These experiments were performed to measure the effects of linolenate deficiency upon neutral lipids of plasma and liver, and to search for a metabolic interaction between dietary choline and linolenic acid. Rats were fed for two generations on a linolenic acid-deficient diet containing methyl linoleate as the only source of lipid. Control rats were supplemented with methyl linolenate.
View Article and Find Full Text PDFThese experiments were performed to find the reasons for the increased concentrations of docosahexaenoyl phosphatidylethanolamines (PE) in livers of choline-deficient rats. We measured the activity of ethanolamine kinase, which catalyzes the first step in PE formation. We also measured the compositions of PE and phosphatidylcholines (PC) and concentrations and fatty acid compositions of diacylglycerols (DG), which are precursors of PE.
View Article and Find Full Text PDFDissociation of apolipoprotein A-I from pig and steer high density lipoproteins (HDL) deficient in apoA-II was determined by exposing native HDL fractions to 6 M guanidine hydrochloride (Gdn-HCl) at 37 degrees C for periods from 5 min to 18 h. Bovine high density lipoprotein (HDL-B) was isolated at d 1.063--1.
View Article and Find Full Text PDFLinolenic acid deficiency has not been demonstrated clearly in warm blooded animals, yet circumstantial evidence suggests that n-3 fatty acids may have functions in these animals. The fact that several species of fish definitely require dietary n-3 fatty acids indicates that n-3 fatty acids have important and specific functions in these animals and suggests that such functions may also be present in warm blooded animals. It is also true that n-3 fatty acid distribution in tissues of birds and mammals appears to be under strict metabolic control, and that this complex metabolic control mechanism apparently has survived evolutionary pressure for a very long time.
View Article and Find Full Text PDFRats were fed for two generations a purified, linolenic acid-deficient diet in which the only source of lipid was purified methyl linoleate. This diet contained about 38 mg linolenic acid/kg diet. Control rats were given the same diet supplemented with methyl linolenate (2,500 mg/kg diet).
View Article and Find Full Text PDFRats were raised for 2 generations on a diet in which 1.25% methyl linoleate was the only source of fat. Control rats were given 1.
View Article and Find Full Text PDFTo see how the metabolism of specific phosphatidyl choline fractions might be affected when only a limited source of methyl groups was available, rats were fed for 7 days a low methionine, choline-deficient diet or one supplemented with either choline or methionine. Prior to killing, they were injected with -14C-methyl methionine and liver and plasma phosphatidyl choline isolated and separated by argentation chromatography into 3 major unsaturated fractions. Fatty acid composition and radioactivity of the fractions were determined.
View Article and Find Full Text PDFBiochim Biophys Acta
February 1967
1. Groups of intact male and female rats and castrated rats injected with oestradiol or testosterone were given a diet containing hydrogenated coconut oil for 9 weeks, and at intervals the amounts and fatty acid compositions of the carcass and liver lipids were determined. 2.
View Article and Find Full Text PDF1. Four-week-old male and female rats were given choline-deficient diets for 2 weeks. Deficient animals gained nearly as much weight as normal controls of the same sex.
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