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PubMed1975

Adipose tissue metabolism in essential fatty acid deficienty. Effects of prostaglandin e1, epinephrine, and ACTH.

In an effort to better define some of the metabolic changes that accompany essential fatty acid deficiency (EFAD), we studied glucose metabolism in adipose tissue of EFAD and normal mice under basal conditions and in the presence of prostaglandin E1 (PGE1), epinephrine, and ACTH1-18. Isolated fat cells were incubated in Krebs-Ringer bicarbonate medium containing glucose 1(-14C) or 6(-14C), and the incorporation of radioactive carbon into CO2, total fat, fatty acids, and glyceride-glycerol was determined. It was found that EFAD increased glucose uptake over controls which could be attributed to increased oxidation to CO2 and fatty acid synthesis. The contribution of the pentose cycle to glucose oxidation was 50-80% higher in EFAD adipocytes as compared to controls. ACTH1-18 (0.1 mug/ml) suppressed this by 18 and 30% in the control and EFAD groups, respectively, while epinephrine decreased pentose cycle activity by 83 and 55% in the two groups, respectively. PGE1 alone had no significant effect, but in combination with epinephrine it abolished the inhibitory action of the catecholamine in both groups. It is suggested that, although EFA serve as prostaglandin precursors, the effects of EFAD on the metabolism of fat cells cannot be reversed by PGE1, in vitro. However, these fat cells retain their responsiveness to the action of both lipolytic (ACTH and epinephrine) and antilipolytic (PGE1) agents.

Adipose Tissue↗
PubMed1989

Essential fatty acid deficiency delays the onset of puberty in the female rat.

This study assessed the effect of a dietary deficiency in the essential fatty acids (EFA) linoleic and linolenic acids on the onset of female puberty. EFA deficiency was produced in female rats by means of a semipurified diet and was biochemically documented by analyzing serum and erythrocyte fatty acid levels of more than 30 fatty acids, including all members of the n-6 and n-3 series. Levels of linoleic acid (18:2 n-6) and all n-6 derivatives, particularly arachidonic acid, were strikingly reduced. A less pronounced but clear-cut decrease in n-3 fatty acids, including docosahexaenoic acid (22:6 n-3) was also found. The times of puberty and first ovulation, as assessed by the ages at vaginal opening and first diestrus, were significantly delayed in EFA-deficient rats. The mechanisms underlying this delay appear to reside at both hypothalamic and ovarian sites. Simulation of preovulatory plasma estradiol (E2) levels via implantation of E2-containing Silastic capsules evoked a LH surge 30 h later in control juvenile rats, but not in EFA-deficient animals, indicating a delay in the development of the hypothalamic component of E2-positive feedback in the latter group. This delay appears to be due at least in part to reduced prostaglandin E2 (PGE2) synthesis, as the ability of the neurotransmitter norepinephrine to induce PGE2 release from median eminence nerve terminals was markedly reduced in EFA-deficient rats compared with that in controls. The decrease in hypothalamic PGE2 release was related to the EFA deficiency and not to reduced PG synthase activity, as determined by HPLC analysis of PG synthase products derived from exogenous [14C]arachidonic acid. Basal and hCG-stimulated PGE2 synthesis was also compromised in ovaries from EFA-deficient rats. Depressed gonadal function resulting from the EFA deficiency was further evidenced by a reduced gonadotropin receptor content, a blunted E2 response to hCG in vitro, and an increase in mean serum FSH levels. These results suggest that the delay in puberty resulting from EFA deficiency is due to a reduced availability of arachidonic acid for synthesis of bioactive metabolites. This results in delayed development of both the hypothalamic and ovarian components of the reproductive axis.

Animals↗
PubMed1984

The role of essential fatty acids and prostaglandins in cercarial penetration (Schistosoma mansoni).

We used rat skin membranes to test the putative role of prostaglandins (PG) and essential fatty acids (EFA) in the penetration response of Schistosoma mansoni cercariae. To examine the effects of EFA on cercarial penetration an EFA-deficient rat model was used. Dams were fed an EFA-deficient diet during lactation and the pups were weaned to this diet. Cercarial penetration of EFA-deficient rat skin membranes was not reduced from control levels until 12 wk on the diet. At this time a decrease of 64.3% was observed. This decrease remained constant up to 16 wk, after which the study was terminated. Other normal rats were treated with 20 mg/kg ibuprofen, a PG inhibitor, to examine the role of PG in the penetration response. Treated rat skin contained a mean of 2 micrograms ibuprofen per 30 mm3 of skin (25-mm skin disc) at 1.5 hours post-injection. Skin from treated rats inhibited penetration by over 81%. These studies indicate that skin EFA and PG may have a critical role in the completeness of penetration by cercariae through the skin, although it is not clear whether cercarial or host PG are involved in the penetration response.

Animals↗
PubMed1982

Influence of dietary essential fatty acid level on fatty acid composition in peripheral nerve and muscle.

Two groups of rats of different lines were divided into two lots. The four lots, whose dams received a fat-controlled diet, were fed with diets containing different levels of essential unsaturated fatty acids, namely linoleic (18:2 (n-6)) and linolenic (18:2 (n-3)) acid, in the oil. Nerve and muscle fatty acids were analyzed at adulthood. When the linolenic acid level was less than 0.6 p. 100 of the total fatty acids in the diets (peanut oil and sunflower oil), the level of long-chain polyunsaturated fatty acids (PUFA) of the (n-3) series decreased. This decrease was associated with an increase in the PUFA of the (n-6) series. Total PUFA ((n-3) + (n-6)) remained similar in the same group of rats, whatever the diet. On the contrary, when dietary linolenic acid reached 7.6 p. 100 (soya oil) or 8.5 p. 100 (rapeseed oil) of the total fatty acids, in the presence of a very high linoleic acid level, the PUFA of the (n-6) series decreased and that of the (n-3) series increased in nerve and especially in muscle. It appears that preferential PUFA biosynthesis from linolenic acid occurred when the ratio (n-6)/(n-3) was low enough in the dietary oil.

Animals↗
PubMed1978

Essential fatty acids, prostaglandins, and respiratory distress syndrome of the newborn.

The lungs are a major metabolic site for the synthesis, release, and degradation of prostaglandins. Prostaglandins of the E and F series exert a potent physiological effect on the smooth muscle of blood vessels and the tracheobronchial tree; prostaglandin E dilates while prostaglandin F constricts. Thus, altered prostaglandin metabolism may contribute to the pathophysiology of respiratory distress syndrome (RDS). Twenty-one infants with RDS and ten age- and weight-matched controls were studied by analyzing their plasma for prostaglandins and their precursor essential fatty acids. The two groups showed no differences in the essential fatty acid prostaglandin precursors, dihomo-gamma-linolenic and arachidonic acids. During the acute phase of RDS, plasma levels of the primary prostaglandins E and F are significantly elevated compared with control values and the ratio of prostaglandin E to prostaglandin F significantly reduced. Prostaglandins E and F returned to control values on recovery from the acute stage of the disease. Two infants with persistent patent ductus arteriosus had significantly elevated prostglandin E values in their plasma compared with controls. The elevated levels of circulating plasma prostaglandins E and F and the reversal of their ratio during the acute phase of RDS may have adverse pulmonary and multisystem effects.

8,11,14-Eicosatrienoic Acid↗
PubMed1967

Fatty acid changes in liver and plasma lipid fractions after safflower oil was fed to rats deficient in essential fatty acids.

1. Fatty acid patterns of liver and plasma triglycerides, phospholipids and cholesteryl esters were determined at intervals during 24hr. after essential fatty acid-deficient rats were given one feeding of linoleate (as safflower oil). 2. Liver triglyceride, phospholipid and cholesteryl ester fatty acid compositions did not change up to 7hr. after feeding. Between 7 and 10hr., linoleic acid began to increase in all fractions, but arachidonic acid did not begin to rise in the phospholipid until 14-19hr. after feeding. 3. Oleic acid and eicosatrienoic acid in liver phospholipid began to decline at about the time that linoleic acid increased, i.e. about 9hr. before arachidonic acid began to increase. 4. Changes in linoleic acid, arachidonic acid and eicosatrienoic acid in phosphatidylcholine resembled those of the total phospholipid. Phosphatidylethanolamine had a higher percentage content of arachidonic acid before the linoleate was given than did phosphatidylcholine, and after the linoleate was given the fatty acid composition of this fraction was little changed. 5. The behaviour of the plasma lipid fatty acids was similar to that of the liver lipids, with changes in linoleic acid, eicosatrienoic acid and arachidonic acid appearing at the same times as they occurred in the liver. 6. The results indicated that linoleic acid was preferentially incorporated into the liver phospholipid at the expense of eicosatrienoic acid and oleic acid. The decline in these fatty acids apparently resulted from their competition with linoleic acid for available sites in the phospholipids rather than from any direct replacement by arachidonic acid.

Animals↗
PubMed1979

The use of essential fatty acid deficient rats to study pathophysiological roles of prostaglandins. Comparison of prostaglandin production with some parameters of deficiency.

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 (omega9:omega6) ratio much higher than the value of 0.4 used as a criterion for EFA deficiency by nutritionists. Changes in body weight, serum omega9:omega6 and platelet PG production were not correlated with each other. Feeding rats on a diet containing less than 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 omega9:omega6 ratio of 6 or over was achieved. This high ratio may be taken as an indicator of the degree of EFA deficiency required for studies on PG deprivation, but PG production by the tissue investigated or by platelets should preferentially be measured.

Animals↗
PubMed1975

The effect of non-steroid anti-inflammatory drugs, dibutyryl cyclic 3',5'-adenosine monophosphate and phosphodiesterase inhibitors on platelet aggregation and the platelet release reaction in normal and essential fatty acid deficient rats.

A comparison was made of the action of three classes of substances with platelet aggregation inhibiting effect in normal and essential fatty acid deficient rats. In the latter group, the effect of indomethacin was considerably reduced, whereas the difference was smaller with aspirin. Dibutyryl cyclic AMP had the same inhibiting effect in both groups. Of the phosphodiesterase inhibitors tested, dipyridamole was inactive, whereas the inhibiting effects of caffeine and papaverine are slightly reduced in the deficient animals. The same differences between the two groups were seen in the magnitude of the release reaction after 14C-serotonin labelling. These data support the idea that the non-steroid anti-inflammatory drugs act by inhibiting the formation of an aggregation-inducing substance from arachidonic acid.

Animals↗
PubMed1982

Incorporation and turnover of essential fatty acids in phospholipids and neutral lipids of rainbow trout.

1. The turnover of rainbow trout (Salmo gairdneri) lipid was monitored in fish receiving essential fatty acids (EFA) replete and EFA deficient diets using [1-14C]-linolenic acid (C18:3 omega 3). 2. Forty percent of administered radioactivity was recovered in total lipid after 7 days. 3. Eighty-five percent of incorporated label was recovered in C18:3 omega 3 derivatives, primarily docosa-hexaenoic acid (22:6 omega 3). 4. Over 10 weeks, 14C activity in neutral lipid (NL) remained constant whereas that in phospholipid (PL) declined due to loss of label from shorter chain omega 3 fatty acids. The mass and specific activity of longer chain omega 3 fatty acids remained constant. 5. There was an accumulation of 14C activity and C22:6 omega 3 in PE at the expense of PC. 6. The pattern of incorporation of 32P inorganic phosphate into molecular classes of phosphatidylcholine (PC) of EFA deficient fish indicated that the rate of turnover of docosahexaenoyl PC was not diminished by EFA deficiency. 7. It is hypothesized that retention of C22:6 omega 3 in EFA deficiency is due to the presence of an efficient recycling system during membrane turnover.

Animals↗
PubMed1996

Essential fatty acid status of fetal plasma phospholipids: similar to postnatal values obtained at comparable gestational ages.

Hardly any direct information is available on the essential fatty acid (EFA) status of the fetus during intrauterine development. Therefore, we studied 86 umbilical plasma samples obtained by trans-abdominal puncture during ongoing pregnancies (18.3-39.0 weeks of gestational age). These were compared with 51 samples of umbilical cord blood, collected immediately after birth (gestational ages, 28.5-39 weeks). The total amounts of fatty acids in fetal plasma phospholipids (mg/l) did not change during gestation. The relative amounts of linoleic acid (% of total fatty acids) showed a slight increase (P = 0.03) during fetal maturation. Arachidonic acid (20:4n-6) decreased (both absolute (mg/l) and relative (% wt/wt) P < or = 0.0001), while docosahexaenoic acid (22:6n-3) increased (absolute P < 0.003, relative P < 0.0001) when pregnancy progressed. The EFA profiles of fetal samples were in general comparable with postnatal results of infants born at similar gestational ages. However, the fetal linoleic acid status was lower than the linoleic acid status of the neonates. The same was true for the overall EFA status. The results of this study indicate that the low EFA status observed in preterm infants at birth, is a developmentally related phenomenon.

Fatty Acids, Essential↗
PubMed1996

Essential fatty acid requirements in carp.

Till date, many workers have demonstrated the nutritive value of dietary lipids and the qualitative and quantitative requirements for essential fatty acid (EFA) in many cultivable fish. From the data accrued, a categorization can be made for the EFA requirement as follows: Type I (require n-6 fatty acids), Type II (require both n-6 and n-3 fatty acids) and Type III (require n-3 fatty acids). Common carp Cyprinus carpio and grass carp Ctenopharyngodon idella are codified as Type II fish based on their EFA needs. The requirement of both fish for dietary n-6 and n-3 fatty acids is found to be 1% and 0.5-1%, respectively. Our recent experiment clearly indicated that grass carp fed diet without EFA show deficiency symptoms like vertebral column curvature (VCC), indicating lordosis. The manifestation is similar to SEKOKE DISEASE which is characterised by apparent muscular dystrophy. However, grass carp fed an EFA-deficient diet did not exhibit the apparent muscular dystrophy. Recently, we have also investigated the interaction between EFA and vitamin E (VE), and the metabolism of linoleic acid (LA) using the isotope technique. These results are to be reviewed.

Animals↗
PubMed1982

Triacylglycerol secretion in rats: effects of essential fatty acids and influence of dietary sucrose, glucose or fructose.

The rate of triacylglycerol (TG) secretion into plasma was determined in vivo in essential-fatty-acid(EFA)-adequate and EFA-deficient rats fed for 8-10 weeks on diets containing either sucrose, glucose or fructose (66.5% wt/wt) as the sole source of carbohydrate. The rate of TG secretion was increased in EFA-deficient rats, irrespective of the type of dietary carbohydrate. The secretion rate in EFA-deficient rats fed fructose was 50% higher than the rate in similar animals fed glucose or sucrose, although in the EFA-adequate rats, the secretion rate with fructose was not significantly higher than with sucrose or glucose. The concentrations of triacylglycerols and cholesteryl esters in plasma were generally reduced in EFA deficiency, whereas the concentrations of these lipids in liver were increased. Plasma free fatty acid concentrations were unchanged. The fatty acid composition of plasma and hepatic lipids was altered both by EFA deficiency and to a smaller extent by the type of dietary carbohydrate. The concentration of plasma glucagon was reduced in the deficient animals, although plasma insulin concentration was not affected. The resulting increase in the plasma insulin:glucagon molar ratio may explain some of the alterations in lipid concentrations and in lipid metabolism observed in EFA deficiency.

Animals↗
PubMed1988

Regulation of essential fatty acid intake in the rat: self-selection of corn oil.

The present investigation was conducted to determine if rats can recognize the essential fatty acid (EFA) in the diet. Weanling rats were pre-fed a 30% hydrogenated coconut oil (30HCO) diet containing 1% cholesterol for 2 or 4 weeks to produce EFA deficiency, then allowed to choose between the fat-free (FF) diet and the 0.5, 1.0, or 2.0% corn oil diet, and between the 0.5% HCO diet and 0.5% corn oil diet. Rats pre-fed the 30HCO diet for 2 weeks selected the corn oil-containing diets for a few days at the beginning of the experiment, but the rats pre-fed for 4 weeks could not recognize the EFA-containing diet. The non pre-fed animals continued to prefer the EFA-containing diet for about 2 weeks. From these results we could demonstrate that rats have a mechanism to distinguish the EFA in their diet, but this EFA selection ability was only in the early period of the experiment, and diminished soon after.

Animals↗
PubMed2000

The control of blepharospasm by essential fatty acids.

Dopamine depletion induced by administration of Ro4-1284 produces a condition of rapid and repeated eye blinking in rats. This condition mimics the human disorder, blepharospasm, which often accompanies parkinsonism and other dopamine deficiency disorders. When given a 3-week course of a compound (SR-3) developed from a specific ratio of two free polyunsaturated fatty acids - linoleic acid and alpha-linolenic acid - the eye blinking rate following administration of Ro4-1284 is reduced to saline and no drug control levels. These results suggest a favorable prospect for essential fatty acids in general, and SR-3 in particular, to provide an improved therapeutic option for the clinical management of benign essential blepharospasm.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1998

Essential fatty acids and breast cancer: a case-control study in Uruguay.

The relationship between frequency of intake of different types of fat and breast cancer was investigated in a case-control study conducted in Montevideo, Uruguay, during the time period 1994-1996. Our study comprised 365 cases and 397 controls. A moderate and non-significant increase in risk of breast cancer, associated with total fat intake, was found. Saturated and monounsaturated fat intake were not associated to an increased risk of this malignancy, whereas polyunsaturated fat and linoleic acid were associated with a significantly reduced risk (OR 0.26, 95% CI 0.13-0.53). On the contrary, both alpha-linolenic acid and cholesterol intakes were associated with an increased risk of breast cancer (OR for the upper quartile of intake of alpha-linolenic acid 3.79, 95% CI 1.53-9.40). When alpha-linolenic was examined at different levels of intake, the OR's were significantly higher at low levels of linoleic acid intake (OR 7.5, 95% CI 1.9-28.8).

Adult↗