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