In vitro lipid metabolism in the rat pancreas. I. Basal lipid metabolism.

1. The in vitro basal lipid metabolism of rat pancreatic fragments was compared with that in adipose tissue fragments and liver slices. 2. [1-14C]Acetate added to the media was mostly incorporated into palmitic acid and to a lesser extent into oleic acid. In addition, pancreatic tissue exhibited a marked capacity for elongation of polyunsaturated fatty acids by [1-14C]acetate and resulting desaturation when compared to adipose tissue and liver. 3. Data obtained in the presence of [U-14C]glucose, [1-14C]palmitate and 3H20 indicate that acetyl-CoA derived from glucose and from beta-oxidation of fatty acids contributed to de novo lipogenesis. 4. Oxidation of [1-14C]palmitic acid was 9-13 times higher in the pancreas than in adipose tissue or liver when expressed on a wet weight basis. 5. The fatty acid moiety of pancreatic glycerolipids could be derived from de novo synthesis, fatty acids added to the medium, or from fatty acids formed from the hydrolysis of endogenous lipids. The glycerol moiety could be derived either from glucose, or directly from glycerol through participation of glycerol kinase.     

Lipid metabolism by the gall-bladder. I. The in situ uptake and metabolism of lysophosphatidylcholine

Accumulation of lysophosphatidylcholine in gall-bladder bile is involved in the pathogenesis of acute cholecystitis. [1-14C]oleoyl- or [1-14C]palmitoyl-lysophosphatidylcholine was thus instilled in the in situ guinea pig gall-bladder and the absorption and metabolism of the lipid were determined. We found that, after 6 h instillation, 53% of the oleoyl derivative was adsorbed by the gall-bladder, whereasee only 37% of the palmitoyl derivative was absorbed. Although some differences in the metabolism of these two lipids were observed, a major portion of the absorbed radioactivity was found in the gall-bladder wall as phosphatidylcholine. To determine the mechanism of phosphatidylcholine formation from lysophosphatidylcholine by the gall-bladder mucosa, we used lysophosphatidylcholine which was labelled in the fatty acid moiety with 14C and in the choline moiety with 3H. Our data suggest that the mechanism of phosphatidylcholine formation from lysophosphatidylcholine involved acylation with an acyl donor other than a second molecule of lysophosphatidylcholine. We hypothesize that this mechanism as well as others described serve to prevent accumulation of lysophosphatidylcholine within the gall-bladder lumen and thus prevent damage to the gall-bladder mucosa.     

Hepatic lipid metabolism. Age-related changes in triglyceride metabolism.

Age-related changes in hepatic triglyceride formation have been described in developing rats. Triglyceride formation was measured in vitro in the presence of [14C]glycerol-3-phosphate, palmitate, ATP, CoA, and Mg2+ by using liver homogenates and microsomal fractions derived from various age groups of animals. Triglyceride formation was most active in one-day-old rats and then decrease with age. The increase in triglyceride formation following birth was prevented by the administration of puromycin or by denying suckling. In addition, changes in plasma and hepatic triglyceride concentrations, were also determined as functions of age. These studies suggest that the age of the animal significantly influences triglyceride metabolism.