No abstract

The present study was done to determine the effect of the interaction of ethanol and an average or high-fat diet on pancreatic acinar cell function. Weight-matched groups of Sprague-Dawley rats were fed regular rat feed or average fat and high-fat liquid diets with or without 5% (w/v) concentration of ethanol for 3 months. Trypsinogen secretion was increased by the high-fat diet but not by ethanol; chymotrypsinogen secretion was decreased by the combination of ethanol and a high-fat diet, while lipase secretion was increased by a high-fat diet. Pancreatic secretory trypsin inhibitor was not significantly altered by ethanol or fat in the diet. Ethanol feeding together with a high-fat content of the diet caused complex and nonparallel changes in the secretion of the pancreatic enzymes. These data are of interest in view of the reported positive correlation between alcoholism and a high-fat content of the diet in the causation of alcoholic pancreatitis in humans.

To determine the effect of riboflavin deficiency on the rat pancreas, one-third of a group of rats was fed a purified riboflavin-sufficient diet ad libitum and two-thirds were fed isocaloric amounts of riboflavin-deficient diet for 13 wk; one-half of the latter group was replenished with daily intraperitoneal injections of riboflavin for the last 3 wk. Body weight, pancreas weight, DNA, protein, amylase, chymotrypsinogen, and trypsinogen decreased in riboflavin-deficient animals. In vitro basal secretion of chymotrypsinogen decreased and basal and bethanechol-stimulated secretions of trypsinogen increased in riboflavin-deficient rats. These changes were considered to be caused by relative inanition resulting from decreased food consumption. On replenishment of riboflavin, amylase content reverted to that of animals fed ad libitum whereas increases in body weight, pancreas weight, DNA, protein, chymotrypsinogen, and trypsinogen were not statistically significant. Both basal- and bethanechol-stimulated secretions of chymotrypsinogen increased. These data indicate that riboflavin deficiency, which commonly accompanies chronic alcoholism, may contribute to the pancreatic injury in chronic alcoholism.