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Results for “FATTY ACIDS, ESSENTIAL”

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PubMed1985

Effects of different dietary intake of essential fatty acids on C20:3 omega 6 and C20:4 omega 6 serum levels in human adults.

Four diets which differed in fatty acid composition were provided for five months each to a group of 24 healthy nun volunteers. The diets contained 54% carbohydrates, 16% proteins and 30% lipids. One-third of the lipid part remained unchanged during the whole study, and two-thirds were modified during each period. For this latter portion, one of the following dietary fats was used: sunflower oil, peanut oil, low erucic acid rapeseed (LEAR) oil or milk fats. This procedure allowed an evaluation of the effects of various amounts of dietary linoleic acid (C18:2 omega 6) and alpha-linolenic acid (C18:3 omega 3) on the serum level of their metabolites. A diet providing a large amount of linoleic acid (14% of the total caloric intake) resulted in low levels of dihomo-gamma-linolenic acid (C20:3 omega 6) and arachidonic acid (C20:4 omega 6) in serum phospholipids and cholesteryl esters. A diet providing a small amount of linoleic acid (0.6% to 1.3% of the total caloric intake) induced high levels of omega 6 fatty acid derivatives. Intermediate serum levels of C20:3 omega 6 and C20:4 omega 6 were found with a linoleic acid supply of about 6.5% of the total caloric intake. Serum levels of omega 6 metabolites were not different after two diets providing a similar supply of C18:2 omega 6 (4.5% to 6.5% of the total caloric intake), although in one of them the supply of C18:3 omega 3 was higher (1.5% for LEAR oil versus 0.13% for peanut oil).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Effects of essential fatty acid administration on cardiovascular responses to stress in the rat.

This study examined the effects of 18:2(n-6), 18:3(n-6), 20:4(n-6) and 18:3(n-3) on cardiovascular responses to isolation stress in male rats. Group-acclimated rats were fasted for 2 days, then placed on a fat-free diet. Two wk later animals were divided into six groups (six animals per group) and given eight-wk intraperitoneal osmotic pumps releasing 1.47 X 10(-7) mol/hr of either olive oil (OL), or of 18:2(n-6), 18:3(n-6), 20:4(n-6) or 18:3(n-3) in OL. Another group received dummy pumps. Two wk after pump implantation, animals were isolated for four wk. Blood pressure (BP), heart rate and body weight were followed before and during stress. Following the stress period, animals were assessed for cardiovascular reactivity to norepinephrine (NOR) and angiotensin (ANG). Prior to isolation, 18:3(n-6) lowered BP vs OL (p less than 0.01). Stress increased BP within 24 hr in all groups except 18:3(n-6) and 20:4(n-6). Treatment with 20:4(n-6) vs OL prevented the BP rise (p less than 0.001) only for the first two wk of stress. Administration of 18:3(n-6) vs OL prevented any BP increase over the four-wk stress period (p less than 0.001). Stress increased heart rate in all groups except 20:4(n-6). Heart rate was lowered by 18:3(n-6) vs OL (p less than 0.01) before and during stress. Vascular reactivity to NOR was unaffected by treatment, but OL and 18:3(n-6) decreased responses to ANG infusion. These data suggest that 18:3(n-6) supplementation attenuates cardiovascular responses to chronic stress, and that delta 6- and delta 5-desaturase activity are inhibited during chronic psychological stress.

Angiotensins↗
PubMed1986

Desaturation and chain elongation of essential fatty acids in isolated liver cells from rat and rainbow trout.

Isolated hepatocytes from rainbow trout and rat were incubated with 14C-labeled linoleic acid, linolenic acid, dihomogammalinolenic acid or eicosapentaenoic acid. The most striking difference in the desaturase activity was the lower level of delta 5 desaturase in trout than in rat. No delta 4 desaturation of 22:4(n-6) to 22:5(n-6) was observed in either of the two species, while the conversion of 22:5(n-3) to 22:6(n-3) was significant in both groups and highest in rainbow trout. The chain-elongating activity was remarkably similar in the two species, except for the "dead-end" elongation which was distinctly more important in fish.

Animals↗
PubMed1988

Effect of essential fatty acid deficiency on the size and distribution of rat plasma HDL.

Rat plasma high density lipoproteins (HDL) are comprised of two major particle size subpopulations, HDL1 (255 A-140 A) and HDL2 (140 A-84 A), in which the proportion of arachidonate in fatty acids of cholesteryl esters is greater than 50%. To determine whether decreased availability of arachidonate for cholesterol esterification would alter the distribution and/or amounts of the HDL subpopulations, we compared HDL subpopulations in EFA-deficient and control rats. To separate the effects of EFA deficiency and fat deficiency and to evaluate effects of different saturated fats, we used EFA-deficient diets that were fat-free or that contained 5% saturated fat. The control diets were the EFA-deficient diets plus 1% safflower oil. The saturated fats were hydrogenated coconut oil, hydrogenated cottonseed oil and saturated medium-chain triglycerides. All EFA-deficient diets decreased the proportion of the HDL1 subpopulation and the peak diameter of the HDL2 subpopulation. These changes appeared after quite brief EFA depletion in young rats and may be related to the increased liver cholesteryl ester concentrations typical of EFA-deficient rats.

Animals↗
PubMed1991

The role of n-3 essential fatty acids in brain and behavioral development: a cross-fostering study in the mouse.

A cross-fostering design was used to examine the effects on brain and behavioral development in mice of pre- and/or postnatal dietary supplementation with n-3 fatty acids. Pregnant mice were fed either of two liquid diets, control (con) or experimental (exp). Each diet provided 3% of the calories in the form of n-6 fatty acids; the experimental diet was supplemented with an additional 1.5% from long chain n-3 fatty acids derived from fish oil. There were four treatment groups, with all pups fostered at birth. These groups were (prenatal diet/postnatal diet): Group 1. exp/exp; Group 2, exp/con; Group 3, con/exp; Group 4, con/con; a fifth control group (unfostered) was fed lab chow (LC) throughout the study. Animals from the exp/exp and con/con groups were weaned onto lab chow for later behavioral assessment. Prenatal n-3 supplementation resulted in a small acceleration of behavioral development. The adult animals did not differ on visual discrimination learning nor did they differ in visual acuity. During development the fatty acid composition of the brain membrane phospholipids reflected closely that of the pre- and postnatal dietary conditions. Levels of 22:5n-3 and 22:6n-3 increased in the n-3 supplemented groups, accompanied by a decrease in levels of 22:4n-6 and 22:5n-6; the net effect of these changes was to increase the total levels of C22 fatty acids. While these results support considerable plasticity of the fatty acid composition of the developing brain with respect to the immediate dietary availability of n-3 compounds, they do not support long term effects on learning capacity of n-3 supplementation during the developmental period.

Animals↗
PubMed1989

Increased liver lipase activity in rats with essential fatty acid deficiency.

Liver lipase activity was measured in EFA-deficient rats (long-term) and in control rats and rats fed an EFA-deficient diet for two weeks (short-term). Liver lipase activity was significantly enhanced by EFA deficiency, both in long-term and short-term experiments. The enhanced liver lipase activity could be normalized by feeding these rats normal laboratory chow for 14 days. Since during EFA deficiency prostaglandin synthesis is impaired, the possible involvement of prostaglandins in the observed changes in liver lipase activity during EFA deficiency was studied. Administration of the prostaglandin synthesis inhibitor indomethacin (5 mg/kg body weight, i.p.) to normally fed rats for two days led to an increase of liver lipase activity. Prostaglandin E2 was found to inhibit the secretion of liver lipase activity by freshly isolated parenchymal liver cells in vitro. These results indicate that the increase in liver lipase activity during EFA deficiency may be due to an impairment of the prostaglandin synthesis.

Animals↗