Gomez R L, Nichoalds G E, Singh M, Simsek H, LaSure M M
Pancreatic Research Laboratory, Veterans Administration Medical Center, Augusta, GA 30910.
Am J Clin Nutr. 1988 Sep;48(3):626-31. doi: 10.1093/ajcn/48.3.626.
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.
