IT HAS BEEN WELL ESTABLISHED that parenteral insulin given in amounts sufficient to lower the blood sugar below 40 to 50 mg% stimulates gastric acid secretion within 1 to 2 hr in the vagally innervated stomach.1,2 Since vagotomy eliminates this response, insulin-induced gastric secretion has been thought to result from hypoglycemic stimulation of a parasympathetic center in the brain. It is not the insulin in itself which affects the central nervous system center, but the critical level of hypoglycemia it produces. The reasons for this conclusion include the observation that the blood sugar must be below 50 mg% to obtain a secretory response. Also, diabetics with high fasting blood sugars (FBS) require a much greater dose of insulin, compared with nondiabetics, to obtain the same critical hypoglycemic level or again the gastric secretory response will not become manifest. Furthermore, regardless of the amount of insulin administered, if the induced