P. Ghosh et Mr. Lakshman, CHRONIC ETHANOL-INDUCED IMPAIRMENT OF HEPATIC GLYCOSYLATION MACHINERYIN RAT IS INDEPENDENT OF DIETARY CARBOHYDRATE, Alcoholism, clinical and experimental research, 21(1), 1997, pp. 76-81
In recent years, a number of studies have been reported that have clea
rly established that hepatic glycosylation machinery is affected by ch
ronic ethanol treatment in rats. We have previously reported that chro
nic ethanol treatment in rats resulted in decreased glycosylation of t
ransferrin and apolipoprotein E with concomitant decreases in enzymati
c activities of Golgi galactosyltransferases and sialyltransferases. I
n all these studies investigators have invariably used the well-accept
ed dietary formulation of alcohol diet as proposed by Lieber and DeCar
li. However, questions were raised whether the lower carbohydrate cont
ent in Lieber's alcohol diet may be responsible for observed effects o
f ethanol on hepatic glycosylation machinery. Therefore, to verify whe
ther or not the crucial effects of chronic ethanol treatment on hepati
c glycosylation machinery as observed in our studies, were truly cause
d by ethanol, we have extended our studies on protein glycosylation wi
th the inclusion of a third dietary group that was compensated for car
bohydrate content In this investigation, rats were fed with three diet
ary regimen corresponding to control, ethanol, and carbohydrate compen
sated ethanol group and studies were done on (i) labeled leucine, gala
ctose and N-acetylmannosamine incorporation into transferrin and apoli
poprotein E, and (ii) hepatic galactosyltransferase and sialyltransfer
ase activities in Golgi rich fraction in rat. Our results clearly show
ed that regardless of the carbohydrate content, marked decreases in th
e incorporation of labeled sugars into transferrin and the enzymatic a
ctivities of galactosyltransferase and sialyltransferase occurred in r
ats administered chronic ethanol. Thus, it is reasonable to conclude t
hat it is not the carbohydrate content of the diet but ethanol per se,
when administered chronically, greedy impairs the glycosylation machi
nery of rat liver and that the magnitudes of these effects are selecti
vely specific with regard to the type of sugar or the glycosylation en
zyme.