Serum gastrin has been measured by radioimmunoassay in normal subjects and patients with proven duodenal ulcer in response to insulin hypoglycaemia in conjunction with manoeuvres to decrease the intragastric acidity. Insulin hypoglycaemia alone caused a rise in the serum gastrin level from 5 ± 1·0 to 49 ± 2·9 pg/ml in duodenal ulcer and from 17 ± 5·6 to 42 ± 7·7 pg/ml in normals. With complete intragastric neutralization of acid and the same stimulus, the rise in duodenal ulcer was from 5 ± 1·3 to 128 ± 13·6 pg/ml and in normals from 13 ± 2·6 to 84 ± 2·6 pg/ml.
These studies suggest an increased production rate of gastrin in response to vagal stimulation in duodenal ulcer, and indicate the precise role of acid inhibition in the control of gastrin release and support the concept of both an increased `G cell' mass and parietal cell mass in duodenal ulcer. They have also offered an explanation of the variable vagal stimulation of gastrin release in normal subjects.
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Part II Effect of insulin hypoglycaemia
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