Gastric acid, plasma gastrin, and somatostatin responses to feeding and exogenous gastrin alone and in combination in conscious cats

Abstract

Meat in the stomach or duodenum potentiates pentagastrin-induced acid secretion in cats, presumably by a humoral mechanism. In the present study on cats, a meat meal significantly augmented the maximal acid response from a Heidenhain pouch (HP) to pentagastrin or to human synthetic gastrin I by 31 and 30%, respectively. The maximal HP acid response to pentagastrin was augmented also by peptone instilled into the stomach through a gastric fistula. Intravenous infusion of amino acids stimulated acid secretion but did not augment the maximal acid response to pentagastrin. The plasma concentrations of gastrin and somatostatin increased during infusion of pentagastrin and gastrin I and were not further altered by simultaneous feeding. The present results indicate that the mechanism for potentiation of gastrin-induced acid secretion is of physiological significance, since feeding augmented also the acid response to heptadecapeptide gastrin, the only gastrin secreted from the antrum and duodenum in cats. The potentiation of acid secretion is not dependent on the vagal excitation induced by oral feeding, since potentiation was demonstrated also by intragastric peptone instillation. The mechanism for the potentiation is not due to absorbed amino acids or a decrease of plasma somatostatin.

Antrum participates in the postprandial augmentation of the acid response to exogenous gastrin in conscious cats

“…The lack of potentiation after antrectomy, duodenal exclusion and gastrojejunostomy demonstrates that meat in the jejunum does not potentiate the acid response to pentagastrin in cats, even in the presence of bile and pancreatic juice. It also supports our previous conclusion (Fernstrom et al 1987) that the potentiation is not caused by absorbed amino acids.…”

“…denostomy ( In conclusion, the present study on cats has demonstrated that the HP acid, plasma gastrin and somatostatin responses to feeding were abolished after antrectomy and duodenal exclusion. The present and previous (Fernstrom et al 1984, 1987, Fernstrom & Emds 1985) studies on cats suggest a postprandial mechanism that potentiates the maximal acid, but not the pepsin response to pentagastrin. The mechanism is localized in the antrum and duodenum (Fernstrom et al 1984) and activated by protein-rich food such as a meat or peptone meal (Fernstrom et al 1987).…”

“…The present and previous (Fernstrom et al 1984, 1987, Fernstrom & Emds 1985) studies on cats suggest a postprandial mechanism that potentiates the maximal acid, but not the pepsin response to pentagastrin. The mechanism is localized in the antrum and duodenum (Fernstrom et al 1984) and activated by protein-rich food such as a meat or peptone meal (Fernstrom et al 1987). It is probably a hormonal mechanism, not caused by absorbed amino acids, nor by a decrease in plasma somatostatin (Fernstrom et al.…”

“…The mechanism for somatostatin release is not fully known. In a previous study on cats with normal gastro-intestinal continuity, the plasma somatostatin response to gastrin-17, pentagastrin or feeding seemed to be related to the plasma gastrin concentration, and it was suggested that somatostatin is released by endogenous and exogenous gastrin (Fernstrom et al 1987). Antrectomy with duodenal exclusion abolished both the postprandial somatostatin and gastrin responses, which suggests a release of somatostatin by endogenous gastrin.…”