Reversal by Glucose of Pancreatic Amylase Insufficiency in Chronic Alcoholic Rats

Abstract

Carbohydrate consumption regulates pancreatic amylase synthesis in rats. The Lieber-DeCarli 36% alcohol diet employed in chronic alcohol studies and the isocaloric control diet contain 11 and 47% of total calories from carbohydrates, respectively. Young rats fed ad libitum the 36% ethanol diet for 2 weeks obtained 1.2 glday of carbohydrate, whereas those pair-fed with control diet received 5.8 g/day. Rats fed the 36% ethanol diet and given an intramuscular injection of a solution of 1.5 g of glucose daily for 2 weeks received twofold greater amounts of carbohydrate than saline-injected controls (2.7 versus 1.2 g). These changes in carbohydrate intake produced proportionate changes in pancreatic amylase levels. The secretory responses to cholecystokinin-octapeptide (CCK,) of acini from control and glucose-injected rats were significantly higher compared with those in the saline-injected or noninjected alcohol groups. The blood alcohol levels in glucose-injected rats were markedly reduced compared with other alcohol groups (71.7 versus 274.9 mg/dl) despite similar amounts of ethanol ingestion daily (2.4 g) in the three groups. In vitro experiments with acini from rats fed a nutritionally optimal diet revealed that high pharmacologic concentrations of ethanol, while inducing basal secretion, inhibited CCK,-stimulated amylase secretion. These results indicate that: (a) the amount of alcohol consumption does not correlate with either the levels of blood alcohol or of pancreatic amylase; (b) the carbohydrate availability in rats regulates pancreatic amylase levels despite significant levels of alcohol in blood; and (c) blood alcohol levels observed in vivo may not affect synthetic and secretory processes of amylase in pancreatic acini. Key Words: Liquid diets-Chronic ethanol feeding-Isolated acini-Nutritional adequacyCholecystokinin-octapeptide-Pancreatic amylase.Ethanol, both in vivo and in vitro, has been reported to affect the exocrine pancreas (1-1 1). Since the pancreas does not metabolize ethanol (12), it is apparent that ethanol-induced effects on the pan-

Regulation of Pancreatic Amylase by Dietary Carbohydrate in Chronic Alcoholic Rats

“…Although other blood alcohol-related effects cannot be discounted, our observations in the present study and those reported earlier (41) emphasize that carbohydrate inadequacy, rather than ethanol consumption per se, is the principal cause of pancreatic amylase insufficiency in chronic alcoholic rats.…”