Methylprednisolone therapy decreases short-term mortality in patients with severe alcoholic hepatitis manifested either by spontaneous hepatic encephalopathy or a markedly elevated discriminant function value.

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A B S T R A C T The effect of feeding diets containing 75% glucose or fructose on liver triglyceride formation in the rat was studied by both in vivo and in vitro techniques. The results were compared with those from control rats fed laboratory chow.Both high-sugar diets increased the capacity for triglyceride formation from sn-glycerol-3-P by rat liver homogenates and correspondingly increased incorporation of [1,3-14C]glycerol into hepatic triglyceride by the intact animal.These independent measures of hepatic triglyceride production changed with a similar time-course characteristic for each diet. The 75% fructose diet produced a greater increase in both determinations, reaching a maximum after 11 days.Despite the increase in hepatic triglyceride formation by both high-sugar diets, only the 75% fructose diet resulted in a consistent and sustained increase in serum triglyceride. This results most probably from differences in the fractional rate of serum triglyceride removal between the two groups.

A B S T R A C T The effect of clofibrate (CPIB) on hepatic glycerolipid formation has been studied in vivo and in vitro in the rat. Feeding 0.25% CPIB in laboratory chow significantly reduced serum triglyceride levels by 6 hr and concomitantly decreased the rate of glycerol-4C incorporation into hepatic and serum glycerides, in vivo. These changes persisted for at least 14 days. A similar decrease in serum triglyceride and glycerol incorporation into hepatic glycerides was observed in rats fed high glucose diets containing 0.25% CPIB. Serum glycerol was reduced by feeding CPIB for 14 days. The formation of diglyceride and triglyceride from 14C-snglycerol-3-P by rat liver homogenates was inhibited by addition of 1-40 mm CPIB to the reaction mixture. These results suggest that CPIB reduces hepatic glycerolipid synthesis, possibly by inhibition of one or more reactions in the esterification of sn-glycerol-3-P. This change may account for the early fall in serum triglyceride. At later time periods, serum glycerol levels fall and in some experiments, hepatic triglyceride content increases. Therefore, it is likely that additional metabolic alterations may contribute to the sustained hypotriglyceridemic effects of CPIB.

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