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Biomedical subjects

D L Young

Publications and source records attributed to D L Young.

22 records · Page 2Linked to original sources
PubMed1972

Effect of bile salts on hepatic phosphatidylcholine synthesis and transport into rat bile.

The effect of transport of micelle-forming and non-micelle-forming conjugated bile salts on phosphatidylcholine synthesis and transport into bile was studied in the ex vivo perfused rat liver. Single additions of sodium taurocholate, a good micelle-forming conjugated bile salt, caused an increase in bile flow associated with increased phosphatidylcholine and taurocholate concentration. The specific activity of phosphatidylcholine with respect to incorporated [1,2-(14)C]choline and [(3)H]methyl of l-[Me-(3)H]methionine was not significantly altered by the increased transport of phosphatidylcholine. The data suggested that bile phosphatidylcholine is synthesized to a great extent, although not exclusively, by phosphorylcholine glyceride transferase. Single additions of the glycine conjugate of dehydrocholate, a poor micelle-forming bile salt, caused an increase in bile flow comparable to that seen with sodium taurocholate administration. However, the concentrations of phosphatidylcholine in bile decreased. Thin-layer and gas-liquid chromatographic analyses of bile secreted before and after glycodehydrocholate administration revealed no significant increase in bile salt secretion other than the administered glycodehydrocholate. Investigations utilizing radiochemically pure [(14)C]glycine dehydrocholate revealed that increased bile flow after [(14)C]-glycine dehydrocholate administration occurs concomitantly with the secretion of 75-95% of the administered [(14)C]glycine dehydrocholate as a single peak into bile. Thus the increased bile flow without increased phosphatidylcholine concentration noted after glycodehydrocholate administration is due to transport of an intact, nonmetabolized, conjugated bile salt with poor micelle-forming properties. The data indicate that the formation of a bile salt-phosphatidylcholine micelle is responsible for phosphatidylcholine transport into bile.

Animals↗
PubMed1971

Estradiol- and testosterone-induced alterations in phosphatidylcholine and triglyceride synthesis in hepatic endoplasmic reticulum.

Pathways of phosphatidylcholine and triglyceride biosynthesis were studied in hepatic endoplasmic reticulum from castrated and noncastrated male rats pretreated with estradiol or testosterone. In vitro measurements of hepatic microsomal enzymes which catalyze phosphatidylcholine biosynthesis revealed a significant increase in the specific activity of the enzyme governing phosphatidylcholine biosynthesis by the sequential methylation of phosphatidylethanolamine in the estradiol-treated castrate animals. The specific activity of phosphorylcholine-glyceride transferase was decreased by estradiol treatment in both castrate and noncastrate animals. The specific activity of diglyceride acyltransferase, which catalyzes triglyceride biosynthesis, was decreased by estradiol pretreatment in both castrate and noncastrate animals and was increased by testosterone in the castrate animals. The changes in specific activity of the enzymes governing phosphatidylcholine biosynthesis may account for the previously noted increased in vivo incorporation of methyl groups of l-methionine into hepatic phosphatidylcholine in female and estradiol-treated animals; the data suggest that in female and estradiol-treated rats a greater proportion of hepatic phosphatidylcholine is synthesized by the stepwise methylation of phosphatidylethanolamine. The decrease in diglyceride acyltransferase specific activity seen after estradiol administration may account for the lipotropic-like effect of estradiol.

Acyltransferases↗
PubMed1971

Phenobarbital-induced alterations in phosphatidylcholine and triglyceride synthesis in hepatic endoplasmic reticulum.

Biosynthetic pathways of phosphatidylcholine and triglyceride were studied in proliferating hepatic endoplasmic reticulum of rats pretreated with phenobarbital. Phosphatidylcholine accounted for the major increment in membrane phospholipid. In vitro measurements of hepatic microsomal enzymes which catalyze phosphatidylcholine biosynthesis revealed a significant increase in specific activity of the enzyme governing phosphatidylcholine synthesis by sequential methylation of phosphatidylethanolamine. The specific activity of phosphorylcholine-glyceride transferase, which catalyzes phosphatidylcholine synthesis from d-1,2-diglyceride and CDP-choline, was not altered. Specific activity of diglyceride acyltransferase, which catalyzes triglyceride biosynthesis, was increased to a degree comparable to the increase in specific activity found in the phenobarbital-induced drug-metabolizing enzyme which oxidatively demethylates aminopyrine. In vivo incorporation of methyl-(3)H from l-methionine-methyl-(3)H into microsomal phosphatidylcholine was significantly increased, resulting in an increased methyl-(3)H to choline-1,2-(14)C incorporation ratio of more than three times that found in control animals. A comparable increase in this incorporation ratio was noted in serum phospholipids. The in vitro enzyme studies, in agreement with in vivo incorporation data, indicate that the increase in phosphatidylcholine content of phenobarbital-induced proliferating endoplasmic reticulum is related to increased activity of the pathway of phosphatidylcholine biosynthesis involving the sequential methylation of phosphatidylethanolamine.

Acyltransferases↗