Techniques were developed to provide direct quantitation of apolipoprotein A-I (apoA-I) synthesis rates in rat small intestine. Following intralumenal administration of a pulse of [3H]leucine, newly synthesized enterocyte apoA-I was quantitated by specific immunoprecipitation and compared to [3H]leucine incorporation into total trichloroacetic acid-precipitable protein. ApoA-I synthesis rates (% total protein) were found to be significantly higher in jejunal enterocytes (1.84 ± 0.20) compared to ileal enterocytes (0.91 ± 0.25) from the same, fasting animals, P < 0.01. It was found that rats consuming regular (4.5% w/w fat) rodent chow had apoA-I synthesis rates, 30 to 240 min after receiving an intraduodenal bolus of 100 mg of triglyceride, that were indistinguishable from control animals receiving either saline or an isocaloric, but fat-free, enteral preparation. By contrast, animals consuming a fat-free chow for 8 days prior to study had a small but significant response to acute reintroduction of dietary triglyceride. Four hours after 100 mg of triglyceride was administered, jejunal apoA-I synthesis (% total protein) was 1.84 ± 0.1 compared to 1.37 ± 0.04 for animals exposed to an isocaloric, fat-free enteral preparation, P < 0.01. External bile diversion for 48 hr, which effectively removed all lumenal sources of lipid, reduced apoA-I synthesis in jejunal enterocytes but produced no more depression than that found in sham-operated controls infused for 48 hr with dextrose-saline or control animals fasted for 30 hr. By contrast, apoA-I synthesis in ileal enterocytes was reduced significantly by external bile diversion (0.59 ± 0.20) in comparison to sham-operated controls (1.19 ± 0.32) P < 0.01. Continuous infusion of 10 mM Na taurocholate for 48 hr or 10 mM Na taurocholate for 44 hr and 80 mg of micellar lipid for 4 hr produced results similar to those obtained by bile diversion alone (0.56 ± 0.2 and 0.61 ± 0.25, respectively) suggesting that bile salt deficiency alone was not responsible for the observed depression in ileal apoA-I synthesis. These results suggest that, under conditions of physiological dietary triglyceride intake, apoA-I synthesis in jejunal enterocytes is not acutely regulated by changes in triglyceride flux. After prolonged dietary triglyceride withdrawal, the reintroduction of fat produces a small, but significant, increase in jejunal apoA-I synthesis. The data further suggest that apoA-I synthesis in jejunal enterocytes is regulated in part by the availability of lumenal lipid, but that the presence of bile does not exert an additional level of control. By contrast, the data obtained with ileal enterocytes suggest that a major aspect of the regulation of apoA-I synthesis in this location is related to biliary lipid flux, although not to the presence of lumenal bile salts. The study suggests fundamental differences exist in the regulation of apoA-I synthesis in jejunal and ileal enterocytes of the rat.

Original languageEnglish
Pages (from-to)368-379
Number of pages12
JournalJournal of lipid research
Issue number3
StatePublished - 1985


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