Apolipoprotein A-IV (apoA-IV) synthesis rates were measured in vivo in rat enterocytes by immunoprecipitation after administration of [3H]leucine into in situ loops of jejunum and ileum. Basal apoA-IV synthesis rates (percent total protein synthesis) were significantly higher in jejunal enterocytes (2.05 +/- 0.54%) compared with ileal enterocytes (0.48 +/- 0.32%) from the same fasted animals. After an acute triglyceride bolus, significant and sustained elevations of apoA-IV synthesis rates were seen in both jejunal and ileal enterocytes with maximal effects noted at 4-6 h. Animals fed diets containing 30% wt/wt triglyceride as saturated (SF) or polyunsaturated (UF) fats for 6 wk had similarly increased rates of apoA-IV synthesis in jejunal enterocytes with both SF (3.73 +/- 0.83%) and UF (3.33 +/- 0.64%) but no change in ileal enterocytes. By contrast, animals consuming a fat-free diet for 3 wk had jejunal apoA-IV synthesis rates indistinguishable from basal values (2.40 +/- 0.45%). Translatable intestinal mRNA levels for pre-apoA-IV after triglyceride increased in parallel to synthesis rates with a 50% increase in jejunum and a 350% increase in ileum observed at 4-6 h. These results suggest that apoA-IV synthesis by rat small intestine increases in response to acute and chronic dietary triglyceride, is maintained in the absence of dietary triglyceride, and may be under pretranslational control.

Page G662: Terri F. Apfelbaum, Nicholas O. Davidson, and Robert M. Glickman. “Apolipoprotein A-IV synthesis in rat intestine: regulation by dietary triglyceride.” Page G663: sentence beginning on line 10, second column, should read “Data are expressed as mean ± 1 SD, and comparisons for both paired and unpaired means were made by Students t test.”

ABSTRACT— We studied two female patients with autoimmune (“lupoid”) chronic active hepatitis whose liver biopsies at initial presentation showed the unusual features of an acute hepatitis. Centrilobular hepatocyte swelling and multinucleation, acidophilic degeneration, cholestasis, mild fatty change and bile duct damage in one case resembled lesions of non‐A, non‐B hepatitis. Lobular and portal infiltrates of plasma cells with piecemeal necrosis suggested transition to chronicity as well as an autoimmune component. This was additionally supported by the presence of hypergammaglobulinemia and auto‐antibodies in both patients. We conclude that liver biopsy features in the acute presentation of lupoid hepatitis may be difficult to distinguish from those seen in acute hepatitis due to virus or drugs.