We studied the absorption and oxidation of enterally administered medium-chain triglyceride (MCT) and long-chain triglyceride (LCT) in peritonitic rats, and also the effects of carnitine supplementation on these parameters. Peritonitis was produced in rats by the cecum ligation and puncture method described by Wichterman. The necrotic cecum was removed from each rat 16h after the operation to allow recuperation. Peritonitis I or II was present in the rats at 24h and 48h, respectively, after cecum removal. The endotoxin reported by Wichterman was detected in the plasma of rats with either peritonitis I or II. Liver function in the model animals was shown to be deranged in comparison with sham-treated rats, and was more severe in peritonitis I than in peritonitis II. The absorption rate of [
14C] MCT or [
14C] LCT was measured by administering either to rats with peritonitis I and II, and keeping the rats in metabolic cages. The expired
14CO
2 was trapped continuously for 10h. In rats with peritonitis I, the cumulative
14CO
2 production from MCT was 66.3±9.2% of the administered dose, whereas that from LCT was only 16.5±3.2%; 87.7±5.1% of MCT and 70.0±12.5% of LCT were absorbed by rats with peritonitis I. In rats with peritonitis II,
14CO
2 production from MCT and LCT was 73.9±1.2% and 44.5±4.3%, respectively, while the absorption rates of MCT and LCT were 96.8±0.2% and 86.1±11.1%. These results indicate that MCT is more effective than LCT as an energy source under the experimental conditions used. Subcutaneous injection of carnitine into rats with peritonitis I neither increased nor decreased the absorption of LCT and MCT. However, cainitine stimulated
14CO
2 production from LCT from 16.5±3.2% to 22.6±3.9%, but suppressed that from MCT from 66.3±9.1% to 52.7±11.8%; carnitine stimulated the oxidation of absorbed LCT but suppressed that of MCT under these conditions.
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