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1.
Studies are reported on the capacity of isolated rat renal papilla (inner medulla) to synthesize and release prostaglandin
(PG) E from endogenous and exogenous precursor(s) during development of an essential fatty acid (EFA) deficiency in the rat.
Weanling (21-day-old) male Sprague-Dawley rats were fed a fat-free diet supplemented with either 5% hydrogenated coconut oil
(HCO) or 5% safflower oil (SO). At approximately 3, 6 and 7 weeks (6, 9 and 10 weeks of age), groups of animals fed each diet
were killed for studies of PGE synthesis in the renal papillae. Differences in the fatty acid composition of the papillae
lipids of the animals of each group were also determined. The in vitro production of PGE from endogenous precursor(s) was
significantly reduced in the papillae from the 6-week-old rats fed the HCO diet compared to the control (SO) rats, and appeared
to be near maximally depressed in the 10-week-old animals compared to that of animals fed an EFA deficient diet for over a
year in an accessory experiment. Analyses of the fatty acids of the papillae lipids of the HCO groups showed that the levels
of 18∶2 and 20∶4 were markedly reduced, and those of 16∶1, 18∶1 and 20∶3 were elevated compared to the controls even in the
6-week-old animals, typical of an EFA deficiency. The papillae lipids of the animals fed the HCO diet were also depleted of
their stores of 22∶4ω6. A fatty acid believed to be derived by chain elongation of 20∶3ω9, 22∶3, was found in large concentrations
in the papillae triglycerides of the EFA deficient rats. Incubations of exogenous arachidonic acid (20∶4) in homogenates and
tissue slices of the papillae of the HCO dietary groups showed that the PG synthetase was not impaired by an EFA deficiency.
The rate of PGE synthesis in the papillae of the EFA deficient animals was generally enhanced when exogenous 20∶4 was added,
indicating that the concentration of available precursor(s) is a primary factor in the control of PGE synthesis in the papilla
of the rat. 相似文献
2.
Studies are reported of the effect of an essential fatty acid (EFA) deficiency on synthesis of triglycerides (TG) and phospholipids
(PL) and secretion of these compounds by livers of male Sprague-Dawley rats. Animals were fed a semipurified diet containing
corn oil or hydrogenated coconut oil (HCO) as the sole source of fat or no fat from weaning to 20 weeks of age. Liver function
of the animals in each group was compared by an isolated liver perfusion technique with perfusates containing erythrocytes
and linoleate, and in vivo experiments via tail vein injection of palmitate-3H. Perfusion experiments showed that an EFA deficiency reduced the ability of the liver to secrete TG and PL. Accumulation
of TG in the liver and its diminished secretion into the blood of EFA deficient animals were demonstrated by in vivo experiments
with palmitate-3H. The rate of conversion of linoleate to arachidonate and synthesis of PL was greater in livers of EFA deficient rats than
in the control, corn oil fed animals. The results suggest a relationship of EFA metabolism to lipid transport.
One of five papers to be published from the Symposium “Lipid Transport” presented at the AOCS Meeting, New Orleans, April
1970. 相似文献
3.
Two nutritional models, essential fatty acid (EFA) deficiency and the feeding of saturated vs unsaturated fats, were used
to determine the effects of dietary lipids on the fatty acid composition of rat lung and lavage. Semipurified diets containing
7% corn oil, 7% hydrogenated coconut oil (EFA-deficient), 10% butter or 10% safflower oil were fed to dams during lactation
and thereafter to their offspring for a total of 24 weeks. Lipids were extracted from the lung lavage and lung tissue and
their fatty acid composition was determined. The content of dipalmitoylphosphatidylcholine (DPPC), the main surfactant in
the lungs, was also determined. The results show that the levels of DPPC in the lungs of rats fed 10% butter decreased although
the decrease in the EFA-deficient rats was greater. Comparing rats fed butter with those fed corn oil, there were also modifications
in the fatty acid composition of the total lipids and phospholipids of lung tissue and lavage as well as in phosphatidylcholine,
phosphatidylethanolamine and phosphatidylinositol +phosphatidylserine fractions isolated from the lung tissue. The changes
in fatty acid composition were somewhat fewer in rats fed butter then in those fed an EFA-deficient diet. The results suggest
that a marginal EFA deficiency produced in rats by long-term feeding of 10% butter may account for the reduction in DPPC levels
and in the changes in fatty acid composition in the lung tissue and lavage. 相似文献
4.
The effect of ethionine on the conversion of stearic acid to oleic acid was studied. Rats were fed essential fatty acid (EFA)
deficient diet for three weeks, after which time half the animals were fed 0.25% DL-ethionine for nine additional days. Seventeen
hours prior to killing, they were fed a slurry of the diet containing 18-14C-stearic acid. Liver triglycerides and phospholipids were extracted and separated and their fatty acid composition and the
distribution of radioactivity between stearic and oleic acid was determined. In the tissues studied, oleic acid was maintained
at control levels in ethionine-fed rats, but eicosatrienoic acid was significantly depressed. Distribution of radioactivity
and specific activity of oleic acid in the triglycerides and phospholipids were significantly reduced by the analogue. In
vitro studies of desaturation and chain elongation reactions, with liver microsomes, using 18-14C-stearic and 1-14C-linoleic acids as substrates, showed that ethionine depressed the synthesis of oleic acid from stearic and γ-linolenic from
linoleic acid. Elongation of linoleic adie to a 20∶2 fatty acid was unaffected by ethionine. Therefore, the results showed
that ethionine inhibited desaturation of stearic to oleic acid in vivo and in vitro and probably also impaired the desaturation
of oleic to octadeca-6, 9-dienoic acid. Maintenance of control levels of oleic acid in the tissues of ethionine-fed, EFA deficient
rats suggested the presence of synthetic pathways for oleic acid other than via desaturation of stearic acid.
Presented in part at the AOCS Meeting, San Francisco, April 1969. 相似文献
5.
Fatty livers and the similarity between the skin lesions in kwashiorkor and those described in experimental essential fatty
acid (EFA) deficiency have led to the hypothesis that protein and EFA deficiencies may both occur in chronic malnutrition.
The relationship between serum very low density lipoprotein (VLDL) and hepatic lipid composition was studied after 28 d of
protein depletion to determine the interactions between dietary protein levels and EFA availability. Rats were fed purified
diets containing 20 or 2% casein and 5% fat as either soybean oil rich in EFA, or salmon oil rich in eicosapentaenoic (EPA)
and docosahexaenoic (DHA) acids, or hydrogenated coconut, oil poor in EFA. Animals were divided into six groups, SOC (20%
casein +5% soybean oil), SOd (2% casein +5% soybean oil), COC (20% casein +5% hydrogenated coconut oil), COd (2% casein +
5% hydrogenated coconut oil), SAC (20% casein +5% salmon oil) and SAd (2% casein +5% salmon oil). After 28 d, liver steatosis
and reduced VLDL-phospholipid contents (P<0.001) were observed in protein-deficient rats. In protein deficiency, triacylglycerol and phospholipid fatty acid compositions
in both liver and VLDL showed a decreased polyunsaturated-to-saturated fatty acid ratio. This ratio was higher with the salmon
oil diets and lower with the hydrogenated coconut oil diets. Furthermore, independent of the oil in the diet, protein deficiency
decreased linoleic and arachidonic acids in VLDL phospholipids. Conversely, despite decreased proportions of EPA at low protein
levels, DHA levels remained higher in rats fed salmon oil diets. While in rats fed the hydrogenated coconut oil-fed diets
the amount of 22∶5n−6 was lower in liver, it was higher in VLDL lipids at low protein levels. Both EPA and arachidonic acid
are precursors of eicosanoids and their diminution may be related to certain clinical symptoms seen in infants suffering from
kwashiorkor. 相似文献
6.
The influence of dietary fat concentration and saturation on blastogenesis, cytotoxicity, antibody response and fatty acid
composition of murine splenic lymphocytes was studied. Blastogenesis of lymphocytes from dietarily manipulated mice in response
to alloantigens from control mice was significantly greater for those mice fed a diet containing minimal essential fatty acids
(EFA) as the only fat source (EFA control) than those fed an EFA-deficient diet. When the dietary fat concentration was increased,
blastogenic responses decreased compared to the EFA control diet. Lymphocyte-mediated cytotoxicity against allogeneic melanoma
cells was greater for mice receiving diets with EFA only than for those deficient in EFA. However, cytotoxicity responses
of mice fed additional polyunsaturated fat (PUF) decreased as concentration increased, whereas responses of mice fed the saturated
fat (SF) diets decreased only when the dietary fat concentration was greater than 8%. As compared to diets with EFA control,
direct plaqueforming cell (PFC) response was decreased for mice fed high levels of PUF and increased for mice fed high levels
of SF; however, no difference in the percentage of IgM-positive cells was observed. These changes in PFC response were inversely
related to the levels of linoleic acid in the lymphocyte. Thus, high levels of dietary fat, and particularly PUF, suppress
lymphocyte functions when EFA requirements are met, whereas low levels (EFA control) intensify these responses. EFA deficiency,
however, suppresses some lymphocyte responses. Thus, dietary lipids differentially modulate the levels of T- and B-cell responsiveness.
Presented at the 73rd Annual Meeting of the American Oil Chemists' Society in Toronto, Canada, May 1982. 相似文献
7.
Total and relative amounts of neutral lipids (NL) and phospholipids (PL) as well as the distribution of various lipid classes
in these were determined in testes of rats fed different types of partially hydrogenated oils for 5,15 and 26 weeks. The dietary
fats were partially hydrogenated arachis oil (HAO), partially hydrogenated soybean oil (HSO), partially hydrogenated herring
oil (HHO) and, for comparison, arachis oil (AO). An additional series of animals was reared on a fat-free diet throughout
the entire experiment. The total amount of NL is decreased by EFA deficiency parallel with the development of the degenerative
changes of the spermatogenic tissue. The relative amounts of NL in the testis are not influenced by EFA deficiency during
the first stages of degeneration. However, feeding of HHO for 26 weeks resulted in a marked decrease in NL. The total content
of PL is directly related to tissue degeneration. This observation is supported by the data obtained after 5 weeks of feeding
HHO and by the correspondence between the results found after 15 and 26 weeks on HAO and the fat-free diets, respectively.
The relative amount of PL is less influenced by EFA deficiency, but severe degenerations as found for the group fed HHO are
followed by decreases. The neutral lipids had three main fractions: triglycerides (TG), free fatty acids (FFA) and cholesterol
(Chol). FFA was found to be the main fraction of NL after 5 weeks, whereas TG was the main component of NL after 15 and 26
weeks, especially in the animals with degenerated testes. The presence of the large quantities of FFA is discussed. Cholesterol
was decreased markedly in the EFA deficient rats fed partially hydrogenated oils, but not in the fat-free reared groups. The
variations in the PL distribution during the experiment were small with regard to the two main PL classes, the phosphatidylcholines
and the phosphatidylethanolamines. The most remarkable change among the PL classes was an increase in the percentage of sphingomyelins
when the spermatogenic degenerations developed. 相似文献
8.
Effects of dietarytrans acids on the interconversion of linoleic acid was studied using the liver microsomal fraction of rats fed a semipurified
diet containing fat supplements of safflower oil (SAFF), hydrogenated coconut oil (HCO) at 5 and 20% levels or a 5% level
of a supplement containing 50.3% linolelaidic and 24.3% elaidic acids devoid ofcis,cis-linoleic acid (TRANS). Growth rate was suppressed to a greater extent with the animals fed the 20% than the 5% level of the
HCO-supplemented diets and still further by the TRANS diet compared to the groups fed the SAFF diets. Food intake was greater
in the groups fed the HCO than the SAFF-supplemented diets, demonstrating the marked effect of an essential fatty acid (EFA)
deficiency on feed efficiency. In contrast to an EFA deficiency produced by the HCO supplement, which stimulated the in vitro
liver microsomal biosynthesis of arachidonic acid, diets containing the TRANS supplement exacerabated the EFA deficiency and
depressed 6-desaturase activity of the liver microsomal fraction. The liver microsomal fraction of the animals receiving this
supplement also was more sensitive to fatty acid inhibition of the desaturation of linoleic acid than those obtained from
animals fed either the SAFF or HCO diets. It is suggested that dietarytrans acids alter the physical properties of the 6-desaturase enzyme system, suppressing its activity, which increases the saturation
of the tissue lipids and, in turn, the requirement for EFA or polyunsaturated fatty acids. 相似文献
9.
L. G. Cleland M. A. Neumann R. A. Gibson T. Hamazaki K. Akimoto M. J. James 《Lipids》1996,31(8):829-837
n-9 Eicosatrienoic acid (ETrA), also known as Mead acid, is a minor fatty acid in essential fatty acid (EFA)-sufficient healthy
subjects but is found at increased levels in EFA deficiency. This study examined the influence of dietary ETrA from a biological
source on plasma and tissue ETrA. A synthetic fat-free diet was prepared to which was added Mut 48 oil which contains 19%
ETrA (wt%) as well as other n-9 fatty acids. Blends of vegetable oils were used to achieve overall diets with 5% fat (wt%)
and varying amounts of ETrA at two different dietary levels of linoleic acid (LA), approximately 4.4 and 19% of total fatty
acids. These diets were fed to 5-week-old Dark Agouti rats for four weeks. Plasma lipid fractions and liver, spleen, and peritoneal
exudate (PE) cells were analyzed for fatty acid composition. ETrA was present at up to 20% total fatty acids in plasma triglyceride,
cholesterol ester, and phospholipid fractions. ETrA also accumulated to substantial levels in phospholipids of liver and spleen
(up to 15% of total fatty acids) and PE cells (up to 11%). ETrA was found in plasma and tissue phospholipids in proportion
to the amount of ETrA present in the diet. The incorporation was reduced in diets with higher LA content compared to diets
containing similar amounts of ETrA but lower LA. All rats remained apparently healthy, and histological survey of major organs
revealed no abnormality. While the long-term implications for health of ingestion of diets rich in ETrA remain to be established,
rats appear to tolerate high levels of dietary ETrA without adverse effects. Dietary enrichment with ETrA warrants further
investigation for possible beneficial effects in models of inflammation and autoimmunity, as well as in other conditions in
which mediators derived from n-6 fatty acids can affect homeostasis adversely. 相似文献
10.
In a retrospective study on essential fatty acid deficient, (EFAD) rats used to study pathophysiological roles of prostaglandins
(PGs) slight increases in the linoleic acid content of the diet were found to gradually restore the depressed growth rate
and to increase the reduced endogenous PG production. These apparently poorly deficient animals had a serum triene tetraene
(ω9:ω6) ratio much higher than the value of 0.4 used as a criterion for EFA deficiency by nutritionists. Changes in body weight,
serum ω9∶ω6 and platelet PG production were not correlated with each other. Feeding rats on a diet containing <0.1 mg/g/linoleic
acid led to decreasing platelet PG production as the degree of EFA deficiency increased. At this high level of deficiency,
a serum ω9∶ω6 ratio of 6 or over was achieved. This high ratio may be taken as anindicator of the degree of EFA deficiency required for studies of PG deprivation, but PG production by the tissue investigated or by
plalets should preferentially be measured. 相似文献
11.
Essential fatty acid (EFA) deficiency in rat causes severe degeneration of spermatogenic tissue. Previously it was shown that
the distribution of lipid classes changes very little during tissue degeneration. However it is well known that the fatty
acid spectrum in lipids from testicular tissue is altered drastically during EFA deficiency. The molecular binding of lipids
in membrane structures might be altered when a larger amount of ω9-acids is present in the various lipid classes in testes
of EFA-deficient rats. In the present studies comparison was made of the binding of lipids in testicular mitochondrial membranes
from rats fed a fat-free diet or a diet containing 6% peanut oil for 26 weeks. Isolated mitochondria were coated on glass
beads, then dried and packed into a column, whereafter the membrane lipids were eluted with solvents with increasing dielectric
constants. The differences between the binding of lipid classes in supplemented and EFA-deficient rats were not pronounced,
but a tendency to a weaker binding in the EFA-deficient rats was observed. However for both groups the various extracts showed
marked differences in the distribution of lipid classes concurrent with the change of the eluent. This indicates a different
kind of binding in the membrane, not only for different lipid classes, but also within a special lipid class. Thus both phosphatidylcholines
(PC) and phosphatidylethanolamines (PE) were found in extracts with quite different dielectric constants. The fatty acid composition
of PC and PE in the major fractions eluted with chloroform and ethanol, respectively, was essentially the same. This indicates
that the successive release of phospholipids (PL) in these two fractions was not based on fatty acid solubility properties
but on variable binding in the membrane structure. The introduction of ω9-polyenoic fatty acids instead of ω6-polyenoic fatty
acids in the PL of mitochondria membranes from EFA-deficient rats seems to be the only deviation in the lipid pattern of EFA-supplemented
and EFA-deficient animals, and might therefore be responsible for the symptons of EFA deficiency.
Presented in part at the AOCS-ISF World Congress, Chicago, September, 1970. 相似文献
12.
The effects of long term (8–14 wk) essential fatty acid (EFA)-deprived diets in rats are well documented. In the present study,
we compared, in weanling rats, the effect of a short term (two wk) hydrogenated coconut oil, EFA-deprived, diet (D) with that
of a corn oil, EFA-adequate, diet (A), using either sucrose (SU) or starch (ST) as carbohydrate. After two wk, rats fed the
sucrose/hydrogenated coconut oil diet developed some characteristic features of EFA deprivation: slower growth rate, decreases
in linoleic and arachidonic acid of plasma phospholipids and an increase in n−9 eicosatrienoic acid of plasma phospholipids.
When rats ate the starch/hydrogenated coconut oil diet, there was a similar decrease in linoleic acid of plasma phospholipids,
but only a small effect on growth rate and no change in the arachidonic acid content of plasma phospholipids. EFA deprivation
and sucrose had opposite effects on plasma triglyceride (TG) levels: deprivation induced a decrease, whereas the sucrose induced
an increase in very low density lipoprotein (VLDL) triglycerides. The observed decrease in plasma triglyceride during EFA
deporivation might result from an activation of lipoprotein lipase during the early stages of deprivation. 相似文献
13.
Studies are reported on the effect of an essential fatty acid (EFA) deficiency in male Sprague-Dawley rats and its exacerbation
by inclusion oftrans fatty acids in the diet on the level and composition of serum lipoproteins. Weanling male Sprague-Dawley rats were fed diets
containing all essential nutritients and a 5% fat supplement of safflower oil (SAFF) or hydrogenated coconut oil (HCO) in
2 experiments, one for 31 wk and the other for 17 wk. For the final 3 wk of each experiment, animals were switched from each
group to a 5% supplement of a concentrate of ethyl linolelaidate (TRANS). In addition, a group of animals fed the HCO diet
in the first experiment were also switched to the SAFF Diet. With the development of an EFA deficiency in the HCO group, there
was a decrease in the high density lipoprotein (HDL) and an increase in the very low density plus the low density (VL-LDL)
lipoprotein fractions separated by heparin-manganese precipitation. Switching animals of the HCO group to the TRANS supplement
exaggerated this effect and produced a very low ratio of HDL-to-VL-LDL. Analysis of the serum lipoproteins by polyacrylamide
disc gel electrophoresis showed that an EFA deficiency produced a marked alternation of the HDL fraction. Changes also appeared
to be produced in the VL-LDL fraction by an EFA deficiency and particularly upon switching EFA-deficient animals to the TRANS
supplemented diet. Switching animals of the SAFF group to the TRANS supplement brough about an immediate reduction in HDL
with a corresponding decrease in serum arachidonic acid. The data suggested a general relationship between arachidonic acid
and the level and composition of HDL on the one hand, and 18∶1 and VL-LDL on the other. Accordingly, the ratio of HDL-to-VL-LDL
appears to provide a sensitive biochemical index of the EFA status of the rat. 相似文献
14.
Experimental allergic encephalomyelitis (EAE) was induced in rats of the Lewis strain fed diets adequate or deficient in essential
fatty acids (EFA). After induction of the disease, the diets were supplemented with aspirin (3.75 g/kg diet), and the effects
of the drug on the course of EAE and on the synthesis of prostaglandin F (PGF) by brain slices from diseased animals and their
Freund controls were examined. Aspirin supplementation delayed the onset of EAE in both dietary groups. EFA-deficient rats
experienced an incidence and severity of the disease similar to that of aspirin-free, EFA-deficient rats, while the EFA-adequate
group showed a greater severity but not an increased incidence, compared to aspirin-free controls. Aspirin treatment led to
an increased PGF production by brain slices from rats on either diet and not subjected to an immunochallenge. When the diet
was deficient in EFA, challenge with antigen plus adjuvant or adjuvant alone tended to decrease PGF synthesis by brain slices,
and when the diet was adequate in EFA, immunochallenge caused a marked depression on PGF synthesis. It was concluded that
the PG synthetase inhibitor aspirin can alter the course of EAE in the rat, providing further evidence that PGs or related
metabolites may be involved in the immune response in this disease.
Part of a thesis submitted by Patricia G. Weston to the University of Illinois in partial fulfillment of requirements for
the Ph.D degree. 相似文献
15.
To test whether vitamin E deficiency might influence the course of essential fatty acid (EFA) deficiency, Long Evans rats
were fed diets containing a marginal amount (1.5% of calories) of 18∶2ω6 or 18∶3ω3 fatty acid with complete absence of the
other and with or without vitamin E. Vitamin E contents decreased continuously in serum and liver in all rats fed the E-free
diets but in the brains of only the rats fed the marginal 18∶3ω3, E-free diet. It is considered that the vitamin E is cooxidized
in the liver with 22∶6ω3, since this fatty acid is very low in livers of the rats fed the marginal 18∶2ω6 diet but much higher
in livers of the rats fed the marginal 18∶3ω3 diet. Brain 22∶6ω3 values are comparable for both groups. The source of 22∶6ω3
is evidently in the mother's milk, since following weaning there is a precipitous drop in 22∶6ω3 in serum, liver and carcass
of rats on the 18∶2ω6-containing diet. No significant signs of EFA deficiency were seen in the E-deficient rats.
Operated for the U.S. Department of Energy by the University of California under contract no. DE-AC03-76-SF00012. 相似文献
16.
The effect of dietary zinc deficiency in the rat on the lipid composition of the erythrocyte membrane was determined. Weanling
male Wistar rats were fed an egg whitebased diet containing <1.0 mg Zn/kg dietad libitum. Control rats were either pair-fed orad libitum-fed the basal diet suppelemented with 100 mg Zn/kg diet. A zinc refed group was fed the −Zn diet until day 18 and then pairfed
the +Zn diet until day 21. The voluntary feed restriction associated with dietary zinc deficiency resulted in erythrocyte
membranes that had depressed phospholipid/protein and elevated cholesterol/phospholipid ratios. Similarly, all feed restricted
groups had elevated 22-carbon n−3 polyunsaturated fatty acid (PUFA) and depressed 22-carbon n−6 PUFA concentrations in alkenylacyl
and diacyl glycerophosphoethanolamine, phosphatidylserine and phosphatidylcholine; they also had depressed 24∶2n−6 levels
in sphingomyelin. The relative concentrations of phospholipids in the membrane was similar between −Zn and +Zn (ad libitum) groups; however, the −Zn group had significantly less phosphatidylserine relative to +Zn (pair-fed) controls. 相似文献
17.
Groups of rats were fed from weaning with diets containing 5% by wt of hydrogenated coconut oil (HCO), safflower oil, or a
concentrate of ethyl elaidate and linolelaidate (TRANS) as the sole source of dietary fat. Fatty acid composition of the lipid
classes from serum, liver, heart, and kidney was determined, and the serum lecithin: cholesterol acyl transferase (LCAT) activities
were assayed for each animal. Serum LCAT activity was increased by both the HCO and TRANS diets in the early stages of the
development of an essential fatty acid (EFA) deficiency but was suppressed in the animals of the TRANS group as they became
older. The HCO and TRANS groups exhibited changes in tissue lipid fatty acid composition, as well as reduced growth, characteristic
of an EFA deficiency. Conversion of oleic acid to eicosatrienoic acid was impaired in the animals fed the TRANS diet, greatly
increasing the octadecenoic acid content of the tissue lipids at the expense of eicosatrienoic acid. The TRANS diet also suppressed
incorporation of eicosatrienoic acid into cholesteryl esters of tissue and serum, indicating that, when fed as the sole source
of unsaturated fat,trans fatty acids influenced the metabolism of unsaturated fatty acids and cholesterol. 相似文献
18.
Essential fatty acid (EFA) deficiency modifies several biological parameters, i.e., growth, metabolic rate and water balance
and induces functional changes in liver, kidney and lung tissues. The brain fatty acid changes reported in the literature
are generally smaller than those observed in other tissues. However, EFA deficiency initiated in rats prior to birth and continued
for a prolonged period of time results in decreased brain weight, brain lipid and phospholipid content and in considerable
changes in polyunsaturated fatty acid distribution, especially in the ethanolamine phosphoglyceride fraction. The unsaturation
level of this phospholipid is maintained at a constant level in spite of the fatty acid distribution changes. Brain lipid
analyses, carried out at various time intervals in EFA deficient animals, indicate that brain weights are already reduced
in 10-day-old deficient rats, that brain phospholipids decrease, especially in the males after three months, and that fatty
acid distribution changes begin rather early. The latter consist of a decrease of tetraenes and increase of trienes and of
the triene-tetraene ratios as early as at 10 days, a decrease of hexaenes after six months, and after six months, an increase
of pentaenes, which are elevated at birth but usually disappear after three months of age. Similar changes are observed in
myelin. The induced changes are not completely reversed upon return to normal diet.
One of five papers to be published from the Symposium “Lipid Transport,” presented at the AOCS Meeting, New Orleans, April
1970.
On leave of absence from the Department of Biochemistry, Medical School of the University of Mississippi, Jackson, Mississippi,
Research Career Development Awardee (6-K3-HE-18, 345), National Heart Institute of U.S. Public Health Service. 相似文献
19.
The impact of a moderate Zn deficiency on growth and plasma and liver lipids was investigated in two 4-week experiments with
male weanling rats fed fat-enriched diets. Semisynthetic, approximately isocaloric diets containing 3% soybean oil were supplemented
with either 7 or 100 mg Zn/kg diet and with 22% beef tallow (BT) or sunflower oil (SF). In Experiment 1, which compared the
dietary fat level and the fat source in a factorial design of treatments, all diets were fed ad libitum to 6 × 8 animals,
whereas intake of the high-Zn BT and SF diets was restricted in Experiment 2 (5 × 6 rats) to the level of intake of the respective
low-Zn diets. The low-Zn SF diet consistently depressed food intake and final live weights of the animals to a greater extent
than the other low-Zn diets, while intake and growth were comparable among the animals fed the high-Zn diets. The marginal
Zn deficit per se did not alter plasma triglyceride and cholesterol concentrations nor hepatic concentrations of triglyceride,
cholesterol and phospholipids. The fatty acid pattern of liver phospholipids did not indicate that chain elongation and desaturation
of fatty acids was impaired by a lack of zinc. It was concluded that dietary energy and fat intake, and fat source have a
greater effect on plasma and liver lipids than a moderate Zn deficiency. Marginally Zn-deficient diets enriched with sunflower
oil as a major energy source cause a greater growth retardation than diets rich in carbohydrates or beef tallow. 相似文献
20.
The growth of female rats was depressed further by the incorporation of DDT into a ration deficient in essential fatty acids
(EFA). With female rats fed a ration supplemented with EFA, DDT produced a slight stimulation in growth. DDT also produced
an increase in the 20∶3ω9/20∶4ω6 ratio in liver lipids of male rats fed a ration deficient in EFA. These data indicate an
effect in EFA nutrition. Substantial changes in the fatty acid composition of liver lipids resulted from the feeding of DDT.
The proportion of 16∶0 was decreased, while that of 18∶0 was increased. With rats on the supplemented rations an increase
in the proportion of 20∶4ω6 was observed, while in the deficient rats a comparable increase was observed in the proportion
of 20∶3ω9. These changes in fatty acid composition have been related to the proliferation of hepatic smooth endoplasmic reticulum
induced by the DDT, and it is suggested that this effect could increase the demand for EFA by the liver, thus influencing
EFA nutrition.
Technical Paper No. 3156, Oregon Agricultural Experiment Station. 相似文献