Intestinal Transit of Fat Depends on Accelerating Effect of Cholecystokinin and Slowing Effect of an Opioid Pathway.
Lin, Henry C. MD; Zaidel, Oren MD; Hum, Susan MSc
[Miscellaneous Article] Digestive Diseases & Sciences. 47(10):2217-2221, October 2002.

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Fat has been described to both accelerate and slow intestinal transit. We hypothesized that the fat-induced jejunal brake depends on the combined accelerating effect of CCK and the slowing effect of an opioid pathway. Using a multifistulated model, intestinal transit was measured in four dogs, while 60 mM oleate was delivered into the proximal gut with either 0 or 6 mg naloxone, and 0.1 mg/kg devazepide (a peripheral CCK-A-receptor antagonist) administered intraluminally and intravenously, respectively. In a second study, intestinal transit was measured in seven dogs, while naloxone was delivered intraluminally at 0-, 3-, 6-, or 12-mg doses. Compared to the jejunal brake (marker recovery of 50.1 /- 2.6%), intestinal transit was slowed by the CCK-A antagonist (36.4 /- 8.3%; P < 0.05) and accelerated by naloxone (82.0 /- 6.8%; P < 0.05). The accelerating effect of CCK occurred early in the transit response, while the dose-dependent effect (P < 0.05) of naloxone occurred later. We conclude that fat-induced jejunal brake depends on the early accelerating effect of CCK and the later slowing effect of a naloxone-sensitive opioid pathway.

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