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)
Leukotrienes have been shown to play an important role as mediators in various disease processes, including asthma and inflammation; thus, their synthesis is tightly regulated. The major precursor of leukotrienes is arachidonic acid (20:4n-6). Fatty acids which are structurally similar to 20:4n-6, such as eicosatrienoic acid (20:3n-6; dihomogammalinolenic acid) and eicosapentaenoic acid (20:5n-3; timnodonic acid) have been found to inhibit leukotriene biosynthesis. Because of the structural similarity of octadecatetraenoic acid (18:4n-3; stearidonic acid) with 20:4n-6, the present study was undertaken to determine whether stearidonic acid also exerts an inhibitory effect on the 5-lipoxygenase pathway. Human leukocytes were incubated with 18:4n-3 (20 microM or 10 microM), 20:5n-3 (20 microM) or 20:3n-6 (20 microM) and subsequently stimulated with 1 microM ionophore A23187 and 20:4n-6 (20 microM or 10 microM). The 5-lipoxygenase products were then measured by high-performance liquid chromatography. Leukotriene synthesis was reduced by 50% with 20 microM 18:4n-3 and by 35% with 10 microM 18:4n-3. Formation of 5S,12S-di-hydroxy-eicosatetraenoic acid and of 5-hydroxy-eicosatetraenoic acid was decreased by 25% with 20 microM 18:4n-3 and by 3% with 10 microM 18:4n-3. The inhibition observed with 20 microM 18:4n-3 appeared to be of the same order as that observed with 20 microM 20:5n-3; the inhibition observed with 18:4n-3 was shown to be dose-dependent. The inhibition produced by 20 microM 20:3n-6 was greater than that observed with either 20 microM 18:4n-3 or with 20 microM 20:5n-3.(ABSTRACT TRUNCATED AT 250 WORDS)
Fatty acid composition of phospholipids in red blood cell membranes was studied in 32 severely head-injured or cerebral stroke patients receiving enteral nutrition for 3 weeks. During this study the effects of three diets differing only by their lipid composition were investigated. The daily energy intake of each patient amounted to 2950 kilocalories, of which the lipid fraction represented 45.7%. Diet A contained only soybean oil, diet B consisted of a 50% soybean oil and 50% medium-chain triglycerides mixture, and diet C was an emulsion of 50% soybean oil, 42.5% medium-chain triglycerides, and 7.5% black-currant seed oil. Our results showed no biochemical signs of fatty acid deficiency in red blood cell membranes for the patients at the beginning of the study, after a comparison with a control group of 20 healthy adults. Inhibition of delta 6-desaturase activity on linoleic acid (C18:2 omega 6) after diet A was suggested by an increase of linoleic acid without a corresponding increase of dihomo-gamma-linolenic acid (C20:3 omega 6). Replacing 50% of soybean oil by with medium-chain triglycerides (diet B) prevented this enzyme inhibition. Supply of black-currant seed oil rich in gamma-linolenic (C18:3 omega 6) and stearidonic (C18:4 omega 3) acids (diet C) induced significant increases of dihomo-gamma-linolenic and eicosapentaenoic (C20:5 omega 3) acids, without influencing arachidonic acid (C20:4 omega 6) levels. This balance was evaluated through the ratio (C20:3 omega 6 + C20:5 omega 3)/C20:4 omega 6.
The intravenous administration of parenteral fat emulsions is widely used in total parenteral nutrition (TPN) to supply essential fatty acids and concentrated energy in a relatively small volume of isotonic solution. They contain very high amounts of linoleic acid and usually about 8% of alpha-linolenic acid calculated in the fat phase (10 or 20% of the total emulsion). Most of the time one emulsion is given as the sole source of fat, giving direct venous entry to a fatty acid composition substantially different from that encountered in a normal diet. Since the latter greatly influences the fatty acid composition of phospholipids which are critical determinants of membrane structural properties influencing a variety of membrane functions (Fig. 1) (enzyme activity, membrane transport, receptor function) and functional precursors of intracellular and intercellular mediators (diacylglycerols, prostaglandins, leukotrienes, hydroxy fatty acids), do we provide the right fatty acid at the right place and the right time for efficient cell cell interaction? In other words, given the three roles of fatty acids--energetic, structural, functional--are we using the best strategy to avoid imbalances between the three roles?
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