Histological changes in adipose tissue of rats fed a vitamin E deficient diet high in cod liver oil

1946 ◽  
Vol 94 (3) ◽  
pp. 265-287 ◽  
Author(s):  
Karl E. Mason ◽  
Henrik Dam ◽  
Humberto Granados
Keyword(s):  
Adipose Tissue ◽  
Vitamin E ◽  
Cod Liver Oil ◽  
Deficient Diet ◽  
Histological Changes

scholarly journals Vitamin E and stress

1967 ◽  
Vol 21 (1) ◽  
pp. 69-101 ◽  
Author(s):  
J. Green ◽  
A. T. Diplock ◽  
J. Bunyan ◽  
D. Mchale ◽  
I. R. Muthy
Keyword(s):  
Fatty Acids ◽  
Ascorbic Acid ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Vitamin E ◽  
Dietary Fat ◽  
Methyl Esters ◽  
Cod Liver Oil ◽  
Deficient Diet

1. A critical analysis of the biological antioxidant theory of vitamin E function has been made and the implications of the theory have been tested.2. When small amounts of [5-Me-14C]α-tocopherol were present in lipid systems subject to autoxidation in vitro, it was found that, whether the tocopherol was the sole antioxidant or was in synergistic combination with a secondary antioxidant (ascorbic acid), peroxidation did not occur without concomitant destruction of the tocopherol. This was so, whether a simple fat substrate or a liver homogenate (subject to catalysis) was used. The decomposition of tocopherol took place even when the secondary antioxidant was in large excess, as would occur under physiological conditions in the vitamin E-deficient animal, and accelerated as the induction period neared its end.3. When [5-Me-14C,3H]α-tocopherol and ascorbic acid were used as a synergistic antioxidant couple in vitro, tocopherol recovered from the peroxidizing system always had the same isotopic ratio as the starting material. This means that regeneration of tocopherol by the secondary antioxidant cannot involve, as an intermediate, a tocopherol carbon radical formed by loss of hydrogen from the 5-methyl group. Such radicals probably dimerize before they can be regenerated. The same result was found when doubly labelled α-tocopherol was given to the rat and recovered later from its tissues.4. In a series of experiments, rats were rigorously depleted of vitamin E for periods up to 7 months and then given as little as 50 μg [14C]D-α-tocopherol. They were then given, either by stomach tube daily or by dietary addition, large amounts of methyl linoleate or vitamin E-free polyunsaturated fatty acid methyl esters prepared from cod-liver oil and compared with controls given methyl oleate for up to 31 days. When the possibility of interaction between the lipid and tocopherol in the gut was eliminated, analyses of liver, kidney, testis, adrenal, adipose tissue, whole carcass and faeces showed that there was no effect of the polyunsaturated fatty acids on either the metabolism or recovery of [14C]α-tocopherol in any of the animals.5. When interaction between the administered fatty acid esters and tocopherol in the gut was allowed to take place, a marked destruction of [14C]α-tocopherol in the tissues was observed in animals given the polyunsaturated esters. The importance of oxidative destruction of tocopherol in the gut before absorption was demonstrated in a nutritional trial, in which cod-liver oil and lard were compared and the degrees of resistance of rats' erythrocytes to dialuric acid-induced haemolysis was used as an index of vitamin E depletion.6. Similar experiments with [14Cα-tocopherol in weanling rats given large amounts of cod-liver oil methyl esters also showed little effect. Although there was a suggestion that prolonged feeding of partly peroxidized polyunsaturated esters could lead to a slight depression of tissue tocopherol concentrations, no significant differences were usually obtained.7. Fourteen-day-old rats were given a vitamin E-deficient diet and received three weekly doses of 0.5 mg α-tocophcryl acetate. The dosage was stopped, the rats were then given a deficient diet containing 4% of either vitamin E-free linseed oil fatty acids or oleic acid, and the rate of their tocopherol depletion was measured by the erythrocyte haemolysis test. No effect of the polyunsaturated fatty acids was found. Nor was there any effect on the concentrations of ‘secondary antioxidants’ (glutathione and ascorbic acid) in liver, kidney, testis, muscle or adipose tissue.8. The results of the experiments in vivo contrast strongly with those in vitro. They lead to the conclusion that lipid peroxidation, if it occurs in the living animal, is irrelevant to the problem of vitamin E function. This conclusion has been substantiated by a critical review of the literature on the quantitative aspects of the vitamin E-dietary fat relationship.9. The effects of dietary fat stress in vitamin E-deficient animals are, we believe, due to two causes: (1) destruction of tocopherol in the diet or in the gastro-intestinal tract of the animal, and (2) the existence of an increased requirement for vitamin E for the metabolism of certain long-chain fatty acids. The specific effects of certain of these substances in producing or accelerating some vitamin E deficiency diseases may be related to the toxic states known to be induced in vitamin E-deficient animals by other stress factors.

scholarly journals On the relationship between vitamin A and vitamin E in the rat

1968 ◽  
Vol 22 (1) ◽  
pp. 133-143 ◽  
Author(s):  
M. A. Cawthorne ◽  
J. Bunyan ◽  
A. T. Diplock ◽  
Elspeth A. Murrell ◽  
J. Green
Keyword(s):  
Weight Gain ◽  
Vitamin E ◽  
Vitamin A ◽  
Methyl Esters ◽  
Tocopheryl Acetate ◽  
Cod Liver Oil ◽  
Deficient Diet ◽  
Weanling Rats ◽  
The Relationship

1. The effect of vitamin E on the metabolism, utilization and storage of vitamin A has been studied in the rat.2. Male weanling rats were given a vitamin A-deficient, vitamin E-deficient diet until growth had ceased for 3 days, and each rat was then given 50 i.u. vitamin A palmitate. The rats were divided into four groups and given the diet with the addition of 10% methyl oleate or 10% cod-liver oil methyl esters, or either of these diets supplemented with 100 ppm D-α-tocopheryl acetate. There was no increase in maximum weight-gain response in the two groups given vitamin E. There was a significantly lower weight-gain response in the groups given cod-liver oil methyl esters. This effect was not influenced by the presence of vitamin E in the diet.3. Weanling rats of both sexes were made deficient in vitamins A and E and then divided into two groups. One group received, every other day, 1·75 i.u. vitamin A palmitate and 0·6 mg D-α-tocopherol given together; the second group received the two vitamins, in the same amounts, on alternate days. After 28 days there was no difference in the growth of the two groups of rats, irrespective of sex.4. Vitamin A-depleted, vitamin E-deficient rats were given 17·51 μg ‘14C-carbinol’retinyl acetate and then a vitamin A-deficient, vitamin E-deficient diet or that diet supplemented with 100 ppm D-α-tocopheryl acetate. After 6 days, the total remaining ‘14C’retinol and its lipidsoluble metabolites were measured in the carcasses of the rats. Vitamin E administration did not affect the metabolism of the vitamin A dose or its effect on growth.5. Vitamin E-deficient rats were given vitamin A until their liver reserves exceeded 30000 i.u. and were then divided into two groups. One group received a diet deficient in vitamins A and E and the other received, in addition to this diet, a weekly oral supplement of 1 mg D-α-tocopheryl acetate. The vitamin E supplement significantly decreased the rate of vitamin A depletion from the liver during the next 6 weeks. This effect, which was not found to occur when the initial liver reserves were only 3000 i.u., suggests a role for vitamin E in connexion with the capacity of the liver to bind vitamin A.6. The relationship between vitamin A and vitamin E in vivo cannot, in the light of these results, be regarded as that between an antioxidant and a peroxidizable substrate.

scholarly journals Effects of vitamin E deficiency on total polyunsaturated fatty acids in rats and chicks

1967 ◽  
Vol 21 (1) ◽  
pp. 217-224 ◽  
Author(s):  
J. Bunyan ◽  
A. T. Diplock ◽  
J. Green
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Vitamin E ◽  
Cod Liver Oil ◽  
Pufa Content ◽  
Specific Nature ◽  
Vitamin E Deficiency ◽  
Exudative Diathesis ◽  
Total Pufa

1. The total polyunsaturated fatty acid (PUFA) content of tissues of vitamin E-deficient rats and chicks has been measured by the lipoxidase method.2. Vitamin E deficiency did not depress total PUFA in rat liver, kidney, heart, spleen, brain, adrenal and adipose tissue during experimental periods up to 13 months.3. Liver PUFA was not depressed by deficiency of vitamin E and selenium in rats at 9 weeks or 8 months of age.4. Rats given a muscular dystrophy-producing diet (containing oxidized cod-liver oil) showed a severe depletion of PUFA in muscle, but not in kidney or adipose tissue.5. Exudative diathesis induced in chicks by a deficiency of vitamin E and Se did not depress liver PUFA.6. It is considered that in vitamin E deficiency there is no general decrease in PUFA due to peroxidative loss. Changes of a more specific nature occur, as found by other workers.

Fish Oil-induced Yellow Fat Disease in Rats I. Histological Changes

1978 ◽  
Vol 15 (1) ◽  
pp. 114-124 ◽  
Author(s):  
L. H. J. C. Danse ◽  
P. M. Verschuren
Keyword(s):  
Adipose Tissue ◽  
Vitamin E ◽  
Fish Oil ◽  
Early Stage ◽  
Subcutaneous Fat ◽  
Reticuloendothelial System ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Fat Depots ◽  
Fat Depot

Yellow fat disease was induced in young rats given a vitamin E-deficient diet supplemented with 15% fish oil. The changes in adipose tissue of this oil-induced disorder were different from those of natural yellow fat disease in horse, pig and mink. In the natural disease all fat depots had the early stage of yellow fat disease with interstitial lipofuscin-laden macrophages exclusively. In the rat, however, this change was seen only in the subcutaneous fat depot. Moreover, affected adipose tissue of animals with natural disease had extensive fibrosis, but in the rat fibrosis was always absent. Rats with fish oil-induced yellow fat disease had degenerative changes in various fat depots that occurred at various times but in the horse, pig and mink fat depots were affected simultaneously. Lipofuscin accumulated in the reticuloendothelial system in rats. Accumulation in spleen and liver was dependent on vitamin E deficiency, but only the accumulation in the Kupffer cells was correlated with yellow fat disease. Lipofuscin accumulation in the mesenteric lymph node did not depend on vitamin E deficiency.

scholarly journals Plasma and tissue concentrations of α-tocopherol during vitamin E depletion in sheep

1993 ◽  
Vol 69 (1) ◽  
pp. 225-232 ◽  
Author(s):  
J. M. Fry ◽  
G. M. Smith ◽  
M. C Mcgrath ◽  
E. J. Speijers ◽  
J. G. Allen
Keyword(s):  
Adipose Tissue ◽  
Vitamin E ◽  
Heart Muscle ◽  
Skeletal Muscles ◽  
Experimental Conditions ◽  
Deficient Diet ◽  
Tocopherol Concentration ◽  
Muscle Tissues ◽  
The Relationship

To determine the relationship between plasma and tissue α-tocopherol concentrations during vitamin E depletion, weaned lambs were placed on a vitamin E-deficient diet for 0, 1, 2, 4, 8 and 12 weeks. α-Tocopherol was measured in plasma, erythrocytes, liver, adrenal, adipose tissue, three different skeletal muscles and heart muscle. The α-tocopherol concentration in plasma fell at the same rate as the α-tocopherol concentration in skeletal muscles, heart muscle, adrenal and adipose tissue. The α-tocopherol concentration in liver and erythrocytes fell at a faster rate than that of plasma and all muscle tissues. There were significant correlations between α-tocopherol concentration in plasma and α-tocopherol concentrations in all the tissues measured. Different skeletal muscles had significantly different concentrations of α-tocopherol which may relate to their differing susceptibility to nutritional myopathy. The increase in malondialdehyde in oxidatively-stressed muscle tissue and the correlation with α-tocopherol concentration in most muscle tissues indicated that the muscles had reduced antioxidant capacityin vitroas a result of vitamin E depletion. It was concluded that during vitamin E depletion in sheep α-tocopherol concentration in plasma was a good index of vitamin E status under the experimental conditions employed.

Biochemical Basis of Heart Function. IV. Energy Metabolism and Calcium Transport in Hearts of Vitamin E Deficient Rats

1971 ◽  
Vol 49 (10) ◽  
pp. 909-918 ◽  
Author(s):  
Margaret Fedelesova ◽  
Prakash V. Sulakhe ◽  
John C. Yates ◽  
Naranjan S. Dhalla
Keyword(s):  
Vitamin E ◽  
Sarcoplasmic Reticulum ◽  
Heart Function ◽  
Adenine Nucleotides ◽  
Creatine Phosphate ◽  
Normal Diet ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Biochemical Basis

Feeding a vitamin E deficient diet to rats for 10 weeks was found to decrease myocardial creatine phosphate, ATP, ATP/ADP ratio, NAD+, NADP+, and NADPH, whereas the level of ADP was increased without any changes in the levels of AMP, total adenine nucleotides, NADH, and ATP/AMP ratio. The levels of ATP and pyridine nucleotides were restored fully, whereas creatine phosphate was restored partially on feeding a normal diet for 4 weeks to animals previously on the vitamin E deficient diet for 10 weeks. Vitamin E deficiency was found to increase cardiac lactate, pyruvate, and lactate/pyruvate ratio and decrease the activities of lactate dehydrogenase and malate dehydrogenase. The activity of Na+–K+-stimulated, ouabain-sensitive ATPase was markedly elevated in the hearts of animals on the vitamin E deficient diet. The ATP-dependent calcium accumulation by the sarcoplasmic reticular fraction in the absence and presence of P1 or oxalate was greater in the vitamin E deficient heart. Vitamin E deficiency also increased the Ca2+-stimulated ATPase activity of the cardiac sarcoplasmic reticulum. Although myocardial contractility of the hearts from vitamin E deficient rats was depressed, no damage to the ultrastructures of mitochondria and sarcoplasmic reticulum was apparent. These results indicate marked alterations in myocardial metabolism due to vitamin E deficiency and it is suggested that such changes are due to abnormalities in the processes of both energy production and utilization.

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