Importance of dietary amines in meal-induced gastrin release

Abstract

The dietary chemical constituents responsible for initiating the gastrin secretory response to a meal have yet to be identified. The evidence supporting the importance of dietary amino acids in the initiation of the postprandial release of gastrin is both conflicting and unconvincing. In this study we investigated the role of the amino acid breakdown products ammonia and the amines in the regulation of gastrin release both in vivo and in vitro. Lyophilization of standard rat food under alkaline conditions results in the volatilization of both ammonia and the amines, which can be subsequently condensed in a cold trap. The normal postprandial release of gastrin is significantly reduced by approximately 50% when rats are fed this freeze-dried diet. Addition of the amine-containing condensate back to the freeze-dried diet completely restores this response to normal. Analysis of the completely restores this response to normal. Analysis of the condensate by thin-layer chromatography revealed that it contained ammonia, methylamine, ethylamine, dimethylamine, and a fourth unidentified aliphatic amine. All of the above compounds significantly stimulated the release of gastrin from isolated G cells. Similarly, addition of ammonia and a synthetic amine mixture to the freeze-dried diet completely restored the postprandial release of gastrin to normal levels. In conclusion, our results suggest that dietary amines and ammonia may play a key role in initiating the gastrin secretory response to a meal.

Amino acids and amines stimulate gastrin release from canine antral G-cells via different pathways.

“…Since proteins are the primary food constituents found to have an acid secretagogue action, it is not surprising that only proteins are capable of significantly stimulating gastrin secretion (1 1, 12). Indeed the metabolic products of proteins, the amino acids, have been reported to be more potent gastrin stimulants than intact proteins (13), and Lichtenberger et al (5,14) have hypothesized further that amino acids must be decarboxylated to their amine-derivative forms before this agonist activity can be observed. We have used a novel preparation of isolated and enriched canine antral G-cells (6) to study the cellular basis for the action of amino acids and amines on gastrin secretion.…”

“…Somatostatin- 14 and bombesin were purchased from Peninsula Laboratories, Inc. (Belmont, CA). Pertussis toxin (PT),' gentamicin, Hepes, dibutyryl cAMP (DbcAMP), chloroquine, isobutyl methylxanthine (IMX), alpha methyldopa, aminooxyacetic acid, 4-deoxypyridoxine, L-amino acids, amines, hydrocortisone, crude collagenase type I, and EDTA were purchased from Sigma Chemical Co. (St. Louis, MO).…”

Effect of inhibition of Helicobacter pylori urease activity by acetohydroxamic acid on serum gastrin in duodenal ulcer subjects.

“…9 In an attempt to elucidate the mechanism of the hypergastrinaemia associated with H pylori infection, we have examined the effect of inhibiting the bacterium's urease activity and ammonia production on serum gastrin in duodenal ulcer patients.…”

Is Helicobacter pylori associated hypergastrinaemia due to the bacterium's urease activity or the antral gastritis?

“…We have examined serum gastrin in 10 patients before and 24 hours after starting triple anti-H pylon treatment consisting of tripotassium dicitrato bismuthate 120 mg four times daily, metronidazole 400 mg three times daily, and amoxycillin 500 mg three times daily. The urease activity, assessed by the 20 minute value of the 14C-urea breath test, fell from a median of 176 (range 116-504) kg% dose/mmol CO2x 100 pretreatment to 5 (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15) at 24 hours (p<0.005). The median antral gastritis score was 6 (4-6) pretreatment and fell to 3 (2)(3)(4)(5) at 24 hours (p<0.02), and this was due to resolution of the polymorphonuclear component.…”