Inhibition of gastric secretion in man by intestinal fat infusion.

The rate of gastric secretion probably depends upon a balance between secretory and inhibitory stimuli; increase of the former or decrease of the latter may lead to excessive acid production (Thompson, 1962). As a possible cause of duodenal ulcer more attention has hitherto been given to increased excitatory than to impaired inhibitory mechanisms. Inhibitory processes originating in the duodenum and small intestine have been shown in dogs. Khizhin, Lobasov, and Sokolov, quoted by Pavlov (1910), demonstrated reduced gastric secretion following the introduction of acid and fat into the duodenum. Since then many workers have confirmed these findings for acid (Sircus, 1958; Andersson, 1960; Konturek and Grossman, 1965) and fat (Lim, Ivy, and McCarthy, 1925; Menguy, 1960; Long, Brooks, and Sandweiss, 1963). In man, although similar mechanisms are assumed to exist, few attempts have been made to define them or correlate them with duodenal ulcer disease. Ewald and Boas (1886), Roberts (1931), and Shay, GershonCohen, and Fels (1939) have demonstrated the effect on gastric secretion of fat in the duodenum in man. Shay and his colleagues (1939) suggested that the inhibitory effect was directed mainly against vagally stimulated rather than chemically stimulated juice, as intraduodenal fat prevented the acid response to insulin but not that to histamine. Card (1941) showed a lessening of the stomach's motility after fat was instilled into the duodenum, and Johnston and Duthie (1964, 1965) a decrease of histamineand gastrin-induced secretion after acid in the duodenum. In the firsit (1964) paper, comparison of normals with duodenal ulcer patients might suggest impaired inhibition in the ulcer group. Shay and his colleagues (1942) have also suggested that the inhibition of gastric secretion and motility following duodenal acidification in duodenal ulcer patients is impaired and may be causally related to ulceration. However, Woodward and Schapiro (1958) found similar motility responses in normals and ulcer patients. Hunt (1957) observed that acidification of stomach contents delayed gastric emptying in both groups whereas secretion was reduced in normals but increased in six of 16 duodenal ulcer patients. We have studied the characteristics of the inhibition of gastric secretion after instilling fat into the distal duodenum and upper jejunum. The results in controls, duodenal ulcer patients, and a group with small intestinal disease are presented.