Abstract
The gastrointestinal site(s) of NTLI [neurotensin-like immunoreactivity] release and the importance of bile and pancreatic juice for fat-induced NTLI release were investigated. Administration of Intralipid (2 ml) into the stomach and oleic acid (0.5 ml) into the duodenum increased the plasma concentration of NTLI (p-NTLI). The increase in p-NTLI levels occurred only when the jejunum and ileum were exposed to Intralipid but not when the exposure was limited to the stomach and duodenum. Exclusion of pancreatic juice significantly reduced the p-NTLI response and exclusion of both bile and pancreatic juice completely abolished the p-NTLI response to duodenally-administered oleic acid. Neurotension is released by a direct luminal exposure of the neurotensin containing N-cells to fatty acids. It seems probable that fatty acids have to be transformed to a micellar form in order to release NTLI.