Endogenous Gastrin and Cholecystokinin Do Not Promote Growth of Rat Liver

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Abstract
Chen D, Ding X-Q, Rchfeld JF, Håkanson R. Endogenous gastrin and cholecystokinin do not promote growth of rat liver. Scand J Gastroenterol 1994;29:688-692 Background: The purpose of the study was to evaluate the trophic effects of endogenous hypergastrinemia and hypercholecystokininemia on intact and regenerating rat liver. We also examined the effects on the liver of portacaval shunting (PCS) alone or together with hypergastrinemia or hyperCCKemia. PCS is known to enhance the trophic effects of gastrin on the so-called enterochromaffin-like cells of the stomach and of CCK on the pancreas. Methods: Hypergastrinemia was induced by treatment with omeprazole (400 μmol/kg/day) or extirpation of the acid-producing part of the stomach (fundectomy). HyperCCKemia was induced by pancreaticobiliary diversion (PBD). After 4 weeks half of the rats were killed; the rest underwent partial hepatectomy and were lulled 60 h later. PCS rats were killed 4 weeks after start of omeprazole treatment or after PBD. The concentrations of circulating gastrin and CCK were measured by radioimmunoassay. The liver weight and DNA content were analyzed. Results: Endogenous hypergastrinemia and hyperCCKemia failed to stimulate growth of either intact or regenerating liver. There were no differences in liver weight and DNA content between rats subjected to PCS and to combinations of PCS and omeprazole treatment, on the one hand, and PCS and PBD, on the other. Conclusion: Gastrin and CCK are unlikely to be physiologically important in the regulation of liver growth and regeneration in the rat.