Glucose-induced inhibition: how many ionic mechanisms?
Version of Record online: 15 MAY 2009
© 2009 The Authors. Journal compilation © 2009 Scandinavian Physiological Society
Special Issue: 16TH ACTA PHYSIOLOGICA INTERNATIONAL SYMPOSIUM ‘10 YEARS OF HYPOCRETINS/OREXINS-PHYSIOLOGY AND PATHOPHYSIOLOGY’
Volume 198, Issue 3, pages 295–301, March 2010
How to Cite
Burdakov, D. and Lesage, F. (2010), Glucose-induced inhibition: how many ionic mechanisms?. Acta Physiologica, 198: 295–301. doi: 10.1111/j.1748-1716.2009.02005.x
- Issue online: 28 JAN 2010
- Version of Record online: 15 MAY 2009
- Received 30 March 2009, revision requested 22 April 2009, revision received 24 April 2009, accepted 24 April 2009
Sensing of sugar by specialized ‘glucose-inhibited’ cells helps organisms to counteract swings in their internal energy levels. Evidence from several cell types in both vertebrates and invertebrates suggests that this process involves sugar-induced stimulation of plasma membrane K+ currents. However, the molecular composition and the mechanism of activation of the underlying channel(s) remain controversial. In mouse hypothalamic neurones and neurosecretory cells of the crab Cancer borealis, glucose stimulates K+ currents displaying leak-like properties. Yet knockout of some of the candidate ‘leak’ channel subunits encoded by the KCNK gene family so far failed to abolish glucose inhibition of hypothalamic cells. Moreover, in other tissues, such as the carotid body, glucose-stimulated K+ channels appear to be not leak-like but voltage-gated, suggesting that glucose-induced inhibition may engage multiple types of K+ channels. Other mechanisms of glucose-induced inhibition, such as hyperpolarization mediated by opening of Cl− channels and depolarization block caused by closure of KATP channels have also been proposed. Here we review known ionic and pharmacological features of glucose-induced inhibition in different cell types, which may help to identify its molecular correlates.