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P Miljanich

Publications and source records attributed to P Miljanich.

18 recordsLinked to original sources
PubMed1980

Effects of linolenic acid deficiency on the fatty acid patterns in plasma and liver cholesteryl esters, triglycerides and phospholipids in female rats.

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. Second-generation linolenate-deficient rats and control rats were fed low-methionine, choline-deficient diets for 2 weeks. Half the animals in each group were given choline-supplemented diets. Plasma and liver total cholesterol, esterified cholesterol, triglyceride and major phospholipid classes, and the fatty acids of these classes were measured. Linolenic acid deficiency reduced the concentrations of plasma triglycerides in both choline-deficient and choline-supplemented rats. Evidence for a metabolic interaction between choline and linolenic acid was not obtained because the rats responded very weakly to the choline deficiency. Linolenate deficiency reduced the proportions of n-3 fatty acids, particularly 22:6n-3, in all the lipids analyzed.

Animals↗
PubMed1979

Dissociation of apolipoprotein A-I from porcine and bovine high density lipoproteins by guanidine hydrochloride.

Dissociation 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--1.100 g/ml while porcine high density lipoprotein (HDL-P) was isolated at d 1.125--1.21 g/ml. Incubation for 5 min with Gdn-HCl resulted in a 45 and 3% loss of apo-A-I from HDL-P and HDL-B, respectively. Exposure to the denaturant for 3 h resulted in a 75% loss of apoA-I from HDL-P and a 30% loss from HDL-B. Analytic ultracentrifugation, patterns paralleled the degree of apoA-I dissociation from each HDL species. The initial flotation peak for HDL-P shifted from F degrees 1.20 2.68 to F degrees 1.20 10.75 after 3 h exposure while HDL-B showed only a small shift from F degrees 1.20 8.30 to F degrees 1.20 8.96 after 3 h exposure. HDL-P particle diameter increased 25% after 5 min of Gdn-HCl treatment and large, flattened structures predominated after 3 h. There was no changes in the size of HDL-B after 5 min exposure and only 16% increase in particle diameter after 3 h. The difference in behavior of HDL-B and HDL-P to Gdn-HCl exposure is discussed in terms of differences in apolipoprotein A-I amino acid composition, interaction of apolipoprotein A-I with phospholipids and the possible involvement of the cholesteryl ester core.

Amino Acids↗
PubMed1979

Ethanolamine kinase activity and compositions of diacylglycerols, phosphatidylcholines and phosphatidylethanolamines in livers of choline-deficient rats.

These 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. Young male rats were fed for one week a low-methionine, choline-deficient diet, or the same diet supplemented with choline. Ethanolamine kinase activity was measured in liver cytosol (100,000 g supernatant). Fatty acids were measured in total liver diacylglycerols and in microsomal PE and PC. Ethanolamine kinase activities were equal in choline-deficient and choline-supplemented rats. Concentrations of DG were elevated 6-fold by choline deficiency. The percentage of docosahexaenoic acid (22:6n-3) in microsomal PE was nearly doubled by choline deficiency. Although the increased concentrations of PE in choline-deficient livers cannot be attributed to increased activity of ethanolamine kinase, the rate of PE formation probably was increased by increases in concentrations of its precursors, including DG. The disproportionate increase in 22:6n-3 PE probably was caused by a selective formation of PE from DG that contain 22:6n-3.

Animals↗
PubMed1979

Linolenic acid deficiency.

Linolenic 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. So far, attempts to produce linolenic acid deficiency in mammals have not revealed an absolute requirement for n-3 fatty acids. If functions for n-3 fatty acids do exist in warm blooded animals, it seems probable that they may be located in the cerebral cortex or in the retina, because these tissues normally contain high concentrations of n-3 fatty acids.

Animals↗
PubMed1978

Linolenic acid deficiency: changes in fatty acid patterns in female and male rats raised on a linolenic acid-deficient diet for two generations.

Rats 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). Male and female rats ranged in age from weaning pups to adults. Lipids were extracted from liver, brain, kidney, spleen, heart, muscle, gastrointestinal tract, lung, ovary, testis, adrenal, plasma, erythrocytes, retina, and adipose tissue. Fatty acids of major phospholipid classes (choline phosphoglycerides, ethanolamine phosphoglycerides, and mixed serine phosphoglycerides plus inositol phosphoglycerides) or of total lipid extracts were measured by gas liquid chromatography. Growth rates and organ weights were similar in control and linolenic acid-deficient rats. The major effect of the deficiency was to lower the proportions of n-3 fatty acids, especially 22:6 n-3, in all the organs analyzed. Docosahexaenoic acid (22:6 n-3) was mainly replaced by 22:5 n-6 in deficient rats. The greatest changes in composition were found in brain, heart, muscle, retina, and liver.

Age Factors↗
PubMed1977

Depletion of docosahexaenoic acid in retinal lipids of rats fed a linolenic acid-deficient, linoleic acid-containing diet.

Rats were raised for 2 generations on a diet in which 1.25% methyl linoleate was the only source of fat. Control rats were given 1.0% methyl linoleate plus 0.25% methyl linolenate. Lipids were extracted from retinas and their fatty acids were analyzed by gas-liquid chromatography. Docosahexaenoic acid accounted for 33.8% of total fatty acids in control retinas, for 13% of fatty acids in first-generation deficient retinas, and for 2.7% of fatty acids in second-generation deficient retinas.

Animals↗
PubMed1975

Effect of low methionine, choline deficient diets upon major unsaturated phosphatidyl choline fractions of rat liver and plasma.

To 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. Deficient rats had reduced total liver phosphatidyl choline when compared with the supplemented groups, but the proportions of 20:4 and 22:6 fatty acids in the total phosphatidyl choline were unchanged. Plasma phosphatidyl choline also was reduced sharply by the deficiency, as was its proportion of 20:4 fatty acid. Specific activities of the liver 22:6, 20:4, and 18:2 phosphatidyl choline fractions showed that deficient rats had less radioactivity in their 20:4 and 18:2 phosphatidyl choline than did the supplemented animals. Plasma phosphatidyl choline fractions presented a similar pattern. Feeding methionine or choline nearly doubled radioactive methyl group incorporation into the 20:4 phosphatidyl choline fraction of liver and plasma, while incorporation into the 22:6 phosphatidyl choline was reduced or unchanged. The results suggested that, in the rat, limited availability of methyl groups altered the metabolism of liver and plasma phosphatidyl choline fractions. Methionine, as a source of labile methyl groups, appears necessary for the normal synthesis of certain unsaturated phosphatidyl choline fractions (particularly 20:4 phosphatidyl choline). Transmethylation of phosphatidyl ethanolamine molecular species to the corresponding phosphatidyl choline species may be an important reaction in normal lipid metabolism and transport. Relative affinities for incorporation of the labeled methyl groups into the phosphatidyl choline fractions of either deficient or supplemented rats were: 22:6 less than 20:4 less than 18:2.

Animals↗
PubMed1965

Influence of sex and gonadal hormones on rat-liver and carcass lipids during the development of an essential fatty acid deficiency.

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. Male rats grew faster and larger, and exhibited typical external essential fatty acid deficiency symptoms sooner than did females. Testosterone-treated castrated male rats were similar to males, and oestradiol-injected castrated male rats resembled females. 3. Intact females maintained a higher linoleic acid concentration in their carcass than did males. Total amounts of carcass linoleic acid remained similar for all groups, only 200mg. being removed in 9 weeks regardless of body size. 4. The amounts of total cholesteryl esters were independent of liver size. They were higher in males and testosterone-treated castrated male rats than in females and oestrogen-treated castrated male rats. 5. Phospholipids represented about 80% of the liver lipids. The total amounts of the phospholipid linoleic acid and arachidonic acid were similar for all groups regardless of liver size, and were not affected appreciably by the deficiency. Females and oestrogen-treated castrated male rats maintained a higher proportion of phospholipid arachidonic acid for longer periods than did their male counterparts. Both the total amounts and the proportions of eicosatrienoic acid and palmitic acid were higher in males than in females. 6. Supplementation of the essential fatty acid-deficient diet with linoleic acid caused a rapid loss of eicosatrienoic acid and palmitic acid with a concomitant increase in stearic acid and arachidonic acid. 7. There were no obvious differences in the way that the essential fatty acids were metabolized or mobilized from adipose tissue of male or female rats during essential fatty acid deficiency. 8. The results indicated that the greater growth rate of the male rats caused them to require and synthesize more phospholipids than did the females. In the absence of adequate amounts of arachidonic acid, eicosatrienoic acid was substituted into the additional phospholipid. The earlier symptoms of essential fatty acid deficiency in the male rat could therefore be ascribed to the higher tissue concentrations of this unnatural phospholipid and its inability to perform the normal metabolic functions of phospholipids.

Journal Article↗