Fatty acid interrelationships in plasma,liver, muscle and adipose tissues of cattle fed safflower oil protected from ruminal hydrogenation

Steers were given diets containing formaldehyde-treated casein-safflower oil supplements, in which the constituent 18∶2 was protected from ruminal hydrogenation. A similar group was given unsupplemented diets. The fatty acid compositions of plasma, liver, muscle and adipose tissue lipids were determined in both groups of cattle after 0, 2, 4 and 8 weeks of experimentation. The proportion of 18∶2 in the triglycerides was markedly increased on feeding the supplement and the rate of incorporation into the plasma triglycerides was higher than that in the triglycerides of muscle and adipose tissue. Associated with this increase there were compensatory decreases in the proportions of 16∶0 and 18∶1 but no consistent change in the proportion of 18∶0. The proportion of 18∶2 in the plasma phospholipids and cholesteryl esters was initially much higher than in the triglycerides and this was further increased by feeding the safflower oil supplement. A linear relationship existed between the proportion of 18∶2 in the phospholipids and cholesteryl esters of plasma. The supplement also caused substantial increases in the proportion of 18∶2, both in phospholipids from liver and muscle and in cholesteryl esters from liver, and there were compensatory decreases in the proportions of other unsaturated fatty acids, e.g., 18∶1, 18∶3, 22∶6. These studies demonstrate that when ruminal hydrogenation was circumvented by feeding formaldehyde-treated casein-safflower oil particles, the linoleic acid was absorbed and the pattern of incorporation into plasma and tissue lipids was similar to that in nonruminants.     

Synthesis of cholesterol esters in the plasma and liver of sheep

A study was made with sheep on the formation in vitro of long chain fatty acid esters of cholesterol by the lecithin-cholesterol-acyltransferase system present in the plasma and the acyl CoA-cholesterol-acyltransferase system present in the liver. The rate of cholesterol esterification in the plasma was 0.024 μmoles/ml/hr. The relative pattern of fatty acids esterified during incubation of the plasma remained constant over the 8 hr period of incubation and was similar to the fatty acids in the plasma cholesteryl esters before incubation began and to the fatty acids in the 2-position of the plasma lecithin. The predominant cholesteryl esters synthesized contained monoenoic and dienoic fatty acids. Unlike the bovine, there was no apparent discrimination in favor of the 18∶2 containing species of plasma lecithin as donors of fatty acids. This difference could be accounted for by the similarity in the 18∶2 content of the phospholipids present in the high density (density >1.062 and < 1.21) and the low density (density > 1.006 and <1.063) lipoprotein fractions of the sheep plasma. The possibility of some discrimination against 20∶4 during cholesterol ester synthesis in the plasma of the sheep cannot be excluded. In the liver, the predominant cholesteryl esters synthesized contained saturated and monoenoic fatty acids; cholesteryl linoleate was synthesized to a very much less extent. There was considerable similarity between the composition of the unesterified fatty acid fraction of the liver before incubation began and the fatty acid composition of the cholesteryl esters synthesized during incubation. Addition of sonicated suspensions of free fatty acids altered markedly the fatty acid pattern of the cholesteryl esters synthesized by the liver slices. From the evidence presented it is concluded that the cholesteryl esters in sheep plasma are syntheized mainly by the plasma lecithin-cholesterol-acyltransferase system. The results are discussed in relation to cholesterol esterification systems demonstrated in the plasma and liver of monogastric animals.     

Effects of dietary cholesterol and triglycerides on lipid concentrations in liver, plasma, and bile

Dietary cholesterol (CHL) and triglycerides (TG) can influence plasma, hepatic, and biliary lipid composition, but effects on lipids in these three compartments during the early stages of CHL gallstone formation have not been studied in parallel. We fed prairie dogs diets containing one of four tes oils (safflower, coconut, olive, or menhaden) at either 5 or 40% of calories, in the presence of 0 or 0.34% CHL, for 3 wk. In the absence of dietary CHL, increases in dietary TG produced 50–200% increases in the concentrations of biliary CHL and hepatic cholesteryl ester (CE), while the concentrations of hepatic free CHL (FC) as well as plasma FC and CE remained relatively unchanged. Increasing dietary CHL to 0.34% resulted in increases in hepatic FC of approximately 50% for all four fats regardless of whether they were supplied at 5 or 40% of calories. CHL supplementation caused more pronounced increases in biliary CHL (200–400%), hepatic CE (50–200%), plasma FC (up to 100%), and plasma CE (up to 150%), and these increases were exacerbated by concurrent supplementation of dietary fat and CHL (biliary CHL: 300–700%; hepatic CE: 100–250%; plasma FC: up to 165%; plasma CE: 100–350%). These results indicate that enhanced secretion of biliary CHL and, to a lesser extent, increased synthesis of hepatic CE, may be primary mechanisms for maintaining the hepatic FC pool. Furthermore, dietary CHL and high levels of fat intake are independent risk factors for increasing biliary CHL concentrations, and adverse effects on lipid concentrations in plasma and bile tend to be exacerbated by ingestion of diets rich in both fat and CHL.     

Effect of dietary cholesterol oxidation products on the plasma clearance of chylomicrons in the rat

Oxidized cholesterols in the diet have been shown to exacerbate arterial cholesterol deposition and the development of atherosclerosis in animal models. Dietary oxidized cholesterols are absorbed through the intestine and incorporated into lymph chylomicrons. The aim of this study was to investigate the effect of oxidized cholesterols on the metabolism of nascent chylomicrons in vivo. It was shown that oxidized cholesterols markedly delay the clearance of chylomicrons from plasma compared to rats given TG alone. However, there was no difference in the clearance of chylomicrons containing oxidized cholesterols vs. purified cholesterol, although the presence of oxysterols did appear to exacerbate the removal of these particles from circulation. The impaired clearance of chylomicrons containing oxidized cholesterols was not due to impaired lipolysis and slower conversion to the remnant form. Moreover, the incorporation of oxidized cholesterols did not alter the hepatic or splenic uptake of chylomicrons compared to chylomicrons isolated from rats given purified cholesterol or TG alone. Collectively, the results of this study suggest that the exacerbated delay in clearance of chylomicron remnants enriched with oxysterols may be due to impaired uptake by tissues other than the liver and spleen. Apolipoprotein (apo) analysis showed that oxysterol incorporation reduced the apoE content and altered the apoC phenotype of chylomicrons, which may have an impact on the removal of chylomicron remnants from plasma. In conclusion, dietary oxysterols appear to have the potential to adversely affect chylomicron metabolism. Therefore, further investigations in humans are required to determine whether dietary oxidized cholesterols found in cholesterol-rich processed foods delay the clearance of postprandial remnants, which may contribute to and exacerbate the development of atherosclerosis.     

Effect of feeding protected cholesterol on ruminant milk fat secretion

Feeding 1–2 g/day of cholesterol protected against ruminal hydrogenation caused a 20–30% drop in the secretion of milk fat by goats and cows. The effect was observed with goats fed conventional rations or with goats and cows fed rations supplemented with protected lipids, but was not observed with cows fed conventional rations, or when unprotected cholesterol and protected β-sitosterol was fed to these animals. The results suggest that this depression in milk fat is due to a decreased uptake of plasma triacylglycerol fatty acids by the mammary gland, induced by dietary cholesterol.     

The effects of dietary cholesterol on blood and liver polyunsaturated fatty acids and on plasma cholesterol in rats fed various types of fatty acid diet

Male rats were fed on a fat-free diet for 8 weeks and then switched to diets containing 10% hydrogenated coconut oil (HCO), safflower oil (SFO) or evening primrose oil (EPO). Half of each group was also given 1% of cholesterol in the diet. After 5 further weeks, plama, red cell and liver fatty acids were measured in the various lipid fractions. Plasma and liver cholesterol also were estimated. In almost all fractions and on all three diets, feeding cholesterol led to accumulation of the substrates of desaturation reactions and to deficits of the products of these reactions. The results were consistent with inhibition of Δ-6, Δ-5 and Δ-4 desaturation of n−6 essential fatty acids. Since the diets were deficient in n−3 fatty acids, levels were very low but were also consistent with inhibition of desaturation. In contrast, cholesterol had relatively less consistent effects on 20∶3n−9, suggesting that desaturation of n−9 fatty acids was less inhibited. Plasma cholesterol levels rose sharply in the HCO and SFO groups but not at all in the EPO group. EPO contains the product of Δ-6 desaturation, 18∶3n−6, suggesting that conversion of linoleic acid to 18∶3n−6 and possibly to further metabolites may be important for the cholesterol-lowering effect of polyunsaturates.     

The effect of dietary fats on the plasma lipid composition of sheep

This study reports on the plasma lipid compositions of sheep fed either a control diet (C), a control diet supplemented with tallow (A) or polyunsaturated fatty acid (B) that had been protected against hydrolysis and hydrogenation in the rumen, or a control diet supplemented with maize oil (D). Diet B considerably increased the 18∶2 content of all the major plasma lipid fractions. Although the feeding of diet D also resulted in an increase in the 18∶2 contents within the cholesteryl ester, unesterified fatty acid, and phospholipid fractions the increases were considerably less than those observed with diet B; the levels of 18∶2 within the triglyceride fraction remained similar to that for the sheep which received the control diet. The effect of feeding diet A was confined solely to the triglyceride fraction where the concentrations of 16∶0 and 18∶1 were increased. The lipoproteins of the plasma were separated into very low density lipoproteins (d<1.006), low density lipoproteins (1.006<d<1.063), and high density lipoproteins (1.063<d<1.21), and the distribution of the major lipids between these lipoprotein fractions was investigated. Diet B increased considerably the proportion of triglyceride found in association with the very low density fraction and the concentrations of 18∶2 within all the lipoprotein fractions; these increases in the concentrations of 18∶2 were not confined to any particular lipid fraction of the lipoproteins. In contrast, the increases in the concentrations of 18∶2 produced as a result of feeding diet D were confined to the low and high density lipoproteins. The effect of feeding diet A was confined to fatty acid changes within the triglycerides of the low and very low density lipoproteins.     

Effect of dietary fat on rat liver microsomal and mitochondrial/lysosomal dolichol,phospholipid and cholesterol

The influence of different fat diets on liver phospholipid, cholesterol and dolichol was studied. Rats were separated into four groups and fed standard laboratory chow (control), a diet containing linolenic acid, a coconut oil diet, or a corn oil-containing diet. After five weeks, microsomes and mitochondrial/lysosomal fractions were prepared from the liver, and lipid compositions were analyzed. No changes in phospholipid content were observed. In control animals, the fatty acid compositions of phosphatidylcholine and phosphatidylethanolamine in the two subfractions were similar. However, these two phospholipids showed different fatty acid patterns, which were altered independently upon dietary treatment. The dietary treatments resulted, in most cases, in decreased cholesterol and dolichol contents and, especially in microsomes, in a decreased level of esterification of both lipids. The fatty acid compositions of cholesteryl esters in the two subfractions showed significant differences and cholesterol was esterified to a large extent with linolenic acid when this fatty acid was supplied in the diet. The same dietary treatment exerted different effects on the cholesterol localized in the two different intracellular compartments. This difference was most pronounced in rats fed the corn oil-containing diet; microsomal cholesteryl esters exhibited increased saturation, whereas cholesteryl esters in the mitochondrial/lysosomal fraction displayed decreased saturation. Dolichyl esters in the two cellular compartments had different fatty acyl compositions, with a considerably higher degree of saturation in microsomes. The various diets influenced the nature of the fatty acid moieties present in the isolated fractions and the effects on the two subfractions were opposite. The diet containing linolenic acid decreased the degree of saturation in microsomal dolichyl esters and increased the degree of saturation in the mitochondrial/lysosomal fraction. The results demonstrate that the fatty acid compositions of both dolichyl and cholesteryl esters display organelle specificity. Both the content of these lipids and their fatty acid compositions are greatly influenced by dietary conditions, and the esterification processes at different cellular locations exhibit independent regulation, regardless of the fatty acid content of the diet.     

Influence of dietary saturated fatty acids on the regulation of plasma cholesterol concentration

The specific effects of individual fatty acids (FA) on plasma cholesterol levels, in the range habitually consumed by humans, is not usually presented by the literature. Conclusions have been made regarding the cholesterolemic effect of individual FA, even though these FA cannot be tested individually. It appears that FA balance of the diet may be more important than individual FA intakes. Variation in plasma cholesterol response to diet is influenced by many factors, such as gene-nutrient interactions. The effect on human health of current processes used in the food industry that are certain to change dietary fat composition and TG structure is yet to be fully explored. Some of the relevant research regarding dietary fat and plasma cholesterol levels is reviewed.     

Protection of dietary polyunsaturated fatty acids against microbial hydrogenation in ruminants

Polyunsaturated fatty acids are normally hydrogenated by microorganisms in the rumen. Because of this hydrogenation ruminant triglycerides contain very low proportions of polyunsaturated fatty acids. A new process is described whereby polyunsaturated oil droplets are protected from ruminal hydrogenation by encapsulation with formaldehyde-treated protein. The formaldehyde-treated protein resists breakdown in the rumen thereby protecting the fatty acids against microbial hydrogenation. When these protected oils are fed to ruminants the formaldehydeprotein complex is hydrolyzed in the acidic conditions of the abomasum and the fatty acids are absorbed from the small intestine. This results in substantial changes in the triglycerides of plasma, milk and depot fats, in which the proportion of polyunsaturated fatty acids is increased from 2–5% to 20–30%. These effects are observed in the plasma and milk within 24–48 hr of feeding while a longer period is necessary to alter the composition of sheep depot fat. The implications of these findings are discussed in relation to human and ruminant nutrition.     

Cholesterol metabolism in the liver and intestine of the chick: Effect of dietary cholesterol,taurocholic acid and cholestyramine

The effect of feeding cholesterol, taurocholic acid, or cholestyramine to chicks on cholesterolgenesis from [1-¹⁴C] acetate in liver and intestine was determined in vitro using tissue slices, and in vivo by i.v. injection of [¹⁴C] acetate. The conversion of cholesterol to bile acids in liver in vivo was measured in the same treatments after i.v. injection of [³H] cholesterol. Hepatic cholesterogenesis in vitro and in vivo was depressed by dietary cholesterol and taurocholate and enhanced by cholestyramine. Intestinal cholesterogenesis in vivo was depressed only by taurocholate whereas ileal cholesterogenesis in vitro was reduced by dietary cholesterol. Conversion of cholesterol to bile acids was enhanced by dietary cholesterol and cholestyramine and depressed by taurocholate. Hepatic cholesterol metabolism in the chick appears to be regulated by mechanisms similar to those reported for other species.     

Effects of dietary protein and cholesterol on phosphatidylcholine and phosphatidylethanolamine molecular species in mouse liver

The present study examined the effects of two atherogenic factors, animal protein and cholesterol, on the distribution of fatty acids and the molecular species of major liver phospholipids in mice. Weanling mice were fed a semisynthetic diet supplemented with either casein or soy protein (20%, w/w) in the presence or absence of 0.5% cholesterol for 4 wk. Results from mouse liver showed that animal protein and, more so, dietary cholesterol modified the fatty acid profiles of the phospholipids. Animal protein had no significant effect on the concentration of lipids, but it altered the relative distribution and fatty acid profiles of the phospholipids, phosphatidylcholine and phosphatidylethanolamine. Dietary cholesterol, on the other hand, significantly increased the concentration of liver lipids, but it did not alter the relative distribution of phosphatidylcholine and phosphatidylethanolamine. In cholesterol-fed mice, the proportions of molecular species containing 18∶2n−6 were increased, whereas those containing 20∶4n−6 were decreased, indicating that dietary cholesterol suppressed linoleic acid metabolism. Since cholesterol feeding selectively decreased the ratio of 18∶0/20∶4n−6 in phosphatidylcholine, whereas it increased the 18∶0/18∶2n−6 ratio in phosphatidylethanolamine, this finding suggests that dietary cholesterol may affect the incorporation of fatty acids but not the rate of synthesis of phosphatidylcholine and phosphatidylethanolamine.     

Effect of cupric ions on serum and liver cholesterol metabolism

Cupric ions were administered subcutaneously to male Sprague-Dawley rats at a single dose of 200 μmol/kg. At 24 hr after administration, a remarkable increase of total and free cholesterol was seen in the rat serum. Also, when lecithin-cholesterol acyltransferase (LCAT) (E.C. 2.3.1.43) activity was expressed as the percentage of the total serum that free cholesterol esterified, the acyltransferase activity in rats treated with cupric ions showed a slight decrease while the triglyceride content in rat serum and liver decreased by 54% and 61%, respectively. However, the content of hepatic cholesterol in rats treated with cupric ions did not show such a marked change. On the other hand, acid cholesteryl ester hydrolase activity (Acid CEH) (E.C. 3.1.1.14) in liver lysosomes of rats treated with cupric ions showed a marked decrease with increasing cupric ion concentration both in vivo and in vitro. Furthermore, cupric ions caused a marked release of the lysosomal enzymes cathepsin D and β-glucuronidase into the cytosolic fraction. The changes in acid cholesteryl ester hydrolase activity induced by cupric ions appear to be a direct effect of cupric ions on the enzyme. These results suggest that excessive cupric ion concentrations could cause various disorders in lipid metabolism.     

Effects of highly hydrogenated soybean oil and cholesterol on plasma,liver cholesterol,and fecal steroids in rats

We investigated the relationship between dietary highly hydrogenated soybean oil (HSO) and cholesterol transport in rats. In the first study, to examine the effects of cholesterol transport of different concentrations of HSO in dietary oil, rats were given one of the three diets containing 0, 25, or 50% HSO in dietary oil with cholesterol (5 g/kg diet) or a diet without HSO and cholesterol for 22 d. Feeding the high concentration of HSO prevented the increase in plasma total cholesterol, hepatic total lipids, and cholesterol and the decrease in high-density lipoprotein-cholesterol, which were caused by dietary cholesterol. Moreover, HSO increased the fecal excretion, fecal lipids, and steroids in a dose-dependent manner. In the second study, to examine the effects on cholesterol transport of redistribution of stearic acid in the triacylglycerol species contained in HSO, rats were given one of the six diets containing HSO (distearoylmonoacylglycerol and tristearoylglycerol)-rich, monostearoylglycerol-rich, or palmitic acid-rich oil with/without cholesterol (5 g/kg diet), for 30 d. Whereas the accumulation of cholesterol in the body was reduced, cholesterol excretion was enhanced effectively in rats given the HSO-rich diet compared with rats given the monostearoylglycerol-rich diet. These results suggested that not only the high concentration of stearic acid but also its uneven distribution in HSO-triacylglycerol contributed to the reduction in intestinal cholesterol absorption in rats.     

Dietary sphingolipids lower plasma cholesterol and triacylglycerol and prevent liver steatosis

The prevalence of dyslipidemia and obesity resulting from excess energy intake and physical inactivity is increasing. The liver plays a pivotal role in the systemic lipid homeostasis. Effective, natural dietary interventions that lower plasma lipids and promote liver health are needed. APOE*3Leiden mice were fed a Western‐type diet, supplemented with different sphingolipids, to determine their effect on plasma lipids and liver steatosis. Hepatic lipid levels and lipid‐related gene expression were also determined. Dietary sphingolipids dose‐dependently lowered both plasma cholesterol (C) and triglycerides (TG) in APOE*3Leiden mice. 1% Phytosphingosine (PS) reduced C and TG by 57 and 58%, respectively. PS (a) decreased the absorption of dietary C and free fatty acid but did not affect the intestinal TG lipolysis, (b) increased hepatic VLDL‐TG production whereas plasma lipolysis was not affected; and (c) increased the hepatic uptake of VLDL remnants. Hepatic mRNA levels indicated enhanced hepatic lipid synthesis and VLDL and LDL uptake. Livers of PS (1%) fed mice were lighter (?22%), less pale, and contained less cholesteryl ester (?61%) and TG (?56%). Furthermore, markers for liver inflammation (SAA) and liver damage (ALAT) were decreased by 74% and 79%, respectively in PS‐fed mice. Sphingolipids lower plasma C and TG and protect the liver from fat‐ and cholesterol‐induced steatosis. In a preliminary small double‐blind cross‐over study with six middle‐aged slightly overweight male volunteers the daily supplementation of one gram of PS to the diet resulted in a ?9.8% (p = 0.0074) and – 13.2% (p = 0.0002) reduction of total C and LDL‐C, respectively. The C/HDL‐C ratio was not significantly affected (p = 0.0571). Due to the relatively low pre‐study levels of TG in the human volunteers, and the individual variability of TG levels, the TG lowering in humans was not significant in this first small study, but per individual there was a clear trend in TG lowering.     

Influence of cholesterol feeding and dietary restriction on cholesterol absorption in rabbits

Plasma cholesterol and cholesterol absorption were measured in rabbits given either a standard or cholesterol-rich diet which were fed either ad libitum or reduced to 50% of the control ration. The results confirmed the aggravating effect of dietary restriction on the plama cholesterol response to cholesterol feeding. Hypercholesterolemia was doubled when cholesterol feeding was associated with reduced dietary intake. The percentage of cholesterol absorbed increased significantly in cholesterolfed rabbits on normal caloric ration, while dietary restriction had no effect on this parameter either with the standard or the cholesterol-rich diet. These data indicate that the mechanisms by which plasma cholesterol increases in response to cholesterol feeding involve increased cholesterol absorption. Nevertheless the aggravating effect of dietary restriction cannot be attributed to increased cholesterol absorption.     

Effect of eicosatetraynoic acid on liver and plasma lipids

Groups of rats were fed a fat-free diet supplemented with 0.5% safflower oil (control) or the control diet containing 0.5% of 5,8,11,14-eicosatetraynoic acid (TYA). Blood was collected weekly and plasma lipids analyzed. After 4 weeks, the animals were killed and the liver lipids were analyzed in detail. The acetylenic fatty acid perturbed plasma neutral lipid and phospholipid class concentrations and reduced growth rates. Liver triglyceride concentrations were reduced dramatically in the TYA fed animals, suggesting interference with complex lipid synthesis. Plasma and liver triglycerides were shifted to higher molecular weight species suggesting that TYA affected fatty acid metabolism. The phospholipids showed an accumulation of 18∶2 and a fall in 20∶4 percentages indicating an inhibition in the conversion of linoleate to arachidonate. All major lipid classes exhibited an increase in 18∶1 levels. Analysis of the octadecenoate positional isomers indicated the proportion of oleate increased substantually in all lipid classes whereas vaccenate proportions had fallen dramatically. All of the data collectively suggest that TYA inhibits the elongation of unsaturated fatty acids. A group of rats bearing hepatoma 7288CTC were also fed the TYA diet. Host liver lipids were affected by TYA similar to normal TYA fed animals, but the effects on hepatoma lipids were marginal.     

The effect of dietary supplementation of cholesterol and its subsequent withdrawal on the liver lipids and serum lipoproteins of chickens

Two groups of male chickens were fed either a control diet (group N) containing a standard poultry ration admixed with 10% corn oil or a cholesterol diet (group C) in which the control diet was supplemented with 1% cholesterol. After 6 weeks on the diets, a negligible amount of very low density lipoprotein (VLDL) was found in the serum from control animals. On the other hand, the serum VLDL from the cholesterol-fed birds was the predominant lipoprotein and carried 72% of the total serum lipids. Surprisingly this lipoprotein from cholesterol-fed animals was very low in triglycrides (6%) and high in total cholesterol (77%). While the level of serum low density liporotein was unaffected by the ingestion of cholesterol, the concentration of total lipids and phospholipids in the high density lipoprotein decreased in cholesterol-fed animals. The greatest change in liver lipids from animals fed cholesterol was found in the cholesterol esters, whereas the unesterified cholesterol, triglyceride and phospholipid varied slightly or remained constant. In normal animals the distribution of cholesterol between the liver and the serum was about equal, whereas in the cholesterol-fed birds the liver accounted for 80% of the cholesterol found in the liver-serum pool. In order to determine how the hypercholesterolemic bird responds to the withdrawal of cholesterol from the ration, a diet-exchange experiment was conducted. In this study the birds that were originally fed the cholesterol diets (group C) for 6 weeks were placed on the control diet (group CN) and the birds fed the control diet (group N) for 6 weeks were given the cholesterol diet (group NC). At periodic intervals, 1, 3, 7 and 14 days following the change of diets, 3–5 animals from each group were sacrificed, and analyses performed on their serum lipoproteins and liver lipids. Within one day after the diet substitution, there was a 31-fold increase and a 46% decrease, respectively, in the serum VLDL concentration in groups NC and CN as compared with their corresponding steady state values (groups N and group C, respectively). The liver cholesterol increased 4-fold and decreased 40%, respectively, in the two groups NC and CN as compared with the values obtained before the diet substitution. It is suggested that the concentration of cholesterol in the liver is the principal factor controlling cholesterol metabolism in chickens fed a hypercholesterolemic diet. This represents a portion of a Ph.D. thesis submitted by A.W. Kruski to the University of Illinois in February 1971.     

Effect of dietary restriction on the plasma apolipoprotein pattern in cholesterol-fed rabbits

Dietary restriction (half of the control ration) was performed in rabbits given either standard or cholesterol-rich diets. The plasma apolipoproteins were studied on the total, d<1.21, lipoprotein fraction using polyacrylamide gel electrophoresis. A marked rise in the amount of both apo-B and apo-E appeared in cholesterol-fed rabbits and was enhanced by dietary restriction. These results reflect the aggravation of hypercholesterolemia when cholesterol feeding is carried out in underfed rabbits. In all groups only one molecular species of apo-B, identified as apo-B-100, was present after overnight fasting. Thus, lipoproteins which accumulate in the plasma following cholesterol feeding, associated with dietary restriction or not, probably are remnants of hepatogenous triglyceride-rich lipoproteins.