Early growth response-1 contributes to XXXX development after acute @entity1068 administration.

@entity1560 @entity7969 @entity167 @entity19 @entity1674 @entity14745 @entity1391 @entity412 @entity382 @entity99 @entity1068
BACKGROUND: Previous work demonstrated that the transcription factor, early growth response-1 ( @entity14745 ), participates in the development of @entity1560 ( @entity1560 ) after chronic @entity1068 ( @entity167 ) administration. Here, we determined the extent to which @entity14745 is involved in @entity1560 development in @entity19 subjected to acute @entity167 administration. METHODS: In acute studies, we treated both wild-type and @entity14745 null @entity19 with either @entity167 or @entity1391 -buffered saline (PBS) by gastric intubation. At various times after treatment, we harvested sera and livers and quantified endotoxin, indices of @entity99 , @entity1560 , and hepatic @entity14745 content. In chronic studies, groups of @entity19 were fed liquid diets containing either @entity167 or isocaloric @entity7969 -dextrin for 7 to 8 weeks. RESULTS: Compared with controls, acute @entity167 -treated @entity19 showed a rapid, transient elevation in serum endotoxin beginning 30 minutes after treatment. One hour postgavage, livers from @entity167 -treated @entity19 exhibited a robust elevation of both @entity14745 mRNA and protein. By 3 hours postgavage, liver @entity412 increased in @entity167 -treated @entity19 as did lipid peroxidation. Acute @entity167 treatment of @entity14745 -null @entity19 showed no @entity14745 expression, but these animals still developed elevated @entity1674 , although significantly lower than @entity167 -fed wild-type littermates. Despite @entity1560 , @entity167 -treated @entity14745 null @entity19 exhibited greater @entity99 . After chronic @entity167 feeding, @entity1560 and @entity382 were clearly evident, but there was no indication of elevated endotoxin. @entity14745 levels in @entity167 -fed @entity19 were equal to those of pair-fed controls. CONCLUSIONS: Acute @entity167 administration induced the synthesis of @entity14745 in @entity19 liver. However, despite its robust increase, the transcription factor had a smaller, albeit significant, function in @entity1560 development after acute @entity167 treatment. We propose that the rise in @entity14745 after acute @entity167 is an hepatoprotective adaptation to acute @entity99 from binge drinking that is triggered by @entity167 metabolism and elevated levels of endotoxin.
