THE FOLLOWING studies on patients with fibrosis of the pancreas were carried out for two purposes: (1) to discover, if possible, an acceptable physiologic explanation for the ravenous appetite of these patients and its abatement with the administration of dried pancreas1 and (2) to determine whether the pancreas is or is not involved in the production of an enterogastrone-like substance which might play a role in the "duodenal mechanism" of Gershon-Cohen.2
That orally ingested fat remains longer in the stomach than other foods has been long recognized.3 That, furthermore, gastric motility4 and gastric secretion5 are decreased following its administration has also been recognized. Lintwarew6 noted that fat placed directly in the duodenum caused a decrease in both peristalsis and the secretory activity of the stomach.
While it is probable that neuronal influences are implicated in the inhibition of gastric secretion and motility, Farrell and
LOWE CU, MAY CD, STAUFFER HM, NEUHAUSER EDB. FIBROSIS OF THE PANCREAS: Enterogastrone and the "Duodenal Mechanism" in Relation to Increased Appetite. Am J Dis Child. 1950;79(1):91–98. doi:10.1001/archpedi.1950.04040010101011
Customize your JAMA Network experience by selecting one or more topics from the list below.
Create a personal account or sign in to: