single islets and single pancreatic [beta]-cells. However, when
islets were perifused with diazoxide and high KCl to maintain high
intracellular free Ca2+, insulin oscillations of similar amplitude
and period still occurred on glucose stimulation, though superimposed
on elevated basal secretion. Several likely possibilities for a
diffusible synchronizing factor were tested, including pyruvate,
lactate, ATP, and insulin itself; nevertheless, perifusion with high
concentrations of these did not prevent insulin oscillations. Clonal
pancreatic [beta]-cells (HIT) and dissociated islets also exhibited
oscillatory insulin secretion, but with the 5-8 min period
oscillations superimposed on 15-20 min period oscillations. These
results indicate that the mechanisms for generating and synchronizing
insulin oscillations reside in the [beta]-cell, though the structure
of the islet may modulate the oscillation pattern.
Received 9 April 1996; accepted in final form 17 June 1996.
APS Manuscript Number E178-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996