title: Estradiol- and testosterone-induced alterations in phosphatidylcholine and triglyceride synthesis in hepatic endoplasmic reticulum.
abstract: 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.
mesh_terms: D000217:Acyltransferases / Q000378:metabolism; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D001565:Benzoates / Q000494:pharmacology; D001835:Body Weight / Q000187:drug effects; D002247:Carbon Isotopes; D002369:Castration; D002794:Choline; D003065:Coenzyme A; D003597:Cytosine Nucleotides; D003864:Depression, Chemical; D004032:Diet; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000201:enzymology*; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D005989:Glycerides; D007279:Injections, Subcutaneous; D008082:Lipotropic Agents / Q000494:pharmacology; D008099:Liver / Q000166:cytology / Q000187:drug effects / Q000201:enzymology; D008297:Male; D008745:Methylation; D008780:Methyltransferases / Q000378:metabolism; D008862:Microsomes, Liver / Q000201:enzymology*; D010713:Phosphatidylcholines / Q000096:biosynthesis*; D010714:Phosphatidylethanolamines / Q000378:metabolism; D010770:Phosphotransferases / Q000378:metabolism; D011422:Propionates / Q000494:pharmacology; D051381:Rats; D012436:S-Adenosylmethionine; D013268:Stimulation, Chemical; D013739:Testosterone / Q000494:pharmacology*; D014280:Triglycerides / Q000096:biosynthesis*
chemical_list: D001565:Benzoates; D002247:Carbon Isotopes; D003597:Cytosine Nucleotides; D005989:Glycerides; D008082:Lipotropic Agents; D010713:Phosphatidylcholines; D010714:Phosphatidylethanolamines; D011422:Propionates; D014280:Triglycerides; D013739:Testosterone; D004958:Estradiol; D012436:S-Adenosylmethionine; D008780:Methyltransferases; D000217:Acyltransferases; D010770:Phosphotransferases; D002794:Choline; D003065:Coenzyme A