Coconut Oil Diet Research Articles

Fatty Acid Composition of Adipose Tissue as an Indicator of Diet: A Preliminary Assessment

In one experiment, male Norway rats (Rattus norvegicus) were provided diets in which oil composition varied systematically from 20% corn oil (and no coconut oil) to 20% coconut oil (and no corn oil). After 5 weeks, samples of adipose tissue (N = four rats/diet) were analyzed for fatty acids. Oleic and linoleic acids (combined) made up the greatest proportion of fatty acids in the samples (? = 53.5%), whereas palmitoleic (? = 3.1%) and acids (f = 3.2%) were relatively least abundant. Lauric and myristic acids, more of which are found in coconut oil than in corn oil, were strongly (r2 = 0.83 and 0.88, respectively) and directly associated with percentage of dietary coconut oil. In a second experiment, three black rats (R. rattus) were maintained on a diet of macadamia nuts for 28 days, and another three were collected in a macadamia grove. Three mongoose (Herpestes auropunctatus) were fed rats for 38 days that had been collected in a macadamia grove, and three were fed rats collected in a sugarcane field. All animals except the latter three mongoose (r2 = 0.49) had proportions of fatty acids that were strongly associated (r2 = 0.84-0.99) with the proportions of fatty acids in the oil of macadamia nuts. The data support the hypothesis that analyses of fatty acids could provide reliable information on the dietary histories of vertebrates in selected agroecosystems and might supplement existing methods, such as radiotelemetry and analyses of stomach contents, as a tool for identifying vertebrate pests and their food-web associates. J. WILDL. MANAGE. 49(1):170-177 Mosby et al. (1974) suggested that, in situations where fat constitutes a large portion of the diet, fatty acid composition of body fat might be used to provide information on the dietary histories of animals. Such a tool might be a useful complement to existing methods (which now include stomach content analyses, marking foods, and direct field observation [Korschgen 1971]) for studying food habits of wildlife and, perhaps, their food-web associates in certain ecosystems. In support of this notion is considerable literature indicating that diet can influence the fatty acid composition of adipose and other tissues in animals (e.g., Hilditch and Williams 1964). For example, Garton et al. (1952) reported that a domestic pig fed from weaning on a diet consisting of 50% whale oil had backfat whose fatty acid composition reflected in part that of whale oil. In general, relations between diet and body fat of livestock are sufficiently understood to allow the use of diet to upgrade the composition of fat before marketing animals (Masoro 1968:25). Evidence also suggests that relationships exist between diet and composition of body fat in rodents. Fatty acids in the adipose tissue reflected diets when various strains of laboratory rats (R. norvegicus) were fed corn oil (Longenecker 1939a), coconut oil (Longenecker 1939b), oddchain fatty acids (Bernardini et al. 1976), or branched-chain fatty acids (Smith et al. 1978). Mosby et al. (1974) reported that composition of fatty acids in the body fat of Polynesian rats (R. exulans) was similar to that found in coconut oil. The rats were collected on the Tokelau Islands where coconuts constitute a major portion of their diets (Mosby et al. 1973). However, factors other than diet can also influence the fatty acid composition of adipose tissue (e.g., Masoro 1968:25). Fatty acids can be subjected to various biochemical transformations that alter overall composition of deposited fats. Mosby et al. (1974), for example, noted a lower ratio of lauric:myristic acids in adipose tissue of R. exulans than occurs in coconut oil, possibly due to an elongation of lauric acid to myristic acid by enzymes known to be present in the rat. Fatty acid composition also differs among species, probably as influenced by diet. Hilditch and Williams (1964:93) characterized the body fat of land mammals as having about 30% (molar) palmitic acid, and the body fat of ruminants, including domestic goats, deer (Cervus elaphus), camels, (Camelus spp.), and hippopotamuses (Hippopotamus amphibius), as stearic rich (p. 99). Stearic acid generally

Effects of Dietary Vitamin E on Serum and Pulmonary Fatty Acids and Prostaglandins in Rats Fed Excess Linoleic Acid

The interrelationships of dietary vitamin E and essential fatty acids and their effects on serum and pulmonary prostaglandin (PG) synthesis and fatty acid precursors were examined. In a preexperimental period, male weanling rats were depleted of essential fatty acids (EFA) by feeding on a hydrogenated coconut oil diet. At the end of 45 days, average serum triene:tetraene ratio for the EFA-deficient rats was 0.76. After a refeeding period with a 20% safflower oil diet and 0, 1 or 50 mg of dl-α-tocopheryl acetate daily, serum and pulmonary fatty acid profiles and PG synthesis were determined. A trend to growth depression on the high vitamin E diet was observed. Vitamin E supplementation seemed to have no significant effect on fatty acid composition or synthesis of PGE1, PGE2, PGF2α or PGI2 in lung. This may be due to the small lipid content and presumed inability of lung to accumulate excess vitamin E. Lung may, therefore, be resistant to such dietary manipulations. Serum PG synthesis was not affected by vitamin E dose, although the C20:4ω6/C18:2ω6 ratio in serum was significantly lowered on the high vitamin E diet.

Effects of saturated and unsaturated dietary fat on aflatoxin B 1 metabolism

Male Fisher 344 rats were fed diets containing either 20% corn oil, 20% coconut oil or 18% cocomnut oil plus 2% corn oil for 3 wk. A single dose of [ 3H]aflatoxin B 1 ([ 3H]AFB 1) was administered ip and the biliary excretion of afflatoxin metabolites and the binding of 3H to nucleic acids were studied. In other experiments the in vitro metabolism of AFB 1 by liver postmitochondrol supernatants prepared from rats fed the different sources of dietry fat was determined. The major nonextractable aqueous metabolite of AFB 1 was the aflatoxin B 1-glutathione conjugate (AFB 1-GSH). Variation in the source of dietry fat did not affect production of the conjugate, nor was in vivo binding of AFB 1 to nucleic acids affected. Aflatoxin P 1 (AFP 1)—mostly conjugated—and aflatoxin M 1 (AFM 1) were also identified in the bile, and the quantities of these metabolites produced were unaffected by the dietary treatments. The metabolites recovered in the in vitro study included aflatoxins Q 1, P 1 and M 1. The corn oil diet produced a higher microsomal cytochrome P-450 level than the coconut oil diet. Associated with the higher level of cytochrome P-450 was increased in vitro coversion of AFB 1 and AFM 1, but not ot AFP 1. The in vitro production of aqueous metabolites and the covalent binding of metabolites to protein was unaffected by the dietary treatments. The results of the in vivo studies suggest that the formation of the putative carcinogenic metabolite, AFB 1-epoxide, which undergoes detoxification through glutathione conjugation, is not affected by the type of dietary fat. These observations further suggest that dietary fat, in particular unsaturated fat, affects AFB 1 carcinogenisis through a mechanism other than by alteration of the metabolic activaqtion of AFB 1.

Influence du remplacement d'une partie du suif d'un aliment d'allaitement par de la tricapryline ou de l'huile de coprah sur l'utilisation de l'énergie et de l'azote par le veau préruminant

The advantages of using caprylic acid in the feed of preruminant calf have been investigated and compared to those of coconut oil. Two trials were carried out. Trial 1 studied the effect on the appetence and digestibility of a conventional milk replacer when tricaprylin ( TC8 ) was substituted for one-half of the tallow in the replacer. Trial 2 investigated diet digestibility and energy and nitrogen balances in 3 groups of 6 Friesian male preruminant calves each, using two open-circuit respiratory chambers. Group 1 was fed a control diet based on skim-milk powder and tallow (diet 1). In group 2, 2/3 of the tallow was replaced by coconut oil (diet 2). In group 3, 1/3 of the tallow was replaced by coconut oil and the other 1/3 by TC8 (diet 3). Apparent digestibility of energy (94.4 vs 90.7%; P less than 0.05) and nitrogen (93.2 vs 89.7%; P less than 0.10) and energy metabolizability , q (91.6 vs 88.1%, NS) were higher with diet 2 than with diet 1. TC8 intake also favoured a higher apparent digestibility of energy (98.0 vs 92.9%; P less than 0.01) and nitrogen (96.9 vs 93.0%; P less than 0.001) in trial 1 but not in trial 2 where diet 3 had only a slightly higher apparent digestibility than diet 1 (92.9% for energy and 90.7% for nitrogen; P less than 0.10). Adjusted protein gains observed in trial 2 were 52.3 +/- 3.4, 58. 9b +/- 5.3 and 56. 5ab +/- 5.4 kcal/d/kg W0 .75, respectively, for each of the 3 diets; adjusted lipid gains were 66. 8a +/- 4.0, 59.6b +/- 4.2 and 61. 2ab +/- 6.7 kcal/d/kg W0 .75; and adjusted energy gains were 119.2 +/- 6.2, 118.4 +/- 6.1 and 117.5 +/- 6.6 kcal/d/kg W0 .75 (a, b = data with different superscripts are significantly different; P less than 0.05). Metabolizable energy (EM) efficiency for tissue deposition was of the order of 0.67 +/- 0.14, and maintenance requirements amounted to an average of 95 kcal EM/d/kg W0 .75.

The dietary regulation of acyltransferase and desaturase activities in microsomal membranes of rat liver.

Dietary manipulation produces marked alterations in desaturase activities of rat liver microsomes with no concomitant changes in acyltransferase activities. Desaturation of stearoyl-CoA (delta 9-desaturase), linoleoyl-CoA (delta 6-desaturase), eicosatrienoyl-CoA (delta 5-desaturase) and eicosatrienoyl-phosphatidylcholine (delta 5-desaturase) was elevated in animals fed a corn oil diet and lowered in those fed a coconut oil diet compared to control animals. The delta 5-desaturase activities were also lowered in starved animals and elevated in starved animals refed a fat-free diet. However, no changes in acyl-CoA:1-acyl-sn-glycero-3-phosphocholine acyltransferase activity were observed in the membranes of animals maintained on any of the dietary regimens studied. These observations suggest that the desaturases of rat liver microsomes are regulated independently of the acyltransferases and that desaturation of eicosatrienoyl-phosphatidylcholine is regulated at the level of the desaturase itself and not by availability of the phospholipid substrate.

Effect of Dietary Fats on the Lipid Composition and Enzyme Activities of Rat Cardiac Sarcolemma

The effect of dietary lipids on the lipid composition and the activites of some enzymes of cardiac sarcolemma were studied. Feeding rats coconut oil-rich diet for 4 weeks resulted in a significant decrease in 5′-nucleotidase, phosphodiesterase I and p-nitrophenylphosphatase activity of cardiac sarcolemma as compared with feeding rats safflower oil. Sarcolemma from animals fed coconut oil diet contained a significantly lower concentration of total polyunsaturated fatty acids and a higher concentration of total monounsaturated fatty acids than that from rats fed safflower oil. Most of the alterations in polyunsaturated fatty acids were found in 20:4, whereas those of the monounsaturates were found in 18:1. Among all the phosphoglycerides, the fatty acid composition of the phosphatidylcholine exhibited the largest alterations as a result of coconut oil feeding. No dietary effect was observed in the sarcolemma content of cholesterol and phospholipid. These studies clearly indicate that manipulation of dietary lipids influences both the fatty acid composition and some functional properties of the sarcolemma membranes.

Independent effects of dietary saturated fat and cholesterol on plasma lipids, lipoproteins, and apolipoprotein E.

Nine normolipidemic males (18-37 years) were fed formula diets containing (as % of calories) egg white protein (15%), glucose polymer:sucrose, 3:1 (54%), and fats (31%) as one of the following: corn oil (corn), corn oil plus 1 gram/day cholesterol (corn+), coconut oil (coco), coconut oil plus 1 gram/day cholesterol (coco+). Two dietary periods of 18 days each were separated by 1 month during which plasma lipid levels returned to prestudy values. A given dietary period consisted of 9 days of either corn or coco feeding allowed by 9 days of corn+ or coco+, respectively. Fasting plasma samples were taken the last 3 days of each 9-day interval. Lipids were determined by standard procedures and the apoE levels in lipoprotein fractions isolated by discontinuous density gradient ultracentrifugation were determined by radioimmunoassay. The biochemical variables measured were: total plasma, VLDL, IDL + LDL, and HDL, cholesterol, triglyceride, and apoE levels, as well as the apoE of plasma d greater than 1.17 g/ml. The effects of apoE phenotype, the type of dietary oil (corn versus coco), the presence or absence of dietary cholesterol, and the day of sampling within triplicates on the above variables were assessed statistically. The type of oil had the only significant effect on any variable. At P less than 0.01, the coconut oil diets were associated with significant elevations (as compared to corn oil) of the following nine variables: total, VLDL, IDL + LDL, and HDL cholesterol; total, VLDL, and IDL + LDL apoE; total and VLDL triglycerides.

The effect of training and diet on lipoprotein cholesterol, tissue lipoprotein lipase and hepatic triglyceride lipase in rats

Treadmill training for 1 hr/day for 10 wk did not significantly affect chylomicron, very low density, low density, or high density lipoprotein cholesterol in rats fed either a high carbohydrate (glucose) or high fat (coconut oil) diet. Lipoprotein lipase activity of heart, adipose tissue, and skeletal muscle fibers was also unaffected by training. Carbohydrate feeding, however, when compared to fat feeding significantly lowered all lipoprotein cholesterol values as well as heart and fast-oxidative-glycolytic muscle fiber lipase activity and, conversely, significantly elevated hepatic triglyceride lipase activity. Thus, in the rat, an alteration in the serum lipid profile did not occur as a result of training, but dietary differences did independently influence serum lipid levels and tissue enzyme activity. It is suggested that human studies need to control for the possible independent influence of dietary differences when investigating the effects of training on lipoprotein metabolism.

Beta-sitosterol: esterification by intestinal acylcoenzyme A: cholesterol acyltransferase (ACAT) and its effect on cholesterol esterification

Rabbits were fed either 10% coconut oil, 10% coconut oil and 1% beta-sitosterol, 10% coconut oil and 1% cholesterol, or 10% coconut oil and 1% beta-sitosterol plus 1% cholesterol for 4 weeks. Microsomal membranes from intestines of animals fed the 1% beta-sitosterol diet had 48% less cholesterol and were enriched twofold in beta-sitosterol compared to membranes from animals fed the coconut oil diet alone. Acylcoenzyme A:cholesterol acyltransferase (ACAT) activity in jejunum and ileum was decreased significantly in animals fed the plant sterol alone. In membranes from animals fed 1% beta-sitosterol and 1% cholesterol, beta-sitosterol content increased 50% whereas cholesterol was modestly decreased compared to their controls fed only cholesterol. Intestinal ACAT was unchanged in the animals fed both sterols when compared to their controls. beta-Sitosterol esterification was determined by incubating intestinal microsomal membranes with either [(14)C]beta-sitosterol-albumin emulsion or [(14)C]beta-sitosterol:dipalmitoyl phosphatidylcholine (DPPC) liposomes to radiolabel the endogenous sterol pool. Oleoyl-CoA was then added. The CoA-dependent esterification rate of beta-sitosterol was very slow compared to that of cholesterol using both techniques. An increased amount of endogenous microsomal beta-sitosterol, which occurs in animals fed 1% beta-sitosterol, did not interfere with the stimulation of ACAT activity secondary to cholesterol enrichment of the membranes. Enriching microsomal membranes three- to five-fold with beta-sitosterol did not affect ACAT activity. Freshly isolated intestinal cells were incubated for 1 hour with [(3)H]oleic acid and beta-sitosterol:DPPC or 25-hydroxycholesterol:DPPC. Incorporation of oleic acid into cholesteryl esters did not change in the presence of beta-sitosterol but increased fourfold after the addition of 25-hydroxycholesterol. We conclude that the CoA-dependent esterification rate of cholesterol is at least 60 times greater than that of beta-sitosterol. Membrane beta-sitosterol does not interfere with nor compete with cholesterol esterification. Inadequate esterification of this plant sterol may play a role in the poor absorption of beta-sitosterol by the gut.-Field, F. J., and S. N. Mathur. beta-Sitosterol: esterification by intestinal acylcoenzyme A:cholesterol acyltransferase (ACAT) and its effect on cholesterol esterification.

Effect of Dietary Essential Fatty Acids on Vitamin A Utilization in the Rat

After their liver reserves of vitamin A were enhanced to ca. 300 µg retinol/g by 5 large daily oral doses of retinyl palmitate, groups of rats (n = 6) were fed a vitamin A-free diet containing 10% corn oil, coconut oil or linseed oil, with or without vitamin E, for a 10-day period. The composition of polyunsaturated fatty acids (PUFA) in liver lipids reflected the dietary composition, with linoleate and linolenate being markedly increased in the livers of rats fed the corn and linseed oil diets, respectively, relative to those fed the coconut oil diet. In contrast, the predominant retinyl ester in the livers of rats on all three diets was retinyl palmitate (>80%), with no dietrelated change noted in the relatively small amounts of retinyl linoleate (1–4%) or of retinyl stearate and linolenate (6–11%) present. The depletion of vitamin A from the liver during the 10-day period was slight (≤10%) and similar on all three diets. Thus, the ingestion of polyunsaturated fatty acids, with or without vitamin E, did not significantly influence either the mobilization rate or the ester composition of liver vitamin A reserves of rats in good vitamin A status. The relationship of these studies to previous investigations in which PUFA was shown to reduce liver and plasma concentrations of vitamin A is discussed.

Selectivity in modification of the fatty acid composition of normal mouse tissues and membranes in vivo.

The fatty acid composition of five normal tissues and purified liver plasma membranes of the mouse was modified by feeding diets rich in either coconut or sunflower oil. The phospholipids from the animals fed the coconut oil diets were enriched in monoenoics, and those from the mice fed the sunflower oil diet contained large percentages of polyenoics. Most importantly, there were differences in the extent and type of modification in each tissue. For example, the phospholipids of the heart from animals fed the sunflower oil diet contained 21% docosapentaenoate compared to less than 6% in other tissues. The bone marrow from animals fed the coconut oil diets contained a high proportion of saturates, including those of medium chain length. The fatty acyl composition of the neutral lipids was also modified, but in some cases the degree of alteration differed from that occurring in the phospholipids. Purified liver plasma membranes demonstrated diet-induced changes but contained smaller amounts of arachidonate, and those from the animals fed sunflower oil diets were less polyunsaturated compared to whole liver phospholipids. We conclude that the modification of fatty acid composition of normal tissues induced by experimental diets differs in extent and type. Furthermore, the liver plasma membrane composition is different from that of liver phospholipids. The differences in the extent and type of modification demonstrate selectivity amongst normal tissues.

The effect of vitamin E deficiency on some platelet membrane properties.

The effects of alpha-tocopherol (vitamin E) deficiency on membrane properties of platelets were studied to determine if vitamin E has a measureable stabilizing role in biological membranes. Three groups of rats and three of mice were studied: two groups consisted of Fisher strain rats and one of Sprague-Dawley rats fed a Draper corn oil diet with and without high levels of supplementary vitamin E. The mice were two groups of BALB/c animals maintained on an 8% hydrogenated coconut oil diet, and one group of CBA/J mice on an 8% lard diet, in each case either deficient in or supplemented with vitamin E. The relative content of fatty acids obtained from both rat platelets and erythrocytes was unchanged by vitamin E deficiency. Depletion of vitamin E had no effect on the degree of fluorescence polarization of 1,6-diphenyl-1,3,5,-hexatriene-labeled rat platelets. No changes in hematocrit values were seen in any of the studies. The platelet count of only the vitamin E-deficient Sprague-Dawley rats was elevated with respect to vitamin E-supplemented counterparts; the others remained constant. Platelet reactivities, as measured by ADP-and thrombin-induced platelet aggregation and by the thrombin-induced changes in platelet transmembrane potential, were unaffected by vitamin E deficiency in all three groups of rats. Our results indicate that a membrane stabilizing effect of vitamin E on rat platelet or erythrocyte membrane fatty acids or on platelet response to external stimuli could not be demonstrated, nor was elevation in platelet count a general phenomenon associated with vitamin E deficiency.-Whitin, J. C., R. K. Gordon, L. M. Corwin, and E. R. Simons. The effect of vitamin E deficiency on some platelet membrane properties.

Diet-Induced Changes in NaCl Preference and Blood Pressure in Rats

The interrelationship between diet, blood pressure and the acceptability of salt solutions was examined. Sprague-Dawley rats were fed high carbohydrate (5% corn oil), all unsaturated fat (20% corn oil) or all saturated fat (20% coconut oil) diets containing either basal (0.15% NaCl) or high (8.0% NaCl) levels of salt. Systolic blood pressure was determined indirectly using an electro-sphygmomanometer. Percent acceptance was determined using a two-bottle preference test. Results from this experiment suggest that postingestional feedback mechanisms rather than blood pressure play an important role in determining the acceptability of salt solutions by the Sprague-Dawley rat.salt solution blood pressure

Polyunsaturated Fatty Acids as Promoters of Mammary Carcinogenesis Induced in Sprague-Dawley Rats by 7,12-Dimethylbenz[<italic>a</italic>]anthracene<xref ref-type="fn" rid="FN2">2</xref><xref ref-type="fn" rid="FN3">3</xref>

The development of mammary tumors was examined in female noninbred Sprague-Dawley rats fed either a low-fat diet or high-fat diets containing different fats and fatty acid esters. Each rat was given 5 mg 7,12-dimethylbenz[a]anthracene by stomach tube 1 week before diets were introduced. Addition of 3% ethyl oleate (an ethyl ester of an unsaturated fatty acid) to a diet high in saturated fat (coconut oil) had no significant effect on tumor development, but the addition of 3% ethyl linoleate (an ethyl ester of a polyunsaturated fatty acid) increased the tumor yield to about twice that in rats fed either the high-saturated fat diet or a low-fat diet. Animals fed the high-saturated fat diet containing 3% ethyl linoleate developed as many tumors as those fed a 20% sunflower seed oil diet, though the sunflower seed oil diet contained about four times as much linoleate. Rats fed a high coconut oil diet containing 3% menhaden fish oil, which contains polyunsaturated fatty acids of the linolenate family (but having little linoleic acid), also developed as many tumors as those fed the 20% sunflower seed oil diet. These differences in mammary tumor yield could not be explained by alterations in the serum levels of prolactin, estrogen, or progesterone. However, the higher tumor yields were associated with increased unsaturation of mammary tissue phospholipids.

Effect of Dietary Lipids on Composition and Glucose Utilization by Rat Adipose Tissue

Feeding rats diets rich in either safflower oil or coconut oil resulted in a significant change in the lipid composition of epididymal fat pads as compared with those obtained from rats fed a commercial stock diet. A safflower oil diet resulted in an increase in tissue cholesterol and a decrease in phospholipid concentration as compared with the stock diet. A coconut oil diet resulted in a decrease in both tissue cholesterol and phospholipid concentrations as compared with the stock diet. Adipose tissue fatty acid composition was also altered due to these dietary manipulations. Glucose utilization by adipose tissue from animals fed the safflower oil diet was 2 and 10 times greater than glucose utilization by adipose tissue from animals fed the stock and coconut oil diets, respectively. The coconut oil diet resulted in an increase in the percentage of glucose incorporated into adipose tissue diglycerides, free fatty acids and cholesterol esters and a decrease in the percentage of glucose incorporated into triglycerides as compared with animals fed the stock or safflower oil diet. The incorporation of glucose into adipose tissue fatty acids was depressed by a saturated fatty acid diet as compared with either a polyunsaturated fatty acid diet or the stock diet.adipose tissue saturated fatty acids glucose utilization

The effect of dietary fat and salt on blood pressure, renal and aortic prostaglandins

The pressor effects of fat and salt were examined in male Sprague-Dawley rats. Rats fed high carbohydrate (5% corn oil), high salt (8% NaCl) diets demonstrated significant elevations in blood pressure within one week of diet introduction which persisted throughout the 9 week experimental period. High saturated fat (5% corn oil-15% coconut oil) diets promoted a significant elevation in blood pressure, irrespective of the level of dietary salt. High dietary salt, as opposed to basal levels, tended to decrease the blood pressure of rats fed a diet containing all unsaturated fat (20% corn oil). The greatest percent increase in the renal vasodilator prostaglandin E 2 was measured in rats fed the high unsaturated-basal salt diet compared to all other dietary treatments. A hypervolemic effect of high levels of dietary salt was demonstrated in the high carbohydrate, all unsaturated fat and high saturated fat groups. These results demonstrate that the amount and type of dietary fat interact with the level of dietary salt to influence blood pressure in rats.

Dietary fat and cholesterol effects on plasma lecithin cholesterol acyltransferase activity in cebus and squirrel monkeys

Plasma LCAT activity was assessed in cebus and squirrel monkeys fed diets containing either corn or coconut oil with or without 0.1% cholesterol. In vitro enzyme activity was determined by measuring the incorporation of [1,2- 3H] cholesterol into cholesteryl ester. Three assay conditions were used to assess overall enzyme activity and to differentiate between the concentration of enzyme and substrate effects. LCAT activity was affected primarily by species and dietary fat and to a lesser extent by dietary cholesterol in squirrel monkeys. Specifically, plasma from both species of monkeys fed corn oil diets had comparable overall rates of LCAT activity (percent esterification and mass esterified/h). In all monkeys fed the coconut oil diets percent esterification was lower than in those monkeys fed the corn oil diets, and was lowest in squirrel monkeys, particularly those fed cholesterol. Coconut oil feeding also resulted in lower substrate activity in all monkeys, whereas cholesterol feeding had no significant effect on substrate activity. Squirrel monkeys always had lower substrate activity than cebus for any diet group. Coconut oil feeding resulted in a lower p]S ratio of HDL phospholipid fatty acids in both species, but the decrease was greater for cebus monkeys. In terms of the mass of cholesterol ester formed (molar rate) during the in vitro assay, plasma from cebus monkeys fed coconut oil diets had greater activity than plasma from other groups. Evaluation of enzyme activity indicated that the greater esterification in cebus monkeys fed the coconut oil diet was associated with the ability of cebus, but not squirrel monkeys, to increase their enzyme activity. In essence, cebus monkeys maintained greater LCAT substrate and enzyme activities than squirrel mon keys when made hypercholesterolemic with coconut oil feeding.

Fatty Acid Alteration of L1210 Murine Leukemia Cells. Growth Rate and Stability of Lipid Changes in Culture<xref ref-type="fn" rid="FN2">2</xref><xref ref-type="fn" rid="FN3">3</xref>

The fatty acid composition of L1210 lymphoblastic murine leukemia cells was altered by experimental diets before the cells were placed in tissue culture for the study of reversion of the lipid modification. Both types of fatty acid-modified cells were cultured in the same fetal calf serum-containing medium designed to maintain the differences. At the time of removal of the L1210 cells from DBA/2J inbred male mice, marked differences existed in the fatty acid composition of the cell phospholipids and neutral lipids. The phospholipids from the mice fed a sunflower seed oil diet contained 16% more polyenoic fatty acids, and phospholipids from mice fed a coconut oil diet contained 18% more monoenoic fatty acids. During 4 days in tissue culture, only limited changes were found in phospholipid fatty acid composition. The polyenoic fatty acids of the phospholipids from mice fed the sunflower oil diet decreased only 3.2%, which was primarily due to decreases in linoleate and long-chain polyunsaturates. Less than a 2% change occurred in the monoenoic fatty acids and saturates. The monoenoic fatty acids of the phospholipids in cells from the coconut oil-fed mice decreased 7.8%, which was primarily due to decreases in palmitoleate and oleate. The polyenoic and saturated fatty acids in the phospholipids of these cells changed less than 2%. Greater changes were found in neutral lipids, which suggests that they may provide a source of fatty acids to stabilize phospholipids. The observation that the cellular content of triglyceride declined in culture, whereas the phospholipid content was unchanged, lends further support to this possibility. No difference was seen in the growth rate or viability between the two types of fatty acid-modified cells. The conclusion was reached that the lipid alterations of L1210 phospholipids are maintained in tissue culture for at least 4 days. Furthermore, the lipid alterations had no effect on the growth rate of the cells in culture.

Decreased formation of porstaglandins derived from arachidonic acid by dietary linolenate in rats

Accumulated evidence now suggests that availability of precursor acid is an important factor controlling the biosynthesis of prostaglandins (PG's). Since linolenic acid inhibits the conversion of linoleic acid to arachidonic acid (PGE2, PGF2 alpha, and thromboxane A2 precursor), rats receiving more linolenic acid are expected to have less arachidonic acid and thus less PG's synthesized from arachidonic acid than those receiving linoleic acid alone. Essential fatty acid-deficient rats, induced by feeding hydrogenated coconut oil diet for 15 weeks, were divided into six groups and fed graded amounts of purified methyl linolenate for 6 weeks. Each group of rats except essential fatty acid-deficient group received the same amount of linoleate. The results showed that the level of arachidonic acid in serum lipids and serum concentrations of PG's synthesized from arachidonic acid by platelets decreased as the amount of dietary linolenate increased. This indicated that biosynthesis of PG's in platelets can be influenced by the availability of precursors, and thus it can be modified by the manipulation of dietary fatty acids.

Quantitative and Qualitative Changes in Phospholipid in the Intestine of the Gerbil and the Development of Lipodystrophy

Female gerbils fed a diet containing 20% coconut oil develop an intestinal lipodystrophy that is not seen in animals fed a diet containing 20% safflower oil or a diet of 20% coconut oil supplemented with 0.1% inositol. The coconut oil diets contained 1.5% safflower oil to prevent essential fatty acid deficiency. The level of inositol in the intestinal tissue of animals fed the coconut oil diet not supplemented with inositol has been shown to be decreased. Phospholipid analyses of the intestinal tissue were undertaken to determine if this decrease in total inositol was reflected in a decrease in phosphatidylinositol or resulted in an altered phospholipid pattern. No difference in the phosphatidylinositol level was seen between animals fed 20% coconut oil with and without inositol supplementation (microgram P/gut section), although animals fed coconut oil diets had lower levels of phosphatidylinositol than animals fed safflower oil diets. Fatty acid analyses of total phospholipid and phosphatidylinositol in gut tissue revealed that animals which deveoped the lesion had an ultered phosphatidylinositol fraction with a depressed level of arachidonic acid and an elevated level of oleic acid. This suggests that the development of the intestinal lipodystrophy may be correlated with qualitative rather than quantitative changes in phosphatidylinositol.