Abstract
Powerful vagal stimulation of gastric secretion was produced in dogs by the administration of 50–200 mg/kg 2-deoxy-d-glucose (2-DG) The secretion could be entirely prevented or immediately abolished by atropine injection, indicating one link which is apparently cholinergic. Studies with glucose, mannose, fructose, galactose, or 3-O-methylglucose injected before or subsequent to the administration of 2-DG indicated that the vagal secretory center is specifically glucose and mannose dependent. 2-DG appears to act by the formation of nonmetabolized 2-DG-6-phosphate resulting in effective cytoglucopenia. While apparently stimulating gastric secretion in the same way as insulin hypoglycemia, 2-DG appears to have definite advantages of reliability and reproducibility. The vagal center appears to be dose responsive and not an all-or-none system, and stimulates all elements of gastric secretion by a single pathway.
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