J. Gutierrezsalinas et al., SUCROSE ADMINISTRATION TO PARTIALLY HEPATECTOMIZED RATS - A POSSIBLE MODEL TO STUDY ETHANOL-INDUCED INHIBITION OF LIVER-REGENERATION, International journal of biochemistry & cell biology, 28(9), 1996, pp. 1007-1016
Although acute ethanol treatment drastically inhibits liver regenerati
on after partial hepatectomy, the exact mechanisms involved remain obs
cure. On the other hand, it is known that early carbohydrate administr
ation promotes a more successful restoration of the Liver mass. Theref
ore, carbohydrate administration could be an experimental approach for
studying ethanol action on the regenerating liver. In rats subjected
to two-thirds partial hepatectomy, ethanol was administered alone or i
n combination with a variety of carbohydrates (glucose, fructose, gluc
ose plus fructose, sucrose and maltose). In liver samples, regeneratio
n parameters and histological assessment were performed. Blood ethanol
and metabolites reflecting liver function were assayed. Ethanol intak
e strongly decreased the incorporation of [H-3]thymidine into Liver DN
A, the concentration of DNA/g of tissue, and thymidine kinase activity
. In this group, severe alterations in cell structure (i.e. abundant f
at droplets and abnormal mitochondria) were found. Carbohydrates readi
ly improved the survival rate of ethanol-intoxicated hepatectomized ra
ts. Sucrose was effective in reverting the ethanol-induced alterations
in li cer structure and the parameters of liver regeneration, and par
tially blocked the ethanol-induced alterations in serum levels of albu
min, triacylglycerols and ammonia without modifying the blood levels a
nd clearance of ethanol. Data suggest that the beneficial action of su
crose might be related to an adequate supply of energetic sources at e
arly times of liver regeneration, rather than altering ethanol bioavai
lability. Thus, the present model could be an experimental approach fo
r studying the metabolic alterations involved in the ethanol-induced i
nhibition of the liver regeneration. Copyright (C) 1996 Elsevier Scien
ce Ltd