CHRONIC ETHANOL-INDUCED IMPAIRMENT OF HEPATIC GLYCOSYLATION MACHINERYIN RAT IS INDEPENDENT OF DIETARY CARBOHYDRATE

Citation
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
Citations number
23
Categorie Soggetti
Substance Abuse
ISSN journal
01456008
Volume
21
Issue
1
Year of publication
1997
Pages
76 - 81
Database
ISI
SICI code
0145-6008(1997)21:1<76:CEIOHG>2.0.ZU;2-L
Abstract
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.