Influence of medium-chain triglycerides on lipid metabolism in the rat

Lipid metabolism was studied in rats fed diets containing corn oil, coconut oil, or medium-chain triglyceride (MCT), a glyceride mixture containing fatty acids of 8 and 10 carbons in length. The ingestion of MCT-supplemented, cholesterolfree diets depressed plasma and liver total lipids and cholesterol as compared with corn oil-supplemented diets. In rats fed cholesterol-containing diets, plasma cholesterol levels were not influenced by dietary MCT, but liver cholesterol levels were significantly lower than in animals fed corn oil. In vitro cholesterol synthesis from acetate-1-¹⁴C was lower in liver slices of rats that consumed MCT than in similar preparations from corn oil-fed rats. Studies of fatty acid carboxyl labeling from acetate-1-¹⁴C and the conversion of palmitate-1-¹⁴C to C₁₈ acids by liver slices showed that chain-lengthening activity is greater in the liver tissue of rats fed MCT than in the liver of animals fed corn oil. The hepatic fatty acid desaturation mechanisms, evaluated by measuring the conversion of stearate-2-¹⁴C to oleate, was also enhanced by feeding MCT. Adipose tissue of rats fed MCT converts acetate-1-¹⁴C to fatty acids at a much faster rate than does tissue from animals fed corn oil. Evidence is presented to show that the enhanced incorporation of acetate into fatty acids by the adipose tissue of rats fed MCT represents de novo synthesis of fatty acids and not chain-lengthening activity. Data are also presented on the fatty acid composition of plasma, liver, and adipose tissue lipids of rats fed the different fats under study.     

Acetoacetate metabolism of rats fed high fat or restricted calorie diets

Ethyl-¹⁴C-acetoacetate was used to trace oxidation and metabolism of acetoacetate when rats were fed a high fat diet (80% of total calories from beef tallow or corn oil, carbohydrate free), a high carbohydrate diet (2% corn oil) or a high carbohydrate diet with restriction of calories to one half of ad lib. consumption for two weeks. The rate of expiration of¹⁴CO₂ in all groups of animals did not differ significantly and was not related to plasma concentration of acetoacetate. The high fat diets slightly enhanced the oxidation of acetoacetate to¹⁴CO₂ over a 3 hr period compared to other diets. Incorporation of acetoacetate into fatty acids did not differ significantly among groups. Rats fed the high carbohydrate diet ad lib. incorporated into liver cholesterol more acetoacetate than did any other group, but dietary unsaturated fat resulted in greater incorporation of acetoacetate into cholesterol than saturated fat. High calorie and high beef tallow groups were ketonemic but the low concentration of plasma acetoacetate in rats fed a high corn oil diet indicates that unsaturated fatty acids are not ketogenic. The data show that utilization of acetoacetate is not significantly reduced in a ketonemic condition and support the premise that overproduction of ketone bodies is the cause of ketonemia. Rats appeared to be normal during the two-week period when no carbohydrate was included in the diet. Presented at the AOCS Meeting, Chicago, October, 1967.     

Effect of dietary fat saturation of absorption and intestinal secretion of cholesterol by the hypercholesterolemic rat

The fate of an oral dose of [4-¹⁴C] cholesterol given to rats grown on diets with 20% safflower oil or 20% hydrogenated coconut oil was determined by analysis of digestive tract, feces and tissues. The pattern of isotope distribution did not support the view that rats fed a saturated fat absorb less cholesterol than those fed an unsaturated fat. Fasted animals growth on the diet with 5% of these two fats and beef fallow showed no clear difference in the amount of digitonin-peecipitable sterol in their intestines. A shorter transit time for intestinal contents was observed with the saturated fat groups. It is concluded that neither absorption of cholesterol from the gut nor secretion of β-hydroxy sterol into the gut accounts for the hypocholesterolemic effect of polyunsaturated fat. Journal Paper No. 4951 AES, Purdue University.     

Effect of dietary fat upon aflatoxicosis in rats fed torula yeast containing diet

This study was designed to study the possible interrelationships between Torula yeast, vitamin E, and the dietary fat source on aflatoxin-induced tumors. Rats were fed Torula yeast-containing basal diets which included 1.7 ppm aflatoxin B₁ with either lard, corn oil or no fat, and with or without vitamin E supplements for 3 months. Thereafter, the respective diets without aflatoxin were fed for ca. 9 months. Animals receiving the vitamin E-deficient diets had a high mortality. Although the vitamin E-deficient, aflatoxin-treated rats had lower wt gains than did the vitamin E-deficient controls, they lived twice as long. In addition, regardless of the dietary fat source, the kidneys and adrenals of these vitamin E-deficient, aflatoxin-supplemented rats were found to be significantly heavier than the controls, and plasma cholesterol levels were elevated. Increased amounts of liver lipid were observed in response to aflatoxin in both corn oil-fed and fat-deficient rats. No such differences were observed in the responses of the vitamin E-supplemented groups to aflatoxin. On the corn oil diet, aflatoxin administration resulted in an increased deposition of polyunsaturated fatty acids in cholesteryl ester and phospholipid fractions in livers of vitamin E-deficient rats and the phospholipid fraction of vitamin E-sufficient rats. The vitamin E-deficient rats exhibited necrosis of the liver, which was alleviated when aflatoxin was included in the diet, and calcification of the kidneys, which was potentiated by the dietary aflatoxin. No tumors were observed in these animals. In animals maintained on vitamin E-sufficient diets for 1 year, growth was depressed as a result of aflatoxin administration with the greatest depression occurring in the group fed corn oil. Spleen wt were decreased in all groups given aflatoxin. However, there were no changes in either plasma or liver cholesterol or total liver lipids which could be attributed to aflatoxin administration. When aflatoxin was fed with lard, the cholesteryl ester, triglyceride, and free fatty acid fractions of plasma had decreased amounts of the C20:4 acid. In the cholesteryl ester fraction only, this change was accompanied by increased levels of C16:0, C18:0, and C18:1 acids. In the liver phospholipids, there were increased levels of mono- and polyunsaturated fatty acids and decreases in the saturated fatty acids. All of the animals receiving aflatoxin exhibited severe necrosis and tumor formation in the kidneys; the animals fed lard had the highest level of involvement and those in the fat-free group the least. Liver pathology was the least marked among the rats fed the fat-free diet. Since aflatoxin-induced tumors are rich in lipids, the fat-free diet may be protective to the animal.     

Synthesis of cholesterol and total lipid by male and female rats fed beef tallow or corn oil

Male and female weanling rats were fed diets containing 2 or 42% of calories as corn oil or 40% as beef tallow plus 2% as corn oil until they were 12 or 18 weeks of age. Incorporation of C¹⁴-acetate into lipids of serum and liver and concentration of lipids in serum, liver, and carcass at the end of these periods were determined. Net synthesis of noncholesterol lipid was repressed by changing the diet from 2% to 42% of calories from either dietary fat in both sexes and at both ages. Cholesterol net synthesis was enhanced 29-fold in males and 22-fold in females fed 42% corn oil compared to 2% corn oil to the age of 12 weeks. It was enhanced only 2.6-fold for males and 3.4-fold for females by 40% beef tallow plus 2% corn oil. At 18 weeks of age cholesterol synthesis in males fed 42% corn oil was 7.3 and in females 9.1 times the value for those fed 2% corn oil. At this age the values for rats fed 40% beef tallow plus 2% corn oil were 1.2 and 3.7 times those for 2% corn oil fed rats of the respective sexes.     

Origin of the high saturated fatty acid content of rat fecal lipids

The biohydrogenation of unsaturated fatty acids and the preferential absorption of unsaturated fatty acids over long chain saturated fatty acids from the gut have been investigated to find the origin of the high saturated fatty acid content of the facal lipids of rats fed soybean oil. Label from dietary (1-¹⁴C)-linoleic acid was recovered in the saturated and monounsaturated fatty acids of the fecal lipid. However, when (9,10-³H)-stearic acid and (1-¹⁴C)-linoleic acid were fed together, the isotope ratio (³H/¹⁴C) of the fecal lipid was 1.9 times that of the diet. It is concluded that both processes occur.     

Influence of medium-chain triglycerides on lipid metabolism in the chick

The effect of corn oil, coconut oil, and medium-chain triglyceride (MCT, a glyceride mixture consisting almost exclusively of fatty acids of 8 and 10 carbons in length) ingestion on lipid metabolism was studied in chicks. In chicks fed cholesterol-free diets, MCT ingestion elevated plasma total lipids and cholesterol and depressed liver total lipids and cholesterol when compared to chicks receiving the corn oil diet. As a consequence of the opposite effects of MCT ingestion on plasma and liver cholesterol and total lipids, the plasma-liver cholesterol pool was not altered. When cholesterol was included in the diets, dietary MCT depressed liver and plasma total lipids and cholesterol as compared with corn oil, consequently also lowered the plasmaliver cholesterol pool. The in vitro cholesterol and fatty acid synthesis from acetate-1-¹⁴C was higher in liver slices from chicks fed MCT than in those from chicks fed corn oil. The percentage of radioactivity from acetate-1-¹⁴C incorporated into the carboxyl carbon of fatty acids by liver slices was not altered by MCT feeding, indicating that the increased acetate incorporation represented de novo fatty acid synthesis. The conversion of palmitate-1-¹⁴C to C₁₈ acids was increased in liver of chicks fed MCT, implying that fatty acid chain elongating activity was also increased. Studies on the conversion of stearate-2-¹⁴C to mono- and di-unsaturated C₁₈ acids showed that hepatic fatty acid desaturation activity was enhanced by MCT feeding. Data are presented on the plasma and liver fatty acid composition of chicks fed MCT-, corn oil-, or coconut oil-supplemented diets. The principles of laboratory animal care, as promulgated by the National Society for Medical Research, were observed.     

Exacerbation of heart and liver lesions in rats by feeding of various mildly oxidized fats

Groups of 40 male Charles River rats were fed diets containing cottonseed oil, olive oil, corn oil, soybean oil, coconut oil, chicken fat, beef fat, butter oil, lard and saturated medium chain triglycerides. The fats were fed fresh and after 40 hr aeration at 60 C, which hardly changed peroxide values. In addition, fresh and aerated soybean oil and lard were fed to W/Fu rats. Body weights and life span were significantly influenced by the kind of fat fed, but not by aeration. Many hearts exhibited unspecific focal myocarditis and focal fibrosis. The latter was graded in a blind test, which revealed highly significant differences in the incidence of severe lesions; those fed corn oil had the most, followed by cottonseed oil, soybean oil, olive oil, beef fat, saturated medium chain triglycerides, butter, chicken fat and lard, in that order. Feeding of aerated fat resulted in an increased incidence with six of the eight fats. The W/Fu rats had lower incidences, but those fed soybean oil had more than those fed lard, and aeration led to a higher incidence. Some heart sections stained with Light Green SF Yellowish revealed areas of muscle fibrils that did not accept the stain, probably as a consequence of cellular damage. Higher incidences of this lesion were associated with the same fats as was severe fibrosis, and feeding of aerated fats led to higher incidences. Many livers revealed marked proliferation of bile ducts. The groups fed cottonseed, soybean, olive and corn oils had higher incidences of severe lesions, and feeding of the oxidized oils led to still higher incidences. None of the results appeared to be associated with the fatty acid composition of the fats, which suggested that these long term effects may have been due to minor constituents in the individual fats. One of seven papers presented in the symposium “Biological Significance of Autoxidized and Polymerized Oils,” JOCS-AOCS Joint Meeting, Los Angeles, April 1972.     

Effect of diet composition and fasting on lipogenesis in lean and polygenic obese mice

A line of mice was developed which exhibited spontaneous obesity when fed commercial laboratory ration low in fat content. Obese mice were compared to a nonobese related line to determine whether energy source in the diet would affect onset of obesity. Experimental diets-beef tallow (38% of calories as beef fat and 2% as corn oil), corn oil (40% corn oil) or low-fat (2% corn oil)-were instituted ad libitum at the time of weaning. When the mice reached 6 months of age, lipogenesis was investigated by injecting intravenously³H₂O and glucose-U-¹⁴C.³H₂O and glucose-U-¹⁴C incorporation into fatty acids of fed mice was greater for obese than for lean mice. Fatty acid synthesis was inhibited by high-fat diets compared to low-fat diet in both lines. Of the 2 high-fat diets, the corn oil diet inhibited fatty acid synthesis about twice as much as beef tallow diet. There was no line effect on tritium incorporation into cholesterol. Cholesterol synthesis from glucose-U-¹⁴C was greater in obese than lean mice. Diets had no effect on tritium and glucose-U-¹⁴C incorporation into cholesterol. Fasting reduced fatty acid synthesis in all mice, but total body fatty acid synthesis was not affected by lines or dietary treatment under fasted conditions. These data suggest that degree of lipogenesis, in part, explains obesity. A failure of inhibition of lipogenesis or an enhanced efficiency in fat deposition by feeding beef tallow compared to corn oil diet may explain the fact that lean mice fed the beef tallow diet tended to be more obese that lean mice fed corn oil or low-fat diets.     

Dietary lipid,fatty acid synthesis and cholesterol metabolism in aging rats

Male and female rats were fed diets containing 2% of calories as corn oil or that plus 40% of calories as beef tallow or corn oil. After 3, 6, 12 and 18 months groups were given 4-¹⁴C-cholesterol ip, and feces were collected for 9 days. Just prior to necropsy³H-acetate was administered ip. Samples of serum, liver, heart and carcass were obtained for analysis. Concentrations of fatty acids and cholesterol, synthesis of those and recovery of ring-labeled steroid are reported. Mortality from acute respiratory disease was very high in male rats fed beef tallow or low fat diets and very low in those fed the corn oil diet. In females, only beef tallow diet resulted in a high mortality rate, and this was lower and at a later age than in males. The most notable effects of age were in relation to fatty acid synthesis and presence of¹⁴C-acidic steroid in the carcass. In 3-month-old rats both fats depressed fatty acid synthesis in comparison to the low fat diet. At later ages beef fat ceased to depress fatty acid synthesis in both sexes. Corn oil continued to depress fatty acid synthesis up to 12 months in males and 18 months in females. The presence of¹⁴C-acidic steroid in carcass was substantial in 6-month-old rats and constituted ca. 40% of recovered¹⁴C in 18-month-old rats. The possibility that the increase in acetate incorporation into fatty acids with age in fat feeding is related to chain elongation rather than de novo synthesis is discussed. Both the presence and amount of acidic steroid in the carcass are notable and may be of importance in constructing models of cholesterol turnover. Presented in part at the AOCS Sterol Symposium, April 1970, and the Federation of American Societies for Experimental Biology, April 1971. Scientific Series Paper No. 1536, Colorado Agricultural Experiment Station.     

Inhibition of cholesterol synthesis in mammary tissue,lung, and kidney following cholesterol feeding in the lactating rat

Pregnant rats were randomly allocated to one of 3 experimental dietary groups: Group 1–15.5% butter, 2% cholesterol, 0.78% sodium cholate purified diet; Group 2-standard rat diet with the addition of 10% lard and 2% cholesterol, and Group 3-standard rat diet. Plasma and milk cholesterol at 10 days postpartum were significantly elevated in dams fed exogenous cholesterol. The rat of incorporation of [1-¹⁴C] acetate into digitonin-precipitable sterols of mammary tissue slices from dams in Group 1 and Group 2 was eight-fold and two-fold, respectively, less than controls. Mammary tissue cholesterol was greater in dams fed dietary cholesterol. Thus, our data, for the first time, demonstrate that cholesterol synthesis in lactating rat mammary tissue is suppressed following cholesterol feeding. In a second experiment, the rate of incorporation of [1-¹⁴C] acetate into digitonin-precipitable sterols in kidney and lung tissue of Group 1 rats was suppressed; however, this response was not as marked as that observed in lactating mammary tissue. The concentration of cholesterol in kidney and lung was greater than controls. These results suggest that extrahepatic inhibition of cholesterol synthesis exists in the rat with a concomitant increase in tissue cholesterol.     

Different metabolism of saturated and unsaturated long chain plasma free fatty acids by intestinal mucosa of rats

During fat absorption, unsaturated long chain fatty acids are esterified at a higher rate than saturated fatty acids of similar chain length. This phenomenon has been attributed to differences in the binding affinity of fatty acids to a cytosolic fatty acid-binding protein. As intestinal mucosa utilizes plasma free fatty acids as well, we investigated whether long chainplasma free fatty acids of different degree of saturation are metabolized also at different rates.³H-Palmitic and¹⁴C-linoleic acid complexed to rat serum were injected rapidly into a tail vein of fasting rats. One, 2 and 4 min later there was no difference between³H and¹⁴C-radioactivity in intestinal mucosa, suggesting equal initial uptake of the two labeled fatty acids from plasma. Despite their equal uptake, the incorporation of the isotopes into ester lipids was significantly different, however: at 2 min, 53.1±3.9% of³H and 73.8±4.6% of¹⁴C were recovered in ester lipids. Phospholipids and triglycerides accounted for most of the mucosal³H and¹⁴C. At 4 min, a similar distribution of isotopes in intestinal mucosal metabolites was found. These data show that despite equal initial uptake by intestinal mucosa unsaturated long chain fatty acids taken up from plasma are esterified to a higher and oxidized to a lower extent than saturated plasma free fatty acids. Unsaturated plasma free fatty acids, therefore, may provide a more important source of fatty acids for endogenous intestinal lipoprotein lipids than saturated plasma free fatty acids. It is speculated that the fatty acid binding protein might be operative not only in the intracellular transport and metabolism of luminal fatty acids but of plasma free fatty acids as well.     

Effect of heated fat upon metabolism of 1-14C-acetate in the rat

Groups of rats were prefed for 18 weeks with fresh or heated corn oil (≈5% nonurea adduct) at 10, 20 and 30% protein levels and at 10% protein+2% cellulose; 1-¹⁴C-sodium acetate was injected intraperitonially into each animal and the radioactivity was measured in expelled CO₂ and also in the lipid fractions of liver. In the groups of rats fed 10% protein, one-half of the administered radioactivity was found 50 min after acetate injection into rats fed fresh oil, whereas 90 min were required to reach the same level in rats fed heated oil. The same trend was found in all the groups of rats receiving different protein levels. The conversion of acetate to CO₂ was significantly higher at a 10% dietary protein level than at the 20 or 30%, but there appeared to be no significant difference in the conversions at the 20 and 30% protein levels. However addition of 2% cellulose to the 10% dietary protein level significantly increased the conversion of the acetate to CO₂ in rats fed heated oil. The livers of animals receiving heated fat diets had a higher lipid content, mainly triglyceride. When the liver lipids from rats fed fresh corn oil were separated by argentation thin layer chromatography, the bulk of the radioactivity was found in the saturated fractions. Monoene, diene and triene fractions from the liver lipid of rats fed heated oil had almost twice the radioactivity of those from fresh oil, suggesting the preferential utilization of acetate in the synthesis of these unsaturated fatty acids. One of seven papers presented in the symposium “Biological Significance of Autoxidized and Polymerized Oils”, JOCS-AOCS Joint Meeting, Los Angeles, April 1972.     

Effect of sterculic acid upon aflatoxicosis in rats fed diets containing saturated and unsaturated fat

Investigations on trout have shown that the cyclopropenoid fatty acids, which occur naturally in small amounts in unrefined cottonseed oil, may act as powerful cocarcinogens when fed in conjunction with aflatoxin. Attempts at confirming these findings in mammals, i.e. rats, have been inconclusive. In this study, the effects of sterculic acid and aflatoxin upon lipid metabolism and tumor formation in male rats have been examined using basal diets containing either saturated or unsaturated fat to which the following additions were made: (A) basal diet (no supplements); (B) aflatoxin B₁ at 1.7 ppm; (C) sterculic acid at 210 ppm; and (D) aflatoxin B₁ at 1.7 ppm, plus sterculic acid at 210 ppm. The rats consumed these diets for 3 months and, thereafter, were fed the unsupplemented basal diet until sacrifice 9 months later. Growth was depressed in rats in groups B, C, and D, but no synergistic inhibition was observed, regardless of the fat source. Liver wt doubled in response to aflatoxin; however, only when the diet contained unsaturated fat did sterculic acid, in combination with aflatoxin, exaggerate the increase in liver wt (a reflection of the more severe liver pathology observed in these rats). In the animals fed the saturated fat diet, aflatoxin administration to animals fed the control or sterculic acid supplemented diets resulted in marked increases in plasma cholesterol levels; the unsaturated fat diets, supplemented with aflatoxin, evoked a slight increase in plasma cholesterol content which was nullified by sterculic acid supplementation.     

Species variation in the atherogenic profile of monkeys: Relationship between dietary fats,lipoproteins, and platelet aggregation

Because lipoproteins and platelet aggregation have been implicated in atherogenesis, relative differences in the response of these variables to dietary fat saturation were compared in three species of monkeys differing in their susceptibility to atherosclerosis (cebus, rhesus, and squirrel monkeys). Both long-term (8–12 years) and short-term (8 weeks) responses to diets containing 31% fat calories were examined in the same monkeys. As expected, long-term feeding of coconut oil by comparison to corn oil produced significantly higher plasma concentrations of total cholesterol, LDL cholesterol, apoB, and triglycerides, as well as higher ratios of LDL/HDL cholesterol and apo B/apo A-I. These responses were characteristic of all species with cebus being most responsive and rhesus the least. The shortterm plasma cholesterol response to animal fats (butter, lard, beef tallow) was significantly less than that to coconut oil. When fish oil was substituted for two-thirds of either corn oil or coconut oil, exceptional decreases occurred in plasma cholesterol and triglycerides, as well as in HDL cholesterol and apo A-I concentrations despite the fact that the fish oil diets contained more saturated fat and less polyenes than the corn oil diet. Platelet aggregation tended to increase with saturated fat consumption and greatly decreased with fish oil intake in all monkeys, although cebus monkeys were ten-fold more resistant to platelet aggregation than the other two species. The molecular species of platelet phosphatidylcholine (PC) varied with both the dietary fat fed and species of monkey. An inverse correlation (r=−0.60; p<0.001) was found between changes in one such PC molecular species (18∶0−20∶4) induced by diet and the platelet aggregation threshold. These results demonstrate that the lipemic and platelet responses to dietary saturated fat depend upon both the type of fat (i.e., the specific combination of dietary fatty acids, including the chain length of saturated fatty acids and the degree of polyunsaturation) and the species of monkey (genetic component) in which the response is elicited.     

Dietary lipid,fatty acid oxidation and incorporation of carbon into cholesterol

Female rats (200 g) were fed a nutritionally adequate diet containing 1% by weight of corn oil (low-fat, LF), 21% of corn oil (CO) or 20% of beef tallow plus 1% of corn oil (BT) for two weeks. Food was removed for 8–12 hr, then each rat was refed for 1 hr. Each rat was injected ip with Na-³H-acetate and U-¹⁴C-Na-palmitate, (P),-oleate (O) or-linoleate (L). Expired CO₂ was collected for 2 hr. Liver, heart and serum were obtained for analysis of total lipid¹⁴C and³H and cholesterol¹⁴C and³H. Oxidation of L was twice as great as O or P when the LF diet was fed. CO and BT diets doubled oxidation of O to equal L, and increased oxidation of P, 50%. In liver and serum P was retained to a greater extent than O or L on BT and CO diets. Incorporation of acetate into total lipid was highest on LF diet and reduced by feeding either CO or BT. Incorporation of acetate into cholesterol was greater when BT or CO was fed than for LF.¹⁴C was incorporated into cholesterol in such small amounts that it was barely detectable and could not be counted accurately. Conclusions are that (a) dietary fat affects rate of oxidation of uniformly labeled palmitate and oleate, but not linoleate, (b) acetate is a more ready precursor to cholesterol than is fatty acid carbon, and (c) the acetate incorporated into cholesterol when polyunsaturated fat is fed is not derived directly from fatty acid carbon. The failure of incorporation of fatty acid carbon into cholesterol within 2 hr of administration opens the question of compartmentation of acetate as to its metabolic source. Colorado Agricultural Experiment Station Scientific Series Paper No. 1510.     

Effect of dietary palm oil and its fractions on rat plasma and high density lipoprotein lipids

Male Sprague Dawley rats were fed semipurified diets containing 20% fat for 15 weeks. The dietary fats were corn oil, soybean oil, palm oil, palm olein and palm stearin. No differences in the body and organ weights of rats fed the various diets were evident. Plasma cholesterol levels of rats fed soybean oil were significantly lower than those of rats fed corn oil, palm oil, palm olein or palm stearin. Significant differences between the plasma cholesterol content of rats fed corn oil and rats fed the three palm oils were not evident. HDL cholesterol was raised in rats fed the three palm oil diets compared to the rats fed either corn oil or soybean oil. The cholesterol-phospholipid molar ratio of rat platelets was not influenced by the dietary fat type. The formation of 6-keto-PGF_1α was significantly enhanced in palm oil-fed rats compared to all other dietary treatments. Fatty acid compositional changes in the plasma cholesterol esters and plasma triglycerides were diet regulated with significant differences between rats fed the polyunsaturated corn and soybean oil compared to the three palm oils.     

Effect of dietary fish oil on the rate of very low density lipoprotein triacylglycerol formation and on the metabolism of chylomicrons

The mechanism by which ω3 fatty acids lower plasma triacylglycerol levels was investigated. Rats were fed fish oil, olive oil (10% fat by weight) or a nonpurified diet 4% fat by weight) for 15 days. Lipoprotein lipase was inhibited by intra-arterial administration of Triton WR 1339 to estimate hepatic triacylglycerol output. Rats fed the olive oil diet showed a higher rate of triacylglycerol formation than rats fed the ω3 fatty acid diet or the low-fat diet. All three groups showed identical rates of removal from plasma of intraarterially administered artificial chylomicrons that had simultaneously been labeled with cholesteryl [1-¹⁴C]oleate and [9,10(n)-³H]triolein. Liver radioactivity and total fat content were lowest in rats fed the fish oil diet, indicating that ω3 fatty acids were preferentially metabolized in liver. Chylomicrons obtained from donor rats fed either fish oil containg [¹⁴C]cholesterol or olive oil containing [³H]cholesterol were removed at similar rates when infused together intraarterially into recipient animals. A slower formation of plasma very low density lipoprotein triacylglycerols in rats fed fish oil is probably due to a faster rate of oxidation of the fatty acid chains in the liver resulting in decreased plasma triacylglycerol concentrations.     

Effects of fish oil,corn oil and lard diets on lipid peroxidation status and glutathione peroxidase activities in rat heart

In this study, we investigated the effect of various types of fats on heart lipid peroxidation status and on blood lipid parameters. Rats were fed either a low-fat diet (2.2% lard plus 2.2% corn oil), a corn oil diet (17%), a salmon oil diet (12.5%) supplemented with 4.5% corn oil, or a lard diet (15%) supplemented with 2% corn oil. All diets were supplemented with 1% cholesterol. Rats were fed for eight weeks. When compared with the low-fat diet, the salmon oil-diet intake resulted in a lower blood cholesterol, triglyceride and phospholipid concentrations (−50, −56 and −30%, respectively). Corn oil only tended to lower blood lipids; this decrease was significant for triglycerides only (−40%). The hypocholesterolemic effect of salmon oil diet is even more pronounced, if blood cholesterol values are compared with those of rats fed the lard diet. Heart lipid composition was not affected by dietary manipulations. Fatty acid composition of cardiac phosphatidylcholines and phosphatidylethanolamines, however, were altered by high-fat diets. In phosphatidylcholine, salmon oil induced a twelvefold decrease in the n−6/n−3 ratio and a 26% increase in the unsaturation index. For phosphatidylethanolamine, the n−6/n−3 ratio decreased 7.7-fold and the unsaturation index increased by 13%. A 50% decrease of the n−6/n−3 ratio was observed in animals fed the lard diet. Ultramicroscopic examination of ventricles revealed that those of the salmon oil group significantly accumulated lipofuscin-like or ceroid material, whereas this accumulation was barely detectable in hearts of the other groups. Seleniumdependent glutathione peroxidase activity tended to be the highest in hearts of rats fed the salmon oil diet; this increase is significant (+36% and +54% for total and specific activities, respectively), if values are compared with those of the rats fed the lard diet. Liver glutathione peroxidase and heart glutathione S-transferases activities remained unchanged. These results indicate that fish oil did not lower the selenium involved in glutathione peroxidase activity. This rules out that a deficiency in this enzyme was at the origin of heart lipofuscinosis. Also, it is concluded that the n−6/n−3 ratio of the diet is likely more determinant in the alteration of heart lipid peroxidation status than is the polyunsaturated/saturated ratio. Part of this work was presented at the International Congress: “Selenium in Medicine and Biology,” Avoriaz, France, March, 15–18, 1988.     

Vitamin E,cholesterol, and lipids during atherogenesis in rabbits

Rabbits were fed diets including cholesterol and 10% butterfat to determine whether polyunsaturated butter (9% 18∶2) would be less atherogenic than normal saturated butter (3% 18∶2) when fed for 12 weeks. The cholesterol diets alone, 0.5% or 2%, produced aortic plaque development, and plasma cholesterol increased 20 times, lipids increased 10 times, and vitamin E increased 5 times. The inclusion of both fat and cholesterol in the diet produced a synergistic effect, doubling these values to 40 times for cholesterol, 20 times for lipids, and 10 times for vitamin E. The higher circulating levels of cholesterol caused increased tissue levels of cholesterol. With 2% cholesterol and fat, liver and aorta cholesterol increased 10 times, heart 4 times, and muscle cholesterol 2 times. The lower 0.5% dietary cholesterol load was successful in limiting the amount of tissue cholesterol increase. Liver, aorta, heart, and muscle levels of cholesterol were only about half the concentration attained when 2% cholesterol was fed. It was concluded that there were no differences in plasma or tissue cholesterol, vitamin E, or atherosclerosis attributable to the polyunsaturated nature of the diet. The 10% butterfat diets alone, whether saturated or unsaturated, did not induce aortic plaques and did not increase blood or tissue cholesterol, lipids, or vitamin E. Our results suggest that the lipid mobilizing effect is mediated by cholesterol, probably by conversion to bile acids and a stimulation in intestinal absorption.