Gastroenterology · 1994
Intracisternal injection of apolipoprotein A-IV inhibits gastric secretion in pylorus-ligated conscious rats.
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Okumura T, Fukagawa K, Tso P, Taylor I L, Pappas T N
Аннотация
BACKGROUND/AIMS: Fat feeding increases not only serum but also cerebrospinal fluid concentration of apolipoprotein (apo) A-IV, a protein produced mainly by the small intestine in the rat. We hypothesized that apo A-IV may have a central effect on gastric secretion.
METHODS: Gastric juice was collected by the pylorus ligation method. Rats underwent pylorus ligation and received intracisternal injection of apo A-IV under brief isoflurane anesthesia. Two hours after the injection, gastric juice was collected and gastric acid output determined.
RESULTS: Intracisternal injection of 0.5 microgram apo A-IV had no effect on gastric secretion. However, gastric acid secretion was significantly inhibited by intracisternal injection of 1 microgram apo A-IV. Furthermore, intracisternal administration of higher doses of apo A-IV (2.0 and 4.0 microgram) resulted in greater inhibition of gastric acid secretion in a dose-dependent manner. On the contrary, 4 micrograms of apo A-I intracisternally injected failed to inhibit gastric acid secretion. Intraperitoneal administration of 15 micrograms of apo A-IV did not alter gastric secretion.
CONCLUSIONS: These results suggest that apo A-IV may act in the brain to inhibit gastric acid secretion. Apo A-IV might be a central enterogastrone, which is a gastric inhibitor produced by the small intestine in response to fat feeding.
METHODS: Gastric juice was collected by the pylorus ligation method. Rats underwent pylorus ligation and received intracisternal injection of apo A-IV under brief isoflurane anesthesia. Two hours after the injection, gastric juice was collected and gastric acid output determined.
RESULTS: Intracisternal injection of 0.5 microgram apo A-IV had no effect on gastric secretion. However, gastric acid secretion was significantly inhibited by intracisternal injection of 1 microgram apo A-IV. Furthermore, intracisternal administration of higher doses of apo A-IV (2.0 and 4.0 microgram) resulted in greater inhibition of gastric acid secretion in a dose-dependent manner. On the contrary, 4 micrograms of apo A-I intracisternally injected failed to inhibit gastric acid secretion. Intraperitoneal administration of 15 micrograms of apo A-IV did not alter gastric secretion.
CONCLUSIONS: These results suggest that apo A-IV may act in the brain to inhibit gastric acid secretion. Apo A-IV might be a central enterogastrone, which is a gastric inhibitor produced by the small intestine in response to fat feeding.