Insulin-induced hypoglycemia stimulates gastric motility in sheep via central vagal excitation, but does not elicit a gastric secretory response.
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Animal data on vagal gastric motility responses are hypothesis-generating; leaves open translation to human dysmotility or diabetes care.
The effect of insulin hypoglycæmia on the motility of the abomasum and rumen has been studied in three sheep prepared with permanent fistulæ of these organs and in a lamb with a denervated pyloric pouch. 2. These experiments have shown that in the sheep, as in the dog and man, the injection of insulin after an initial inhibitory period causes increased gastric motility as a direct consequence of the fall in blood sugar. 3. The effect is dependent upon increased activity of the vagus nerves, since it does not occur in the denervated (vagal) stomach pouch and is inhibited by atropine. 4. It is therefore probable that in the sheep, as in dog and man, hypoglycæmia acts centrally to excite vagal discharge. 5. The absence of a gastric secretory response to insulin in the ruminant suggests therefore that the secretory cells, unlike the musculature, are not under central vagal control.
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K. J. Hill (1954) studied this question.
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