Gastric and Extragastric Gastrin Release in Normal Subjects, in Duodenal Ulcer Patients, and in Patients With Partial Gastrectomy (Billroth I)

Fritsch, W.-P.; Hausamen, T.-U.; Rick, Wirnt

doi:10.1016/s0016-5085(76)80540-9

Cited by 33 publications

(4 citation statements)

References 21 publications

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“…The modest rise in plasma gastrin levels after intraduodenal infusion of protein, but not fat or carbohydrate is in keeping with previous reports of gastrin release following bolus infusion of homogenized meals into the duodenum of man (Fritch et al, 1970) and Blair et al (1 978) state that protein digestion products probably account for this elevation. Similarly, the observation that intraduodenal protein stimulates release of insulin into the systemic circulation is in keeping with the studies using intraduodenal infusion of mixed amino acid solutions in man (Thomas et af., 1978).…”

Section: Discussionsupporting

confidence: 89%

Response of Circulating Somatostatin, Insulin, Gastrin and Gip, to Intraduodenal Infusion of Nutrients in Normal Man

Lucey

Fairclough

Wass

et al. 1984

Clinical Endocrinology

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We have studied the effect of direct infusion of nutrients into the duodenum of normal subjects on circulating plasma somatostatin, insulin, gastrin and gastric inhibitory polypeptide (GIP) levels. Six normal subjects were given on four separate occasions 150 ml of isotonic solutions containing 100 calories of carbohydrate, protein, or fat, and a control solution of saline, by infusion into the second part of the duodenum. Plasma somatostatin rose slightly after carbohydrate, mean basal 30 +/- 3 pg/ml, peak 46 +/- 16 pg/ml at 15 min; and more markedly after protein, peak 57 +/- 9 pg/ml at 30 min. However, fat was the most potent intraduodenal stimulus to plasma somatostatin release into circulation, peak 101 +/- 11 pg/ml at 30 min. The plasma insulin rise was greatest after carbohydrate, peak 68 +/- 10 i.u., but there was a significant rise after protein also, peak 34 +/- 6 i.u. Plasma gastrin rose significantly after protein only, peak 70 +/- 22 pg/ml. Plasma GIP rose markedly after carbohydrate, basal 506 +/- 50 pg/ml, peak 1480 +/- 120 pg/ml. Protein was also a potent stimulus of circulating plasma GIP release, peak 1200 +/- 190 pg/ml, while fat was the least potent, peak 730 +/- 190 pg/ml. Thus, calorie for calorie, fat is the most potent intraduodenal nutrient stimulus of circulating somatostatin. We postulate therefore that somatostatin may be an enterogastrone--a circulating hormone released by intraduodenal fat which inhibits gastric acid secretion. Fat is the least potent intraduodenal nutrient stimulus of circulating GIP release. This is evidence against the hypothesis that circulating GIP acts as an enterogastrone.

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Section: Discussionsupporting

confidence: 89%

Response of Circulating Somatostatin, Insulin, Gastrin and Gip, to Intraduodenal Infusion of Nutrients in Normal Man

Lucey

Fairclough

Wass

et al. 1984

Clinical Endocrinology

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“…In the present study a meat meal failed to stimulate a significant rise in serum gastrin levels following antrectomy with either BI or,BIl anastomosis. The results are in agreement with those of Way et al [3] and Booth et al [8], but are at variance with those of Sjodin and Nilsson [9] in the dog, and both Stern and Walsh [10] and Fritsch et al [11] in humans. The latter workers found evidence for significant release of duodenal gastrin in humans.…”

Section: Dogssupporting

confidence: 91%

Studies on the release of extra‐antral gastrin evidence of vagal inhibition in the dog

Bhattacherjee

Psaila

et al. 1977

World j. surg.

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Serum gastrin concentration was measured in 3 dogs after a meat meal; basal levels rose significantly after 10 minutes. After antrectomy with a Billroth I, and later a Billroth II anastomosis, the tests were repeated. Basal gastrin levels were unchanged but the rise after meat feeding was abolished. Four antrectomized dogs with a BII anastomosis and cannulae in both the duodenum and stomach were used to examine the effect of duodenal perfusion on serum gastrin. Whether the perfusate was 150 mM NaCl, 150 mM HCl or 0.1% acetylcholine, the mean serum gastrin levels did not differ significantly from basal levels. Transthoracic vagotomy in antrectomized dogs produced a significant rise in basal gastrin levels, but did not restore the response to a meat meal or duodenal perfusion.Parallel studies were conducted in 6 antrectomized, vagotomized patients who had undergone Roux‐en‐Y conversion for postgastrectomy bilious vomiting, and in 2 patients after total gastrectomy. Duodenal perfusion via duodenostomy tubes with 150 mM NaCl, 150 mM HCl, fat emulsion, and an amino acid mixture did not raise serum gastrin above basal levels.Since meat feeding and duodenal perfusion in antrectomized dogs and humans failed to stimulate a rise in serum gastrin, we conclude that the intestinal phase of gastric secretion is unlikely to be mediated by gastrin. The results following vagotomy in the dog suggest that extragastric basal gastrin release is vagally inhibited or that vagotomy interferes with the catabolic destruction of gastrin.

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“…Frifsch el al. (2) found that food stimulation caused a rise in serum gastrin after BI resection but that the rise was much lower and with a marked delay as compared to normal subjects. Possible explanations of the contradictory results might be differences in the intragastric pH.…”

Section: Discussionmentioning

confidence: 91%

Gastrin Production Following Antrectomy

Nielsen

Lauritsen

Hansen

et al. 1983

Acta Pathologica Microbiologica Scandinavica Series A :Patholog

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Fifteen patients were studied 3 to 35 years after antrectomy, with a gastroduodenal (Billroth I (BI)) anastomosis in 8, and a gastrojejunal (Billroth II (BII)) anastomosis in 7. The investigations included gastric acid secretion, serum gastrin response to feeding and immunohistochemical search for gastrin‐producing cells in gastric remnant mucosal biopsies. All of the patients had hypochlorhydria. The gastrin response to feeding was minimal. Apart from a significantly higher value of serum gastrin 3 hours post‐prandial in BI operated as compared to BII operated patients, no greater differences were found in the gastrin production between the two groups of patients. No gastrin‐producing cells could be identified in the gastric remnant, not even in areas of pseudopyloric metaplasia. It is concluded that the gastrin production following antrectomy is caused by extragastric G‐cells; these cells are poorly stimulated by food, and do not respond to hypochlorhydria with hypergastrinaemia.

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Gastric and Extragastric Gastrin Release in Normal Subjects, in Duodenal Ulcer Patients, and in Patients With Partial Gastrectomy (Billroth I)

Cited by 33 publications

References 21 publications

Response of Circulating Somatostatin, Insulin, Gastrin and Gip, to Intraduodenal Infusion of Nutrients in Normal Man

Response of Circulating Somatostatin, Insulin, Gastrin and Gip, to Intraduodenal Infusion of Nutrients in Normal Man

Studies on the release of extra‐antral gastrin evidence of vagal inhibition in the dog

Gastrin Production Following Antrectomy

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