Measurement of blood cortisol and acid output in patients with duodenal ulceration and normal subjects during insulin hypoglycaemia.
The blood cortisol and gastric acid responses to insulin hypoglycaemia were investigated in 18 healthy control subjects and 14 patients with endoscopically proven duodenal ulceration. In both controls and patients, insulin hypoglycaemia caused blood cortisol and acid output to rise and peak simultaneously, the rises being significantly greater in patients with duodenal ulcer than in control subjects. The peak acid output and the base to peak cortisol increments were also found to be significantly greater in patients with duodenal ulcer than in control subjects (P less than 0.001 and P less than 0.005 respectively). We conclude that insulin hypoglycaemia causes stimulation of the sympathetic and parasympathetic nervous systems and of the hypothalamo-pituitary-adrenal axis, resulting in the simultaneous elevation of gastric juice acidity and blood cortisol levels. We have shown that synchronous rises in gastric acid and blood cortisol occur during insulin hypoglycaemia and that these rises are greater in patients with duodenal ulcer.
D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D004381:Duodenal Ulcer / Q000503:physiopathology*; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005750:Gastric Juice / Q000032:analysis; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D007003:Hypoglycemia / Q000139:chemically induced / Q000503:physiopathology*; D007328:Insulin; D008297:Male; D008875:Middle Aged; D012907:Smoking; D013997:Time Factors
D001786:Blood Glucose; D007328:Insulin; D006854:Hydrocortisone