Abstract

Metabolism of tri-(G 3) and polyglycerol (G 10) and G 3 and G 10 esters was studied in vivo in the rat, and in vitro with pancreatic enzymes. Fatty acid-labeled (oleic acid and eicosanoic acid), G 10 ∗-labeled esters and 14C-labeled tri-(G 3 ∗) and polyglycerol ( G 10 ∗ ) were used so that the metabolic fate of the fatty acids and of the G 3 and G 10 moieties could be independently determined. Our data showed that the ester bonds were hydrolyzed to a large extent prior to absorption. The free fatty acids were absorbed via the thoracic duct pathway. Eicosanoic acid was not as readily absorbed as was oleic acid. The free or partially esterified polyglycerols were not as well absorbed as the fatty acids; absorption was by a pathway other than the thoracic duct, presumably by the portal venous blood. Distribution of radioactivity among respiratory CO 2, urine, feces and carcass was determined. CO 2 was the major end product of fatty acid catabolism. G 3 ∗ and G 10 ∗ moieties were not catabolized or stored in the carcass, but were excreted unchanged in the urine. Hydrolysis experiments in vitro confirmed that the oleic acid ester bond in the G 3 and G 10 esters was readily cleaved, as is the same bond in triglycerides. The eicosanoate bond was cleaved more slowly than the oleate bond. The slower rate of hydrolysis of the eicosanoate ester linkage coupled with a slower rate of absorption of saturated fatty acids would explain why more of the label from this compound than from oleate was detected in the feces and gastrointestinal contents.

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