J Physiol Boston Smyposia
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Physiol Vol 246, Issue 2 pp 459-478
Copyright © 1975 by The Physiological Society
This Article
Right arrow Full Text (PDF)
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dean, P M
Right arrow Articles by Sakamoto, Y
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dean, P M
Right arrow Articles by Sakamoto, Y

Pancreatic islet cells: effects of monosaccharides, glycolytic intermediates and metabolic inhibitors on membrane potential and electrical activity.

 P M Dean, E K Matthews and Y Sakamoto

1. The effects of monosaccharides, glycolytic intermediates, metabolic inhibitors and anxia, have been studied on the membrane electrical activity of mouse pancreatic islet cells in vitro using a single intracellular micro-electrode for both voltage recording and current injection. 2. In addition to D-glucose (28mM), D-mannose (16-6mM), and L-leucin (10mM), the substances D-glyceraldehyde (11mM), and acetoacetate (20 mM), induced action potentials in islet cells but other glucos analogues and metabolic intermediates including L-glucose dod not. 3. Mannoheptulose 20 mM), but not D-galactose or 2-deoxy-D-glucose, antagonized the electrical activity induced in islet cells by D-glucose, 28mM. Prior treatment of the cells with mannoheptulose caused them to hyperpolarize and completely prevented the appearance of electrical activity on subsequent exposure to D-glucose. 4. Electrical activity induced by D0glucose 28mM, was progressively inhibited by phloridzin, 10mM, if the cells were exposed to D-glucose and inhibitor simultaneously, and abolished on pretreatment with inhibitor for 30-60 min. Phloridzin also caused depolarization of the islet cells which was independent of extracellular glucose. 5. Anoxia completely blocked the electrical activity induced by glucose but not that evoked by D-glyceraldehyde, L-leucine, tolbutamide or glibenclamide. 6. Iodoacetic acid, 5 mM, rapidly blocked glucose-induced electrical activity whilst that elicited by tolbutamide was relatively resistant to inhibition. 7. The nature and possible location of the glucoreceptor in pancreatic islet cells is discussed in relation to the origin and functional significance of glucose-induced electrical activity and insulin secretion.




This article has been cited by other articles:


Home page
 DiabetesHome page
X.-J. Yang, L.-M. Kow, D. W. Pfaff, and C. V. Mobbs
Metabolic Pathways That Mediate Inhibition of Hypothalamic Neurons by Glucose
Diabetes, January 1, 2004; 53(1): 67 - 73.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
L. A. Fahien and M. J. MacDonald
The Succinate Mechanism of Insulin Release
Diabetes, September 1, 2002; 51(9): 2669 - 2676.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
M.-t. Liu, S. Seino, and A. L. Kirchgessner
Identification and Characterization of Glucoresponsive Neurons in the Enteric Nervous System
J. Neurosci., December 1, 1999; 19(23): 10305 - 10317.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1975 The Physiological Society.