AJP - GI Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Gastrointest Liver Physiol 267: G227-G234, 1994;
0193-1857/94 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Hernandez, I.
Right arrow Articles by Chacin, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hernandez, I.
Right arrow Articles by Chacin, J.

AJP - Gastrointestinal and Liver Physiology, Vol 267, Issue 2 227-G234, Copyright © 1994 by American Physiological Society


ARTICLES

Mechanism of cholinergic stimulation of glucose oxidation in isolated gastric glands

I. Hernandez and J. Chacin
Laboratorio de Investigaciones Gastrointestinales, Facultad de Medicina, Universidad del Zulia, Maracaibo, Venezuela.

The mechanisms of cholinergic activation of carbohydrate metabolism were investigated in isolated rabbit gastric glands. Carbachol stimulated the rate of glucose oxidation in a dose-dependent fashion with a half-maximal effect occurring at approximately 9 microM. Atropine and omeprazole, but not cimetidine, completely blocked the stimulation induced by carbachol. Direct activation of the H(+)-K(+)-adenosinetriphosphatase by NH+4 caused a significant stimulation of glucose oxidation that was totally abolished by oligomycin and by the mitochondrial uncouplers dinitrophenol and carbonyl cyanide p-trifluoromethoxyphenylhydrazone. These latter agents did not abolish the stimulating effect of carbachol on glucose oxidation. Ionomycin increased the rate of glucose oxidation in a dose-dependent manner, and this effect was not blocked by oligomycin. The metabolic effect of ionomycin was reduced but not abolished by omeprazole. 1,2-Bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester eliminated the carbachol-induced stimulation of glucose oxidation and partially inhibited the effect of NH+4. The mitochondrial enzymes pyruvate dehydrogenase and oxoglutarate dehydrogenase were activated by physiological concentrations of calcium in the isolated mitochondria. This effect was blocked by incubation with ruthenium red.(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
Exp. Biol. Med.Home page
I. Hernandez-Rincon, M. Olguin-Martinez, and R. Hernandez-Munoz
Enhanced Intracellular Calcium Promotes Metabolic and Secretory Disturbances in Rat Gastric Mucosa during Ethanol-Induced Gastritis
Experimental Biology and Medicine, March 1, 2003; 228(3): 315 - 324.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online