Nutritional factors, especially the protein and fat content of the die
t, may change pancreatic morphology after ethanol induced injury. This
study was performed to delineate the combined effects of a low fat di
et and longterm ethanol ingestion on the rat pancreas. Male Sprague-Da
wley rats were maintained with five different diets for 12 weeks and t
he pancreas removed on the day they were killed. Rats fed a very low f
at diet without ethanol (5% of total calories as lipid) developed maln
utrition, pancreatic steatosis, and reduction in zymogen granules cont
ent. Animals fed a 35% lipid diet with ethanol also developed pancreat
ic steatosis but changes in zymogen granules content were not detected
. Both malnutrition and longterm ethanol consumption increased pancrea
tic cholesterol ester content, and their effects were additive. Pancre
atic steatosis was accompanied with hypercholesterolaemia. Amylase, li
pase, and cholesterol esterase content were reduced in malnourished ra
ts; but longterm ethanol ingestion, regardless of the nutritional stat
e, increased lipase content and decreased amylase. It is suggested tha
t high serum cholesterol concentrations and increased pancreatic lipas
e activity could cause accumulation of cholesterol esters in acinar ce
lls. Fat accumulation in the pancreas has been reported as the earlies
t histopathological feature in alcoholic patients and may be responsib
le for cytotoxic effects on the acinar cells at the level of the cell
membrane. Although it is difficult to extrapolate results in this anim
al study to the human situation, the results presented in this work mi
ght explain the higher incidence of pancreatitis is malnourished popul
ations as well as in alcoholic subjects that is reported in dietary su
rveys.