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J. Biol. Chem., Vol. 269, Issue 45, 27787-27790, 11, 1994
LH Philipson, MP Rosenberg, A Kuznetsov, ME Lancaster, JF Worley 3rd, MW Roe and ID Dukes
Glucose stimulation of pancreatic beta-cell insulin secretion is closely
coupled to alterations in ion channel conductances and intracellular Ca2+
([Ca2+]i). To further examine this relationship after augmentation of
voltage-dependent K+ channel expression, transgenic mice were produced
which specifically overexpress a human insulinoma-derived,
tetraethylammonium (TEA)-insensitive delayed rectifier K+ channel in their
pancreatic beta-cells as shown by immunoblot of isolated islets and
immunohistochemical analysis of pancreas sections. Whole-cell current
recordings confirmed the presence of high amplitude TEA-resistant K+
currents in transgenic islet cells, whose expression correlated with
hyperglycemia and hypoinsulinemia. Stable overexpression of the channel in
insulinoma cells attenuated glucose-activated increases in [Ca2+]i and
prevented the induction of TEA-dependent [Ca2+]i oscillations. These
results, employing the first ion channel transgenic mouse, demonstrate the
importance of membrane potential regulation in excitation-secretion
coupling in the pancreatic beta-cell.
Delayed rectifier K+ channel overexpression in transgenic islets and beta-cells associated with impaired glucose responsiveness
Department of Medicine, University of Chicago, Illinois 60637.
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