Rat Plasma Lipoproteins Research Articles

The effect of a thromboxane A2 synthase inhibitor on the dyslipoproteinemia of an inbred rat strain with spontaneous age-related nephrotic syndrome

We have previously shown that the administration of a thromboxane A2 (TXA2) synthase inhibitor (FCE 22178) reduced the progression of glomerular lesions and proteinuria in MNS rats, an inbred strain which develops an age-related nephrotic syndrome. In the present study we investigated the effect of FCE 22178 on the plasma lipoproteins of MNS rats at 28 weeks of age (with mild proteinuria and moderate dyslipoproteinemia) and at 48 weeks of age (with heavy proteinuria and severe dyslipoproteinemia). Drug treatment reduced proteinuria (by 70% and 36% at 28 and 48 weeks of age, respectively) plasma cholesterol (by 36% and 27% at 28 and 48 weeks of age, respectively) and prevented the decrease of plasma albumin observed in untreated rats (C-MNS) 48 weeks old. In treated rats (T-MNS), the decrease of proteinuria was positively correlated with that of plasma cholesterol. FCE 22178 reduced the elevation in plasma HDL1 (by 17.4%) and HDL2 levels (by 30%), a key feature of nephrotic dyslipoproteinemia in the rat. From 28 to 48 weeks of age plasma apo A-I and apo E increased 217% and 128%, respectively, in C-MNS rats and 191% and 121%, respectively, in T-MNS rats. A significant increase of apo A-I/apo E ratio was found in C-MNS rats from 28 (2.28 +/- 0.36) to 48 weeks of age (3.84 +/- 0.9) but not in T-MNS rats. FCE 22178 altered the lipid composition of VLDL and HDL2 by reducing the content of cholesteryl esters and increasing that of free cholesterol and phospholipids. These findings suggest that the beneficial effect of FCE 22178 on the dyslipoproteinemia of nephrotic MNS rats is secondary to the amelioration in kidney function and to the reduction of proteinuria produced by this drug.

Isoforms of rat apolipoproteins and changes induced by insulin deficiency and fasting

Reasons for the disordered lipoprotein metabolism in insulin deficiency are not completely understood. In this study the apolipoproteins from plasma of fed and fasted streptozotocin-induced insulin-deficient rats were compared with normal control rats. Analysis of the apolipoprotein isoforms by two-dimensional electrophoresis revealed increased proportions of sialylated apo E and of sialylated apo C-III in diabetic rats compared with control rats. Fasting increased the proportion of sialylated apo E but not the proportion of sialylated apo C-III. 3H-labeled leucine was injected into normal and insulin-deficient rats, followed by a chase of unlabeled leucine after 30 min. Blood samples were collected at intervals over 24 h and the apolipoprotein components were separated by two-dimensional electrophoresis. The relative specific activities of sialylated isoforms of apo E were less than the relative specific activities of non-sialylated apo E isoforms. In contrast, sialylated isoforms of apo C-III had higher relative specific activities than non-sialylated apo C-III. No interconversions of apo E or apo C-III isoforms were found within the lipoprotein fractions. In insulin-deficient diabetic rats the relative specific activities of sialylated apo E and apo C-III isoforms were both increased relative to non-sialylated isoforms when compared with control rats. The results of this study suggest that the isoforms of apo E and apo C-III associated with the plasma lipoproteins of diabetic rats are changed in parallel with changes in synthesis of the isoforms. The changes in association with the isoforms of the apolipoproteins possibly contribute to abnormal metabolism of plasma lipoproteins in insulin deficiency.

Stimulation of rat hepatic low density lipoprotein receptors by glucagon. Evidence of a novel regulatory mechanism in vivo.

We studied the influence of glucagon on hepatic LDL receptors and plasma lipoproteins in rats. A dose-dependent (maximum, threefold) increase in LDL-receptor binding was evident already at a dose of 2 x 4 micrograms, and detectable 3 h after injection; concomitantly, cholesterol and apolipoprotein (apo) B and apoE within LDL and large HDL decreased in plasma. LDL receptor mRNA levels were however unaltered or reduced. Hepatic microsomal cholesterol was increased and the enzymatic activities of 3-hydroxy-3-methylglutaryl coenzyme A reductase and cholesterol 7 alpha-hydroxylase in hepatic microsomes were reduced. Insulin alone increased receptor binding and receptor mRNA levels twofold, but plasma cholesterol was unchanged and plasma apoE and apoB increased. Administration of insulin to glucagon-treated animals reduced the LDL-receptor binding to control levels and apoB appeared in LDL particles. Estrogen treatment increased LDL-receptor binding and mRNA levels five- and eightfold, respectively. Combined treatment with glucagon and estrogen reduced the stimulation of LDL-receptor mRNA levels by 80% although LDL-receptor binding was unchanged. Immunoblot analysis showed that glucagon increased the number of hepatic LDL receptors. We conclude that glucagon induces the number of hepatic LDL receptors by a mechanism not related to increased mRNA levels, suggesting the presence of a posttranscriptional regulatory mechanism present in the liver in vivo.

Effect of Amylomaize Starch on Plasma Lipoproteins of Lean and Obese Zucker Rats.

Male Zucker rats either genetically obese (fa/fa) or lean (Fa/-) were fed a semi-purified diet containing either cornstarch or amylomaize starch (Eurylon 7R) rich in amylose (70%). Obese rats were hyperlipidemic (cholesterol, 3.27±0.18; triglycerides, 2.11±0.12g/liter), when compared with lean rats (cholesterol, 1.13±0.03; triglycerides, 0.75±0.05g/liter). The amylomaize diet did not reduce the body weight of the Zucker rats. However, it decreased weight, esterified cholesterol, and triglyceride content of the liver in both lean and obese rats. The amylomaize diet decreased plasma cholesterol levels of obese rats (-42%) and lean rats (-30%), while plasma triglyceride levels were significantly decreased only in the lean rats (-43%). The cholesterol content of chylomicrons, VLDL, LDL1 (1.006-1.040), and LDL2 (1.040-1.063, which contains apo E-rich HDL) was reduced by 40 to 50%, while that of HDL was reduced by only 20% (lean) or 23% (obese). Diet containing amylose-rich starch therefore constitutes a promising new way of nutritional control of hyperlipidemias.

Changes in Rat Plasma Apolipoproteins and Lipoproteins During Moderate Protein Deficiency: Potential Use in the Assessment of Nutritional Status

To test apolipoprotein sensitivity as protein deficiency markers, concomitant evolution of plasma apolipoproteins (apo) and usual nutritional markers (transthyretin, albumin, transferrin) were followed during a 28-d protein restriction in young male Wistar rats. In addition, plasma lipids and chemical composition of lipoproteins were assayed by d 28. The control and the deficient groups were fed 18% and 6% casein diets, respectively. By d 28 the protein-deficient group exhibited hypotriglyceridemia resulting from the decrease in VLDL triacylglycerols; free cholesterol and phospholipids were increased, reflecting the increment in LDL-HLDL1. In plasma total lipoproteins, apo BH, AI and E were not different than controls in the deficient group. Apolipoprotein AIV decreased after d 14 and was significantly less than in controls at d 28. Apolipoprotein BI was considerably reduced by d 14 (43% less) and d 28 (52% less) compared with the control group. Apolipoproteins C + AII were significantly lower in the protein-deficient group by d 14 (43%). By d 28, VLDL apo C were decreased 60% by protein restriction. Transthyretin level was 20% lower in the protein-deficient group by d 7 but returned to control values by d 14. A moderately lower value was observed for albumin by d 7 and d 14 and for transferrin by d 28. These results indicate that, in this model, apo BI and C are more sensitive to protein depletion than usual nutritional markers.

Isolation and properties of nascent lipoproteins from highly purified rat hepatocytic Golgi fractions

Two procedures were used to isolate hepatocytic Golgi fractions from rat liver. One procedure yields a light Golgi fraction (GF1 + 2) and the other "intact" stacks of cisternae. Triglyceride fatty acids in nascent very low density lipoproteins (VLDL) were labeled by injection of [3H]palmitate intravenously, and radiolabeled lipoproteins were injected as markers of potentially contaminating endosomes. GF1 + 2 fractions were enriched manyfold in the endosomal markers, indicative of substantial endosomal contamination, whereas intact Golgi fractions from the same livers were about 7% as contaminated. By electron microscopy, GF1 + 2 fractions contained mainly multivesicular bodies (MVBs), together with some Golgi-derived secretory vesicles. The small endosomal contamination of intact Golgi fractions was further reduced by a simple modification of the procedure, which removed most entrained endosomes. The surface constituents of Golgi VLDL (d less than 1.010 g/ml) released from these highly purified intact Golgi fractions differed from those of plasma VLDL. Golgi VLDL contained fivefold less unesterified cholesterol than plasma VLDL, but twofold more phospholipids. Golgi VLDL and plasma VLDL contained similar amounts of cholesteryl esters and triglycerides. The protein content of Golgi VLDL was substantially lower than that of plasma VLDL. ApoB-100 and apoB-48 were similarly represented, but nascent VLDL contained less of the C apolipoproteins. ApoA-I was present mainly as the proprotein in Golgi VLDL, but was virtually lacking in plasma VLDL. ApoE comprised about 22% of the protein mass of Golgi VLDL as well as plasma VLDL; the distribution of apoE isoforms was also similar. Apolipoproteins E and pro A-I released from ruptured Golgi cisternae were largely bound to the Golgi VLDL or were associated with Golgi membranes. Particles resembling low density lipoproteins (LDL) and high density lipoproteins (HDL) were not seen by electron microscopy in contents of intact Golgi fractions. These observations indicate that nascent Golgi VLDL are the primary particulate precursors of rat plasma lipoproteins of hepatocytic origin, and suggest that particles with the density of plasma HDL and LDL do not exist within the secretory pathway of normal hepatocytes. Thus, the results of this research on the properties of nascent plasma lipoprotein precursors contained within uncontaminated hepatocytic Golgi fractions differ substantially from previous published work.

P-298 - Changes in plasma lipoproteins of rats induced by chlorinated organic solvents.

P-298 - Changes in plasma lipoproteins of rats induced by chlorinated organic solvents.

Effects of intravenous infusions of commercial fat emulsions (Intralipid 10 or 20%) on rat plasma lipoproteins: Phospholipids in excess are the main precursors of lipoprotein-X-like particles

Like most commercial parenteral emulsions, Intralipid ® contains the same amount of phospholipids (12 mg/ml) to stabilize 100 or 200 mg of soybean oil (10 or 20% formula, respectively). By centrifugation, 10 or 20% Intralipid was separated into a supernatant, fat particles containing the bulk of triacylglycerols stabilized by a fraction of phospholipids and an infranatant — called mesophase — consisting mainly of phospholipids used in excess as emulsifier. We observed that the initial triacylglycerol phospholipid ratio of the emulsion ( 100 12 and 200 12 , respectively) determines the size of the triacylglycerol-rich particles (260 and 350 nm) as well as the phospholipid content of the mesophase (6.02 and 4.67 mg/ml). To understand the mechanism of the lipoprotein-X (LPX) accumulation generally reported after intravenous fat infusions, plasma lipid levels and lipoprotein profiles were first compared in the rats after infusion (at a constant rate of 0.5 or 1 ml/h for 43 h) of Intralipid 10 or 20%. For the same intravenous triacylglycerol load (100 mg/h), rats infused with Intralipid 10% at 1 ml/h displayed higher triacylglycerol levels than rats infused with the 20% emulsion at 0.5 ml/h, suggesting that the size of exogenous fat particles modulated the catabolic rate of their triacylglycerols. The plasma levels of LPX varied according to the infusion rate of phospholipids not associated with triacylglycerol-rich particles of the emulsion. Moreover, an apo E and apo B enrichment of plasma and an elevation of the apo B48/apo B100 ratio was always observed after Intralipid infusions. In order to confirm that phospholipids of the mesophase are the main LPX precursors, lipoprotein profiles were then compared in the rats after intravenous infusion, at a constant rate of 1 ml/h, of either the mesophase or a suspension of triacylglycerol-rich particles isolated from Intralipid 20%. As expected, significant LPX amounts were only detected in rats infused with the pure mesophase of the emulsion. It was concluded that products of the lipolysis of exogenous fat particles play only a minor role in the formation of LPX. In fact these abnormal lipoproteins are generated by phospholipids of the mesophase which, like infused liposomes, actively mobilize endogenous free cholesterol. Consequently, in order to be considered as true chylomicron models for safe fat delivery in parenteral nutrition and in order to prevent some detrimental effects on cholesterol metabolism, commercial emulsions should be cleared of phospholipid excess.

Effects of dietary saturated, monounsaturated and polyunsaturated fats on plasma lipids and lipoproteins in diabetic rats*

The effects of altering the type of dietary fat on plasma lipid and lipoprotein levels were investigated in streptozotocin‐diabetic rats fed non‐purified diets containing corn oil, olive oil, cod‐l...

Effects of trichloroethylene, 1,1,1-trichloroethane and carbon tetrachloride on plasma lipoproteins of rats.

Effects of single intraperitoneal administration of trichloroethylene, 1,1,1-trichloroethane, and carbon tetrachloride (positive control) on the plasma contents of lipoproteins were investigated in rats. Plasma was fractionated to VLDL, LDL, and HDL by sequential ultracentrifugation. On the administration of carbon tetrachloride at 30 to 1000 mg/kg, VLDL and HDL were reduced dose-dependently, but the reduction in LDL was not dose-dependent. With trichloroethylene at 30 to 300 mg/kg, the lipid contents of VLDL and LDL fractions were decreased. At 1000 mg/kg, VLDL and LDL was increased by the trichloroethylene. The HDL was decreased with increasing doses of trichloroethylene at 30 to 1000 mg/kg. With 1,1,1-trichloroethane at 100 to 300 mg/kg, VLDL and LDL were increased. The HDL levels rose at 100 mg/kg but fell at 1000 mg/kg. Thus trichloroethylene impairs VLDL formation at low doses. 1,1,1-Trichloroethane stimulates the VLDL synthesis at low doses and inhibits it at high doses. The decreases in HDL at high doses of trichloroethylene and 1,1,1-trichloroethane resulted from the inhibition of HDL synthesis. Liver-to-body weight ratios were raised with increasing doses of carbon tetrachloride, trichloroethylene, and 1,1,1-trichloroethane. Plasma GOT and GPT activities rose at much higher doses of solvents than dose levels which produce the changes in lipoproteins and the increases in liver weights. The liver enlargement appeared to be a sensitive marker of hepatotoxicity related to the changes in lipoproteins, the profile of which was different in three solvents.

Redistribution of cholesterol and beta-sitosterol between intralipid and rat plasma lipoproteins and red blood cells in vivo.

Male Wistar rats were injected intravenously with 2 mL of Intralipid containing 7.5 x 10(5) counts per minute (cpm) [14C]cholesterol and 7.5 x 10(5) cpm beta-[3H]sitosterol. Blood was withdrawn immediately and at 5, 10, 20, 60, 120, and 1440 min after injection from different animals. Plasma and red cells were separated and washed by conventional centrifugation, while lipoprotein density classes corresponding to chylomicrons, very low (VLDL), low (LDL), and high density lipoproteins (HDL) were isolated by ultracentrifugation. Total lipid and sterol compositions were determined by thin-layer chromatography in combination with gas-liquid chromatography, whereas radioactivity was measured by scintillation counting. The ratio of [14C]cholesterol/beta-[3H]sitosterol rose from 1 to 3.65 in the plasma VLDL fraction, whereas that in the LDL and HDL fractions were equilibrated at about 2, following an initial transient increase in favour of cholesterol. The appearance and disappearance of the radioactivity from LDL and HDL fractions exhibited precursor-product relationship owing probably to the conversion of the Intralipid into an intermediate lipoprotein-X-like particle, which possesses a density similar to that of LDL. The radioactive cholesterol and beta-sitosterol were incorporated into the red blood cell membranes at nearly similar initial rates, while at later times the incorporation of cholesterol was much preferred.

Induction of long-lasting hypercholesterolemia in the rat fed a cystine-enriched diet.

The influence of dietary excess (5%) of L-cystine on rat plasma lipoproteins was examined. After only one week of cystine feeding, an increase in the plasma cholesterol level and a decrease in triglyceride levels were observed. The increase in cholesterol level became greater when the duration of cystine-enriched diet increased until eight weeks (+131% after eight weeks), but no further increase occurred between 8 and 20 weeks. This change was essentially due to the progressive increase in cholesterol levels in high density lipoproteins (HDL) and in lipoproteins isolated between 1.040 and 1.063 g/ml, i.e., certain low density lipoproteins (LDL2), and containing mainly apoE-rich lipoproteins (HDL1). The decrease in plasma triglycerides resulted from that of chylomicrons and very low density lipoproteins (VLDL). The effects observed after four or eight weeks of cystine feeding were maintained for eight weeks after replacing the cystine diet by the standard diet. Ingestion of the standard diet containing either cholestyramine (2%) or probucol (0.25%) following eight weeks of cystine feeding significantly decreased plasma cholesterol levels. It is concluded that cystine-fed rats are a useful tool of investigation for understanding mechanisms leading to increased plasma cholesterol level and for hypocholesterolemic drug trials.

Effect of fish oils on rat plasma lipoproteins

Plasma high (HDL) and low (LDL) density lipoproteins were isolated from rats fed a diet supplemented with either fish (menhaden) oil or hydrogenated coconut oil (control). Fluorescence polarization and electron spin resonance of labelled fatty acid probe molecules incorporated into the outer amphiphilic monolayer of HDL indicate molecular motion is restricted in the upper portion of the acyl chain following the fish oil diet, which is consistent with a ‘hook’ conformation predicted by preliminary molecular model calculations for n-3 fatty acids (the predominant component of fish oil). Negligible dependence on diet was observed in LDL. Thus, a HDL specific effect of dietary fish oil on molecular fluidity and order in the outer monolayer of rat lipoproteins is suggested.

Modulation of the synthesis of apolipoproteins in rat hepatoma cells

The present study was designed to investigate whether plasma lipoproteins and albumin can affect the basal synthetic rate of apolipoproteins in differentiated rat hepatoma cells (Fao) incubated in serum-free medium. The synthesis of apolipoproteins was measured by the incorporation of [35S]methionine into medium lipoproteins isolated by density gradient ultracentrifugation. Under all the experimental conditions used, Fao cells synthesized almost exclusively apolipoprotein E. When cells were incubated in the presence of 5-10% rat plasma the synthesis of apolipoprotein E increased 2-3-fold; lipoprotein-deficient serum had a negligible effect. Fatty acid-poor bovine serum albumin (BSA), which had been found to reduce very-low-density lipoprotein secretion in isolated rat hepatocytes, did not modify the synthesis of apolipoprotein E. When Fao cells were incubated in medium containing rat plasma lipoprotein fractions, the synthesis of apolipoprotein E increased. The d less than 1.090 g/ml plasma lipoprotein fraction had the major stimulatory effect. Increased apolipoprotein E synthesis was observed when cells were incubated in the presence of lipids extracted from rat plasma lipoproteins. These results suggest that the intracellular accumulation of lipoprotein-lipids plays an important role in regulating apolipoprotein E synthesis in Fao cells.

L-carnitine effect on plasma lipoproteins of hyperlipidemic fat-loaded rats.

The effect of oral L-carnitine administration to rats fed olive oil has been studied. Carnitine significantly decreased triglyceride, cholesterol and phospholipid levels. Particularly, the levels of chylomicron and very low density lipoproteins in the blood were lowered. Low density lipoprotein levels were not affected, and high density lipoproteins were found to be decreased by 20%. Because carnitine did not change the composition of chylomicron and very low density lipoproteins fraction or affect the gastrointestinal triglyceride residue (about 1/3 of the original load), an effect of carnitine on hepatic fatty acid handling is most likely. The lowering of plasma free fatty acid levels by carnitine administration is in favor of an effect of carnitine on fatty acid handling. The effect on the liver is illustrated by the study of acetoacetate formation in in vitro perfused livers from previously olive oil loaded +/- carnitine-treated rats. Carnitine pretreatment stimulated ketogenesis. It is speculated that carnitine administration, by promoting beta-oxidation, lowers the production of very low density lipoproteins. This may be accomplished partly by an increase in the hepatic level of fatty acid binding protein, which also has been observed.

Similar Effects of Zinc Deficiency and Restricted Feeding on Plasma Lipids and Lipoproteins in Rats

Similar Effects of Zinc Deficiency and Restricted Feeding on Plasma Lipids and Lipoproteins in Rats

Effect of portacaval anastomosis on plasma lipoproteins of lean and obese Zucker rats

The distribution of cholesterol (C), triglycerides (TG), phospholipids (PL) and proteins in the different lipoproteins was studied in lean and obese Zucker rats under 2 conditions: non-operated and after portacaval anastomosis (PCA). All lipoproteins, but mainly the d < 1.006 g/ml (chylomicrons + VLDL) fraction, were increased in obese rats. They were hypertriglyceridemic ( +675 %) and hypercholesterolemic ( +207%). PCA decreased cholesterolemia by about 50% and triglyceridemia by 50–70% in both lean and obese rats. Except for VLDL, enriched in TG in obese rats, proportions of C, TG, PL and proteins in lipoproteins were about the same in obese and lean Zucker rats and were nearly unchanged by PCA, suggesting an increased number of particles in obese rats and a decreased number after PCA. Lipoproteins of obese rats were enriched in apo C and proportions of apo E and apo B were decreased in the d < 1.006 g/ml fraction. PCA decreased the proportion of apo C in all lipoproteins.

Potential mechanisms for redistribution of polychlorinated biphenyls during pregnancy and lactation.

Female mice treated with 14C-2,4,5,2',4',5'-hexachlorobiphenyl (6-CB) two weeks prior to mating eliminated virtually their entire body burden of the compound through milk during one lactation cycle. 6-CB was shown to distribute among rat and human plasma lipoproteins and protein in vitro. It was readily transferred among plasma constituents and its distribution was related to the triacylglycerol:protein ratio in plasma. At one hour following its intravenous administration to virgin rats, 6-CB was primarily distributed to LDL. With the hypertriglyceridemia of late pregnancy, more than 70% of circulating 6-CB was associated with VLDL. VLDL is a major substrate for mammary gland lipoprotein lipase which is elevated during lactation. When 6-CB was complexed with human VLDL and injected i.v. into late pregnant mice, mammary gland concentrations of 6-CB exceeded those of adipose tissue at all sacrifice times between 5 min and 6 h. No differences between adipose tissue and mammary gland concentrations of 6-CB were observed with Emulphor:ethanol:saline as vehicle until 6 h. Isolated hepatocytes were capable of secreting protein and triacylglycerol in the form of VLDL into serum-free media. Eighty percent of 6-CB released from hepatocytes was in association with VLDL, with the remainder in association with protein. Adipocytes isolated from epididymal fat pads of male rats which were pretreated with 6-CB released progressively less radioactivity to incubation media with time after treatment even though PCB content of these cells increased. 6-CB may not be evenly distributed among adipocyte lipids.

Accumulation of cholesteryl esters and triglycerides in cultured macrophages incubated with plasma very low density lipoproteins from rats fed on casein or soybean protein diets containing moderate levels of cholesterol

Even when administered at a comparatively low level, dietary cholesterol produces significant changes in the properties of plasma lipoproteins in rats, particularly the d < 1.006 g/ml fraction (VLDL). The occurrence of these changes is promoted by dietary casein. To test the hypothesis that these dietary-induced perturbations might include properties influencing lipoprotein-cell interactions of relevance to atherogenesis, cultured mouse peritoneal macrophages were incubated with VLDL isolated from male rats fed on diets containing either 0, 0.25 or 0.5% cholesterol with casein or soybean protein, respectively, as the sole source of protein. No increase in cholesteryl ester content, and a comparatively small rise in triglyceride content, was observed in macrophages incubated with VLDL from rats fed on cholesterol-free diets. In contrast, a significant and apparently saturable cellular accumulation of cholesteryl esters as well as triglycerides was produced by VLDL from cholesterol-fed rats. The curves showing cellular lipid accumulation versus VLDL-protein (or VLDL-cholesterol) content in the cell medium indicated different cellular affinity for VLDL from casein-fed rats in comparison with VLDL from soybean protein-fed rats. The apoprotein composition of VLDL differed between groups of rats fed on different types of dietary protein with higher proportions of apo C's in the casein-fed rats. In addition, cholesterol feeding resulted in increased proportions of apo A-I and apo A-IV in the plasma VLDL fraction.

Similar Effects of Zinc Deficiency and Restricted Feeding on Plasma Lipids and Lipoproteins in Rats

The objective of this study was to determine whether alterations in HDL composition observed previously were due specifically to zinc deficiency or to reduction in food intake. Rats were placed into three groups and fed for 21 d a zinc-adequate diet (100 ppm) ad libitum, or a zinc-deficient diet (< 1 ppm) ad libitum, or the zinc-adequate diet at an intake equal to that of the deficient group. Blood plasma was fractionated into VLDL, LDL and HDL fractions, and plasma and the isolated fractions were analyzed for lipids and apolipoprotein composition. Analysis of plasma and liver zinc indicated that animals consuming the low zinc diet were deficient. Zinc deficiency and restricted feeding were associated with lower plasma and VLDL triglyceride levels and lower HDL cholesterol levels. The similarities in overall pattern of lipoprotein composition between the zinc-deficient and restricted-intake groups indicate that reduction in food intake may account for the differences in lipoprotein composition which were observed.