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1.
The objective of this study was to determine whether or not a relationship exists between free fatty acid (FFA) extraction
by skeletal muscle and onset of irreversible shock. Hind limb skeletal muscle vasculature of anesthetized dogs was surgically
isolated from cutaneous tissue and subjected to a modified Wigger's hemorrhage shock protocol which was divided into five
stages (I−V). Since the first signs of irreversibility began in Stage II, this stage of hypovolemic hypotension was subdivided
into IIa, IIb and IIc. Arterial and venous blood samples were taken during each stage for subsequent blood gas and FFA analysis.
The data indicated that the onset of severe tissue ischemia and metabolic acidosis occurs concurrently with increased uptake
of FFA and skeletal muscle vasodilation (decomposition). A possible physiological explanation for these observations could
be related to an increased synthesis and release of PGE1. This agent has been shown by others to inhibit adrenergic neurotransmitter release causing loss of vascular tone.
Presented at the fall American Physiological Society Meetings, St. Louis, MO, October 22–27, 1978. 相似文献
2.
In this study, we examined whether the increased availability of lipids in blood resulting from two types of diet manipulation
regulated metabolic gene expression in the skeletal muscle of rats. Feeding for 4 wk on an isocaloric-sucrose or a hypercaloric-fat
diet increased plasma TAG in the fed condition by increments of 70 and 40%, respectively, and increased fasting insulinemia
(approximately 3-fold) compared with a starch diet. The fat diet impaired glucose tolerance and caused obesity, whereas sucrose-fed
rats maintained their normal weight. We analyzed the expression of genes that regulate the exogenous FA supply (LPL, FAT/CD36,
FATP1), synthesis (ACC1), glucose (GLUT4, GLUT1, HK2, GRAT1, glycogen phosphorylase) or glycerol (glycerol kinase) provision,
or substrate choice for oxidation (PDK4) in gastrocnemius and soleus muscles at the end of the glucose tolerance test. LPL,
FAT/CD36, FATP1, PDK4, and GLUT4 mRNA as well as glycogen phosphorylase and glycerol kinase activity levels in both muscles
were unchanged by the diets. Increased mRNA levels of GLUT1 (1.6- and 2.6-fold, respectively) and GFAT1 (about 1.7-fold) in
gastrocnemius, and of ACC1 (about 1.5-fold) in soleus, were found in both the sucrose and fat groups. In the fat group, HK2
mRNA was also higher (1.8-fold) in the gastrocnemius. Both sucrose and saturated-fat diets prompted hyperinsulinemia and hyperlipemia
in rats. These metabolic disturbances did not alter the expression of LPL, FAT/CD36, FATP1, PDK4, and GLUT4 genes or glycogen
phosphorylase and glycerol kinase activity levels in either analyzed muscle. Instead, they were linked to the coordinated
upregulation in gastrocnemius of genes that govern glucose uptake and the hexosamine pathway, namely, GLUT1 and GFAT1, which
might contribute to insulin resistance. 相似文献
3.
Male Sprague-Dawley rats, 3 weeks of age, were fed semisynthetic diets containing test oils at 20% by weight for 3 days, 1
week, and 16 weeks. The test oils contained up to 22.3% erucic acid. Growth retardation was evident in rats fed rapeseed oil
high in erucic acid, and soybean oil and Tower rapeseed oil diets containing about 5% erucic acid. Cardiac triglyceride accumulation
was found in rats fed diets containing about 5% erucic acid but not in rats fed Tower rapeseed oil which contains 0.2% of
this acid. The cardiac free fatty acid levels were low, 50–100 μg/g of wet heart tissue, and were not affected by feeding
diets containing about 5% erucic acid. Feeding a diet containing a high erucic acid rapeseed oil did result in higher free
fatty acid levels but only at 3 days and 1 week; the level at 16 weeks was similar to the other oils. The fatty acid analysis
of cardiac triglycerides and free fatty acids showed high percentages of erucic acid at 3 days and 1 week; at 16 weeks these
levels had declined significantly. The results indicate that the accumulated erucic and eicosenoic acids, at 3 days and 1
week, accounted for the increase in cardiac free fatty acids when rats were fed the high erucic acid rapeseed oil. There appears
to be no evidence that the early cardiac triglyceride or free fatty acid accumulation is related to the formation of the long
term myocardial lesions.
Contribution No. 739 Animal Research Institute. 相似文献
4.
Brain free fatty acid levels in rats sacrificed by decapitation versus focused microwave irradiation
Values are presented for whole brain free fatty acid levels of rats sacrificed by decapitation vs focused microwave irradiation.
Free fatty acids were quantitated by specific colorimetric analysis. Within ca. 1 min of sacrifice by either decapitation
or microwave, rat whole brain free fatty acid concentrations ranged from ca. 80–100 μg/g fresh tissue. If the brain remained
in the head for a total of 5 min after decapitation, free fatty acid levels increased by over 100%. The free fatty acids at
this time were enriched with arachidonic acid. The increase in free fatty acid levels following decapitation was completely
absent in rats sacrificed by the microwave irradiation. This microwave technique could be a valuable tool in determining free
fatty acid and other heat stable compounds in brain tissue. 相似文献
5.
Rats were fed (for 2 or 6 wk) purified diets containing lard (LD) or menhaden oil (MO) at two levels of dietary fat,i.e., at 11.5 and 20.8% of energy in the low fat (LF) and the medium fat (MF) diets, respectively. Following the diet period,
rats were sacrificed after either an overnight fast or after uninterruptedad libitum feeding. The studies were designed to investigate the dependence of our previously reported effects of MO,i.e. the reduction of plasma free fatty acid (FFA) levels and accumulation of hepatic triacylglycerols, on the dietary fat concentration
and the nutritional state of the animal at the time of sacrifice. Reductions in plasma triacylglycerol and cholesterol levels
in MO-fed relative to LD-fed rats were observed under all conditions. FFA levels were consistently reduced by MO-feeding at
both dietary fat concentrations, but only when blood was sampled fromad libitum fed rats. Under these conditions there was a significant positive relationship between plasma FFA and triacylglycerol concentrations.
Reduction in plasma FFA levels may be an additional mechanism associated with the triacylglycerol-lowering effect of fish
oil (FO). The LF and MF MO diets caused a rise in plasma glucose levels with no significant change in insulin concentration,
indicating that the reduction of FFA by MO was not related to changes in insulin concentration or insulin sensitivity. The
MO diets had no effect on skeletal muscle or epididymal adipose tissue lipoprotein lipase activity, demonstrating that catabolism
of triacylglycerol-rich lipoproteins contributes little, if any, to the MO-dependent reductions of plasma triacylglycerol
and FFA. The previously reported accumulation of hepatic triacylglycerols after high fat (HF; 30% of energy) MO-feeding was
not observed with the LF or MF MO diets, suggesting that the apparent direct inhibition of triacylglycerol secretion by FO
imposes a rate-limitation only when feeding HF diets. 相似文献
6.
Previous studies with cardiac myocytes from homozygous heart-type fatty acid (FA)-binding protein (H-FABP)−/− mice have indicated that this intracellular: receptor protein for long-chain FA is involved in the cellular uptake of these
substrates. Based on the knowledge that muscle FA uptake is a process highly sensitive to regulation by hormonal and mechanical
stimuli, we studied whether H-FABP would play a role in this regulation. A suitable model system to answer this question is
provided by H-FABP+/− mice, because in hindlimb muscles the content of H-FABP was measured to be 34% compared to wild-type mice. In these H-FABP+/− skeletal muscles, just as in H-FABP−/− muscles, contents of FA transporters, i.e., 43-kDa FABPpm and 88-kDa FAT/CD36, were similar compared to wild-type muscles,
excluding possible compensatory mech-anisms at the sarcolemmal level. Palmitate uptake rates were measured in giant vesicles
prepared from hindlimb muscles of H-FABP−/−, H-FABP+/− and H-FABP+/+ mice. For comparison, giant vesicles were isolated from liver, the tissue of which expresses a distinct type of FABP (i.e.,
L-FABP). Whereas in H-FABP−/− skeletal muscle FA uptake was reduced by 42–45%, FA uptake by H-FABP+/− skeletal muscle was not different from that in wild-type mice. In contrast, in liver from H-FABP−/− and from H-FABP+/− mice, FA uptake was not altered compared to wild-type animals, indicating that changes in FA uptake are restricted to H-FABP
expressing tissues. It is concluded that H-FABP plays an important, yet merely permissive, role in FA uptake into muscle tissues. 相似文献
7.
This study compared (i) the relative effects of long-chain triglycerides (LCT) and medium-chain triglycerides (MCT), (ii) the influence of amount of MCT, and (iii) the impact of medium-chain fatty acid position, on plasma and lymphatic triglycerides and portal vein free fatty acids. The animals were fed approximately at 250 kcal/kg · day for 20h. The lymph from lymphatic duct and blood from portal vein and systemic circulation were collected. The results showed that feeding 100% MCT for 20h was sufficiently long to reduce significantly the level of linoleic acid in portal vein fatty acids and plasma and lymph triglycerides. However, this alteration induced by MCT feeding was partially prevented by adding LCT to the diet. The level of arachidonic acid was significantly reduced in plasma triglycerides by any of the diets containing medium-chain fatty acids compared to 100% LCT. When feeding MCT only, palmitoleic acid, presumably reflecting de novo lipogenesis, was increased in lymphatic triglycerides and portal vein fatty acids. Total saturated fatty acids as a total percentage of total fatty acids were also significantly increased in plasma and lymphatic triglycerides and portal vein fatty acids. Thus, when linoleic acid is limiting, the conversion of MCT into long-chain fatty acids by de novo lipogenesis is likely to be an important metabolic route. Providing LCT with MCT or 2-monodecanoin appears to limit this pathway. 相似文献
8.
Skeletal muscle phospholipid fatty acid (PLFA) composition is associated with insulin sensitivity in animal models and in
man. However, it is not clear whether changes in insulin sensitivity cause a change in PLFA composition or vice versa. The
present studies have examined the effects of agents known to increase or decrease insulin sensitivity on PLFA composition
of the major phospholipids, phosphatidylcholine (PC) and phosphatidylethanolamine (PE), in soleus and extensor digitorum longus
muscle. Four groups of Sprague-Dawley rats— control, 0.2% troglitazone (Tgz), 60% fructose fed, and fructose + Tgz—were treated
for 3 wk. Fructose feeding was associated with a decrease in muscle membrane polyunsaturated fatty acids (PUFA) and n-3 fatty
acids in both PC and PE. Administration of Igz alone resulted in an increase in liver (3.75±0.93 to 6.93±1.00 μmol/min/mg
tissue, P<0.05) and soleus muscle (0.34±0.03 to 0.67±0.09 μmol/min/mg, P<0.01) elongase activity, which would be expected to increase membrane PUFA. However, Tgz decreased PLFA associated with greater
insulin sensitivity (e.g., PUFA and n-3 fatty acids) and increased PLFA associated with decreased insulin sensitivity (16∶0
and n-6 fatty acids) in both PC and PE. Co-administration of fructose and Tgz did not reverse the decrease in PUFA observed
with fructose alone. We conclude that the improvement in insulin sensitivity reported with Tgz is associated with an apparently
paradoxical effect to decrease PUFA and n-3 PLFA composition in rat skeletal muscle. These studies suggest that Tgz-mediated
increases in insulin sensitivity do not result in improved PLFA composition. 相似文献
9.
High levels of dietary arachidonic acid triglyceride exhibit no subchronic toxicity in rats 总被引:3,自引:0,他引:3
Arachidonic acid (AA), an n?6 long-chain polyunsaturated fatty acid (LC-PUFA), serves an important role in the body as a structural fatty acid of many tissues including neurological tissues. It is also a precursor of the n?6 class of eicosanoids and is the most abundant n?6 LC-PUFA found in human breast milk. We have optimized the production of a microfungal source of a triglyceride oil (ARASCO®) which is enriched in AA to about 40% by weight. To establish the safety of this oil as a food, we evaluated the effect of ARASCO® in Sprague-Dawley rats (20/sex/group) gavaged at dose levels of 1.0 and 2.5 g/kg/d for a period of 90 d, paying special attention to any potential neurotoxicity of the oil. Two groups of control animals received either untreated standard laboratory diet (untreated control) or the same diet and vehicle oil at the same dose volume administered to the treated animals (vehicle control). Physical observations, ophthalmoscopic examinations, body weight, food consumption, clinical chemistry, hematology parameters, neurobehavioral assessments, and macroscopic as well as microscopic postmortem evaluations were performed. Tissue fatty acid analyses indicated that the AA levels in the brain, heart, and liver of the high-dose ARASCO®-fed animals increased by 8, 59, and 76%, respectively, indicating that the AA in the oil was readily incorporated into tissue lipids. In spite of this high elevation in tissue AA levels, no developmental, histopathological, or neuropathological differences were seen in the animals administered ARASCO® compared with the vehicle control animals. Being highly enriched in AA, ARASCO® offers the means to study the effect of this fatty acid in experimental settings and in human metabolic studies. 相似文献
10.
Young male rats were fed ad libitum for 8 weeks a low iron fat-free (FF-Fe) diet or a fat-free diet supplemented with iron
(FF+Fe). The relative levels of 16∶1 to 16∶0 and 18∶1 to 18∶0 in the total fatty acids of liver and other tissues (plasma,
erythrocytes and intestinal mucosa) were considerably decreased because of a lack of dietary iron. In rats fed the FF-Fe diet,
the levels of essential fatty acids (18∶2ω6+20∶4ω6) in tissues were 2-to 3-fold greater than in the corresponding tissues
of rats fed the FF+Fe diet. Eicosatrienoic acid (20∶3ω9) levels in tissue lipids from rats fed the FF+Fe diet were high (8–16%),
whereas they were low (2–5%) in the case of animals fed the FF-Fe diet. The proportion of 20∶4 in total fatty acids of tissues
was 2-to 3-fold greater in rats fed the FF-Fe diet than when they were fed the FF+Fe diet. Therefore, the relative levels
of 20∶3ω9/20∶4ω6 varied from 1-2.9 in tissue lipids of rats fed the FF+Fe diet, while it varied only from 0.2–0.3 in animals
fed the FF-Fe diet. These results suggest that a lack of dietary iron may reduce the synthesis of 16∶1, 18∶1, 20∶3 and 20∶4
and the metabolism of 20∶4. 相似文献
11.
J. K. G. Kramer E. R. Farnworth B. K. Thompson A. H. Corner H. L. Trenholm 《Lipids》1982,17(5):372-382
A comprehensive statistical analysis had shown a significant correlation between the incidence of myocardial lesions in male
albino rats and the concentration of certain dietary fatty acids. To test this result under controlled conditions, male rats
were fed for 16 weeks diets containing 20% by weight soybean oil or a low erucic acid rapeseed (LEAR) oil. Both dietary oils
contained substantial amounts of linolenic acid, and both groups developed a high incidence of myocardial necrosis. The addition
of dietary saturated fatty acids to the oil in the form of cocoa butter significantly lowered the incidence of heart lesions
in both groups. The addition of cocoa butter resulted in increased absorption of saturates and increased growth. Replacement
of the cocoa butter by at least an equal amount of synthetic triolein resulted in no significant changes in the cardiopathogenic
response compared to the original oils, thus ensuring that the reduction in heart lesions associated with the addition of
cocoa butter was not due to dilution of cardiopathogenic compounds in the original vegetable oils. These results support the
hypothesis that myocardial lesions in male rats are related to the balance of dietary fatty acids and not to cardiotoxic contaminants
in the oils. Changes in the dietary fatty acids did not appear to influence the proportion of the cardiac phospholipids, but
their fatty acid composition was markedly influenced. Dietary linolenic acid affected the C22 polyunsaturated fatty acids
(PUFA) and dietary saturates increased the level of saturates in cardiac phospholipids. The level of arachidonic acid and
total C22 PUFA did not appear to be affected by diet.
Contribution no. 1004 from the Animal Research Centre and No. I-272 from the Engineering and Statistical Research Institute. 相似文献
12.
Male Sprague-Dawley rats were fed, ad libitum for 30 days, a fat-free (FF) liquid diet containing 34% of the calories as ethanol
or a control FF diet in which alcohol was replaced by an isocaloric amount of dextrins. The cytosolic fatty acid synthetase
and the microsomal stearoyl-CoA desaturase activities in the livers of rats fed the alcohol diet were about half of those
observed in the livers of control rats. The conclusion is that chronic ethanol consumption depresses the activities of these
lipogenic enzymes in the liver. 相似文献
13.
The aim of the present study was to investigate whether eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) was responsible
for the triglyceride-lowering effect of fish oil. In rats fed a single dose of EPA as ethyl ester (EPA-EE), the plasma concentration
of triglycerides was decreased at 8 h after acute administration. This was accompanied by an increased hepatic fatty acid
oxidation and mitochondrial 2,4-dienoyl-CoA reductase activity. The steady-state level of 2,4-dienoyl-CoA reductase mRNA increased
in parallel with the enzyme activity. An increased hepatic long-chain acyl-CoA content, but a reduced amount of hepatic malonyl-CoA,
was obtained at 8 h after acute EPA-EE treatment. On EPA-EE supplementation, both EPA (20:5n-3) and docosapentaenoic acid
(DPA, 22:5n-3) increased in the liver, whereas the hepatic DHA (22:6n-3) concentration was unchanged. On DHA-EE supplementation
retroconversion to EPA occurred. No statistically significant differences were found, however, for mitochondrial enzyme activities,
malonyl-CoA, long-chain acyl-CoA, plasma lipid levels, and the amount of cellular fatty acids between DHA-EE treated rats
and their controls at any time point studied. In cultured rat hepatocytes, the oxidation of [1-14C]palmitic acid was reduced by DHA, whereas it was stimulated by EPA. In thein vivo studies, the activities of phosphatidate phosphohydrolase and acetyl-CoA carboxylase were unaffected after acute EPA-EE and
DHA-EE administration, but the fatty acyl-CoA oxidase, the rate-limiting enzyme in peroxisomal fatty acid oxidation, was increased
after feeding these n-3 fatty acids. The hypocholesterolemic properties of EPA-EE may be due to decreased 3-hydroxy-3-methylglutaryl-CoA
reductase activity. Furthermore, replacement of the ordinary fatty acids, i.e., the monoenes (16:1n-7, 18:1n-7, and 18:1n-9)
with EPA and some conversion to DPA concomitant with increased fatty acid oxidation is probably the mechanism leading to changed
fatty acid composition. In contrast, DHA does not stimulate fatty acid oxidation and, consequently, no such displacement mechanism
operates. In conclusion, we have obtained evidence that EPA, and not DHA, is the fatty acid primarily responsible for the
triglyceride-lowering effect of fish oil in rats. 相似文献
14.
Rats of an inbred Sprague-Dawley strain were fed purified diets with low (0.3% of total energy), normal (3%) or high (10%)
content of essential fatty acids (EFA) for at least three generations. Two 30-days-old rats with similar weights were chosen
from one litter. One was killed; weight increase and food consumption of the other rat was measured for 15 days. Total lipid
content and fatty acid composition in total lipid and lipid classes were determined in both rats. Seven pairs of rats from
each group were treated in the same way. Calculations based an amount of linoleic acid ingested and retained in the carcass
lipids showed that 50% of the ingested linoleic acid was retained in the low EFA rats compared to 10–15% in the normal and
high EFA rats. 相似文献
15.
The effect of very low levels of dietary long-chain n−3 fatty acids on Δ6 desaturation of linoleic acid (18∶2n−6) and α-linolenic
acid (18∶3n−3), and on Δ5 desaturation of dihomo-γ-linolenic acid (20∶3n−6), in liver microsomes and its influence on tissue
fatty acids were examined in obese and lean Zucker rats and in Wistar rats. Animals fed for 12 wk a balanced diet containing
ca. 200 mg of long-chain polyunsaturated n−3 fatty acids per 100 g of diet were compared to those fed the same amount of α-linoleic
acid. Low amounts of long-chain n−3 fatty acids greatly inhibited Δ6 desaturation of 18∶2n−6 and Δ5 desaturation of 20∶3n−6,
while Δ6 desaturation of 18∶3n−3 was not inhibited in Zucker rats and was even stimulated in Wistar rats. Inhibition of the
biosynthesis of long-chain n−6 fatty acids was reflected in a decrease in arachidonic acid (20∶4n−6) content of serum lipids
when fasting, and also in the phospholipid fatty acids of liver microsomes. On the contrary, heart and kidney phospholipids
did not develop any decrease in 20∶4n−6 during fish oil ingestion. Docosahexaenoic acid (22∶6n−3), present in the dietary
fish oil, was increased in serum lipids and in liver microsome, heart, and kidney phospholipids. 相似文献
16.
Male and female weanling rats that were born to dams fed a diet low in linolenic acid received diets of 15% lipids by weight
containing 45% elaidic acid (as trielaidin) and 8.5% or 0.1% linolenic acid for 10 weeks. Four other groups, in which palmitic
or oleic acid replaced elaidic acid in the diet, served as controls. The fatty acid profiles of several lipid classes were
determined in adipose tissue, adrenals, testes, heart and brain. Elaidic acid was incorporated into tissue lipids in varying
degrees, depending on the organ and on the lipid class. Feeding elaidic acid induced no changes in the polyunsaturated fatty
acid (PUFA) profiles of testes lipids but resulted in definite modifications of the PUFA patterns of heart phosphatidylcholine
(PC) and phosphatidylethanolamine (PE). In linolenic acid-deprived rats, arachidonic acid was decreased in PC and linoleic
acid was increased in both PC and PE; 22∶5n−6 was strongly depressed in both PC and PE. In linolenic acid-fed rats, 22∶6n−3
was decreased in PC and PE. These changes, on the whole, were more evident in females, and some also were observed in adrenal
cholesteryl esters but only slightly in brain phospholipids. the apparent inhibition of the biosynthesis of PUFA induced by
dietary elaidic acid appeared to be complex and of greater intensity in the n−6 fatty acid series than in their n−3 homologues. 相似文献
17.
Response of free and esterified plasma cholesterol levels in the mongolian gerbil to the fatty acid composition of dietary lipid 总被引:2,自引:0,他引:2
The present study was undertaken to investigate the potential suitability of the Mongolian gerbil as a useful animal model
to study the effects of dietary fats on plasma cholesterol levels. Semipurified diets containing either 20% lard, 20% safflower
oil, or 19.5% beef tallow +0.5% safflower oil were equalized to contain 0.01% cholesterol and 0.05% plant sterol and were
fed for a four week experimental period. The proportions of total calories contributed by fat, protein and carbohydrate (starch/sucrose
ratio of 2∶1) were 40, 14 and 46%, respectively, so as to approach the distribution of calories within the average North American
diet. Free, esterified, and total plasma cholesterol levels of male gerbils were determined weekly by gas liquid chromatography
after drawing blood via a serial sampling technique. After 1, 2, 3, and 4 weeks of feeding the experimental diets, total cholesterol
levels were lowest in the safflower oil fed animals; the corresponding values were 19–64% greater in gerbils fed lard and
68–91% greater in those consuming the beef tallow diet. Cholesterol in the free form generally responded more dramatically
to the type of dietary lipid than did cholesterol in the ester form. Irrespective of the type of dietary lipid or the length
of the feeding trial, 18–23% of the total plasma cholesterol was in the free form and 77–82% was present as the ester. In
view of the similarity to the human of the relative proportions of free versus esterified cholesterol, the type of cholesteryl
esters, and their response to dietary manipulation, the gerbil appears to be a useful animal model for studying the regulatory
effect of dietary lipid on plasma cholesterol levels.
Presented in part at the A.O.C.S. Annual Meeting, San Francisco, CA, May 1979. 相似文献
18.
Isopolyunsaturated lipids isolated from plant and animal sources were included in the diets of mature male rats. Liver and
blood serum cholesterol lowering effects were noted only in the lipid from the vegetable source. The authors suggest that
the cholesterol lowering effect of vegetable oils is associated with the generally betaunsaturated triglycerides found therein.
Journal Article No. 3758, Michigan Agricultural Experiment Station, East Lansing, Mich. 相似文献
19.
Chicks were fed isocaloric and isonitrogenous diets containing 6% (w/w) added fat consisting of various proportions of animal
tallow and flaxseed oil (FSO). No differences among treatments were seen in growth rate, muscular deposition of protein and
lipids nor in the muscle phospholipid (PL) and triglyceride (TG) contents. Prostaglandin (PG)E2 synthesis in isolated skeletal muscle was depressed significantly by feeding FSO or by treatment with naproxen (6-methoxy-α-methyl-2-napthaleneacetic
acid), an inhibitor of PG synthesis. The changes associated with diet may be related to differences in the fatty acid composition
of muscle lipids. Levels of saturated fatty acids in muscle PL and TG were relatively insensitive to dietary treatments. Monounsaturated
fatty acid levels were significantly lower in the FSO-fed groups. FSO diets caused significant depression in muscle PL 20∶4ω6
and almost completely inhibited 22∶5ω6 incorporation. FSO diets decreased ratios of ω6/ω3 fatty acids and increased the unsaturation
index of muscle PL. Muscles of chicks fed FSO showed increased levels of 18∶3ω3, and of its derivatives 20∶4ω3 and 22∶5ω3.
These results suggest that FSO inhibits PG synthesis and modifies the fatty acids of PL and TG of chick muscle. These changes
may have implications for PG-dependent and/or membrane-dependent processes in muscle metabolism. 相似文献