Relationships of dietary zinc/copper ratios to plasma cholesterol and liver trace mineral deposition in young rats fed saturated and unsaturated fats

The effects of copper and zinc supplements on weight gains, plasma total and high density lipoprotein (HDL)-cholesterol levels and liver trace mineral levels were studied in young rats fed either coconut oil or corn oil. Dietary factors included 1.5 ppm and 6 ppm copper, 7.5 ppm and 30 ppm zinc, and the two fat sources. Weight gains and levels of total and HDL-cholesterol were higher in rats fed corn oil than in rats fed coconut oil. Increases in dietary zinc were associated with increases in total and HDL-cholesterol levels in rats fed corn oil, while increases in copper supplements were associated with decreases in total and HDL-cholesterol levels in rats fed either fat source. Supplements of 30 ppm zinc resulted in decreases in total cholesterol/HDL-cholesterol ratios in rats fed coconut oil but had no apparent effect on these ratios in rats fed corn oil. Thus, zinc may be a more important factor than copper in the reduction of this ratio, particularly if saturated fatty acids predominate in the diet. Increases in dietary copper were associated with increases in liver copper levels of rats fed either fat source. Increases in either dietary copper or zinc resulted in decreases in liver iron deposition in rats fed both fat sources. Results of this study indicate that a dietary zinc/copper ratio of 5 may be required for optimum growth of young rats.     

Dietary cholesterol-fat type combinations and carbohydrate and lipid metabolism in rats and mice

In rats fed semipurified cholesterol-free diets, dietary corn oil induced higher levels of liver cholesterol, but lower concentrations of plasma cholesterol, plasma triglycerides and blood D-3-hydroxybutyric acid, than did coconut fat. Addition of cholesterol to the diets (1%, w/w) greatly increased liver cholesterol levels but did not affect the corn oil effect upon liver and plasma cholesterol. In contrast, dietary cholesterol prevented the corn oil effects upon plasma triglycerides and blood D-3-hydroxybutyric acid. Liver glycogen levels in rats increased significantly after cholesterol feeding, the effect being independent of dietary fat type. In mice, dietary corn oil, compared to coconut fat, elevated liver cholesterol only when the diet contained cholesterol. Corn oil caused an increase of liver glycogen in mice in the presence, but not in the absence of dietary cholesterol. This study shows that dietary cholesterol-fat type combinations influence various aspects of lipid and carbohydrate metabolism in rats and mice.     

Serum and liver lipids in rats and chicks fed with diets containing different oils

OBJECTIVES: Because dietary fat composition is determinant for serum cholesterol level, which is related to cardiovascular disease, we evaluated the effects of diets containing saturated (coconut oil) or polyunsaturated fatty acids (soybean oil) supplemented or not with dietary cholesterol on serum and liver lipid composition in two animal species. METHODS: Male Wistar rats (21 d old) were assigned to one of seven groups and fed with commercial diet or diets containing 5% or 20% soybean oil or 20% coconut oil with or without 1% cholesterol. Chicks were assigned to one of four groups and fed with diets containing 15% soybean oil or 15% coconut oil with or without 1% cholesterol. RESULTS: In rats, the accumulations of hepatic cholesterol and triacylglycerols were higher in the group fed 20% soybean oil and 1% cholesterol than in the group fed 20% coconut fat and 1% cholesterol. The highest serum levels of cholesterol and triacylglycerols were observed in the group fed coconut oil and cholesterol, compared with the group fed soybean oil and cholesterol. Triacylglycerol, high-density lipoprotein, and total cholesterol serum levels increased with diet containing coconut oil and cholesterol. In chicks, the highest hepatic cholesterol accumulation occurred in the group fed 15% coconut fat and 1% cholesterol. Total and high-density lipoprotein cholesterol levels increased with diet containing coconut oil and cholesterol, although none of these diets modified serum triacylglycerol levels. CONCLUSIONS: The type of experimental animal model and the diet composition influence lipid metabolism.     

Copper and iron deficiencies: effects on serum lipids and tissue minerals

To study the interrelationship between iron and copper on serum lipid concentrations, four diets were fed to growing rats: iron and copper deficient, copper-deficient, iron-deficient, iron and copper adequate. After 18 weeks, concentrations of iron and copper in organs and lipids in sera were determined. Iron deficiency alone or combined with copper deficiency resulted in reduced body weights, hemoglobin concentrations, hematocrits, and iron concentrations in liver, spleen, and heart. Hepatic copper was elevated 8-fold in iron deficiency. Copper deficiency alone or combined with iron deficiency resulted in reduced copper concentrations of liver and spleen and reduced ceruloplasmin. Serum triglycerides and cholesterol did not differ among experimental treatments. No significant effects of the interaction between dietary iron and copper on serum lipid levels were found.     

Effect of dietary fat on hepatic metabolism of 14C-oleic acid and very low density lipoprotein triglyceride in the gerbil.

In order to compare in vitro and in vivo aspects of lipid metabolism and lipoprotein secretion associated with the hyperlipemia of saturated fat feeding, gerbils were fed a diet containing 15% coconut oil or safflower oil for 6 weeks. In vitro incorporation of fatty acid was determined by measuring 14C-oleic acid incorporation into hepatic lipis in liver fasting gerbils following Triton WR1339 injection. The plasma lipoprotein profile was assessed by agarose electrophoresis. Coconut oil produced a hypertriglyceridemia and hypercholesterolemia associated with the appearance of very low density migrating lipoprotein, not seen with the safflower oil. Coconut oil also increased the hepatic triglyceride content, enhanced 14C-oleic acid incorporation into total lipid, and favored fatty acid incorporation into triglyceride; safflower oil facilitated esterification of oleic acid into phospholipid. Triton blockade of gerbils fed safflower oil resulted in twice the triglyceride secretion rate of those fed coconut oil. Our interpretation of the data is that dietary polyunsaturated fat favors incorporation of fatty acids into phospholipid, enhances both triglyceride secretion and the plasma transport and clearance of triglyceride and cholesterol and that the hyperlipemia of coconut oil feeding reflects a reduced metabolic clearnace of circulating lipid associated with that dietary fat.     

Taurine prevents hypercholesterolemia in ovariectomized rats fed corn oil but not in those fed coconut oil

We studied whether the type of dietary fatty acid influences the preventive effect of taurine on the ovarian hormone deficiency-induced increase in plasma cholesterol concentration in 6-mo-old ovariectomized rats. Rats were fed one of the following four diets for 28 d: purified diets based on corn oil, which is rich in linoleic acid, with or with out taurine (50 g/kg) or purified diets based on coconut oil, which is rich in lauric and myristic acids, with or without taurine. Body mass gain, food intake, liver weight and plasma apolipoprotein (apo) A-I, apo B, LDL and VLDL concentrations were not affected by the diets. On the other hand, taurine lowered the plasma total cholesterol concentration (P < 0.02) in rats fed corn oil, but not in those fed coconut oil. In rats fed both types of oils, taurine increased the LDL receptor mRNA level (P < 0.01), hepatic cholesterol 7alpha-hydroxylase activity (P < 0.01) and fecal bile acid excretion (P < 0.01). Taurine increased the HMG-CoA reductase mRNA level (P < 0.02) in the liver of rats fed coconut oil, but not in those fed corn oil. Taurine increased liver total lipid (P < 0.05) and triglyceride (P < 0.05) concentrations in rats fed corn oil, but not in those fed coconut oil. These results indicate that the effect of taurine on ovarian hormone deficiency-induced changes in cholesterol metabolism is influenced by the type of dietary fatty acids.     

Effect of dietary safflower phospholipid on plasma and liver lipids in rats fed a hypercholesterolemic diet.

The effect of safflower phospholipid (SP) on plasma and liver lipids in rats fed a hypercholesterolemic diet was examined. Triglyceride mixture (SPO) of safflower oil and palm oil (8:2) containing almost comparable amounts of linoleic acid to safflower phospholipid was used as a control diet. Similarly, the effect of paste safflower phospholipid (PSP) which contains approximately 45% of neutral lipid was also compared to safflower oil (SO). Concentrations of total cholesterol in plasma and liver of rats fed the SP diet were markedly decreased in comparison with those of the other diets, but a slight reduction of total cholesterol in plasma and liver was observed in rats fed PSP diet. SP and PSP induced a reduction in the plasma level of low density lipoprotein (LDL) cholesterol as well as an increase in the level of high density lipoprotein (HDL) cholesterol. The activity of plasma lecithin-cholesterol acyltransferase (LCAT) was greatly increased in rats fed SP diet. These results suggest that the safflower phospholipids suppress the elevation of plasma and liver cholesterol and that this effect may depend on the phospholipid content in dietary lipid.     

Effect of dietary fat content and composition during pregnancy on fetal hepatic HMG CoA reductase activities and lipids in rats

The effects of diets containing 20% (wt/wt) safflower, olive or palm oil or 5% (wt/wt) safflower oil when fed throughout gestation on hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase activity and on plasma and liver lipids were studied in fetal rats at d 21 of gestation. Hepatic total and active HMG CoA reductase activity, plasma free cholesterol and liver triglyceride and phospholipid 18:2(n-6) levels were higher in fetuses of rats fed 20% than in those of rats fed 5% safflower oil. Fetuses of rats fed olive oil had higher active HMG CoA reductase levels than fetuses of rats fed 20% safflower or palm oil; their total reductase activity was similar to that of the safflower oil group and higher than that for the palm oil group. Fetal liver and plasma cholesterol and triglyceride, as well as liver phospholipid concentrations, were not altered by the type of oil fed. The diets containing safflower oil resulted in higher 18:2(n-6) and lower 18:1 levels in fetal liver phospholipid and triglycerides than did the diets containing palm or olive oil. These studies demonstrate that fetal liver HMG CoA reductase activity is influenced by the maternal diet fat content and composition although the effect of specific fatty acids is unknown.     

Interrelated effects of the type of dietary fat and carbohydrate on cholesterol metabolism in rats

Rats were fed semipurified diets, differing in the amount of cholesterol and the sources of fat (corn oil or coconut fat) and carbohydrate (sucrose or starch). After 21 days dietary corn oil had induced higher serum cholesterol concentrations than did coconut fat, except for on diets with a high-cholesterol, high-sucrose background. On high-cholesterol diets containing coconut fat, dietary sucrose increased serum cholesterol, when compared with starch; with corn oil sucrose tended to lower serum cholesterol. Such a tendency was not seen on cholesterol-free diets. Cholesterol feeding caused a dramatic increase in liver cholesterol with all dietary carbohydrate-fat combinations. Liver cholesterol was higher in rats fed corn oil than in those fed coconut fat. The influence of the type of dietary carbohydrate on liver cholesterol was dependent on the type of fat and the amount of cholesterol in the diet. Thus effects of a single dietary component on serum and liver cholesterol in rats are strongly influenced by the background of the diet. This implies that published results of experiments on diet and cholesterol metabolism in rats cannot be compared readily.     

Influence of dietary fats and vitamin e on plasma and hepatic vitamin a and β‐carotene levels in rats fed excess β‐carotene

Effects of different dietary lipids and excess vitamin E on plasma and hepatic concentrations of β‐carotene were evaluated in rats fed diets containing a large excess (0.2%) of β‐carotene. Male weanling Wistar Kyoto rats were fed β‐carotene‐supplemented diets containing various dietary lipids as follows: Group I, a saturated fat (coconut oil); Group II, a monounsaturated fat (olive oil); Group III, a polyunsaturated fat rich in ω‐6 fatty acids (safflower oil); Group IV, same as Group III plus vitamin E; and Group V, a polyunsaturated fat rich in ω‐3 fatty acids (menhaden oil). All diets contained 2% saf flower oil to provide sufficient amounts of linoleic acid (an essential fatty acid). Rats were killed after six weeks of feeding the various diets, and the concentrations of Q‐carotene and vitamin A were determined in plasma and liver. Plasma vitamin A levels were not altered by any of the dietary lipids or by an excess of vitamin E. The concentrations of β‐carotene in plasma were the lowest in rats fed the diet containing menhaden oil. The feeding of the diet containing an excess of vitamin E also resulted in a significant decrease in plasma β‐carotene concentration. Similarly, the hepatic β‐carotene concentration was also reduced to about one‐half in rats fed the diet containing an excess of vitamin E. Liver β‐carotene concentration was higher in Groups II and III than in the other three dietary groups. Hepatic vitamin A concentrations were also affected by the type of dietary fat. The highest levels were observed in rats fed the coconut oil diet; the lowest level of vitamin A was in rats fed menhaden oil (Group V). The results of this study suggest that the type of dietary fat and an excess of vitamin E can have a significant effect on 0‐carotene and vitamin A stores in liver and on β‐carotene content of plasma.     

The effect of dietary safflower phospholipid and soybean phospholipid on plasma and liver lipids in rats fed a hypercholesterolemic diet.

The effect of dietary safflower phospholipid (Saf-PL) and soybean phospholipid (Soy-PL) on plasma, liver, and fecal lipids in rats fed a hypercholesterolemic diet was compared with that of triglyceride mixture (controls). Triglyceride mixture (SP-Oil) of safflower oil and palm oil (8:2) contained almost comparable amounts of linoleic acid to safflower phospholipid or soybean phospholipid. Concentration of total cholesterol in plasma of rats fed the Saf-PL and Soy-PL diets were significantly decreased in comparison with that of the SP-Oil diet. Similarly, both Saf-PL and Soy-PL induced a reduction in the concentration of liver cholesterol compared with SP-Oil; Saf-PL indicated the lowest value. Saf-PL only significantly increased the level of high density lipoprotein (HDL) cholesterol. The level of chylomicron plus very low density lipoprotein (VLDL) cholesterol was lower in rats fed the Saf-PL and Soy-PL diets than that of the SP-Oil diet. The activity of plasma lecithin-cholesterol acyltransferase (LCAT) was increased in rats fed Saf-PL and Soy-PL. Saf-PL and Soy-PL caused an enhanced excretion of fecal neutral steroids, but not acidic steroids compared with SP-Oil. These results suggest that, in addition to soybean phospholipid, safflower phospholipid suppresses the elevation of plasma and liver cholesterol and that this effect may be brought about by inhibiting the absorption of cholesterol in the small intestine.     

In vitro effects of selenite and mercuric chloride on liver thiobarbituric acid-reactive substances and non-protein thiols from rats: influences of dietary cholesterol and polyunsaturated and saturated fatty acids

OBJECTIVE: We measured the in vitro effects of mercuric chloride (Hg2+) and selenite (Se4+) on hepatic 2-thiobarbituric acid-reactive substances (TBARS) and non-protein sulfhydryl (NPSH) levels of rats fed diets enriched with polyunsaturated or saturated fatty acids with and without cholesterol. METHODS: Male Wistar rats (21 d old) were assigned to one of four groups and fed diets containing 20% soybean oil, 20% soybean oil plus 1% cholesterol, 20% coconut oil, or coconut oil plus 1% cholesterol. After the feeding period (6 wk), body weight gain was equal in all groups. TBARS levels and NPSH content were measured after in vitro exposure to mercuric chloride (100 microM) and sodium selenite (25 microM) for 1 h. RESULTS: The lipid peroxidation, measured as TBARS levels in the control group, were statistically higher in hepatic homogenates of rats fed diets containing soybean oil than in groups fed coconut oil (P = 0.009). However, cholesterol supplementation did not change TBARS levels. Selenite alone did not modify TBARS production, whereas mercury alone significantly increased TBARS levels. Moreover, Se4+ protected against mercury-induced lipid peroxidation only in rats fed diets containing coconut oil. In the control group, dietary fat acids did not change NPSH levels. Selenite produced higher oxidative effects toward NPSH content, whereas Hg2+ decreased NPSH levels only in liver from rats fed diets containing soybean oil. NPSH levels were higher after concomitant exposure to Se4+ and Hg2+ chloride that after exposure to Se4+ alone, suggesting an interaction between Hg2+ and Se4+. Catalase activity was higher in animals fed diets containing soybean oil. Dietary cholesterol decreased glutathione peroxidase activity. CONCLUSION: Together these results indicated that the protective effect of Se4+ against mercury-induced lipid peroxidation depends on dietary fat saturation.     

Accelerative effect of olive oil on adrenal corticosterone secretion in rats loaded with single or repetitive immersion-restraint stress

The present study was performed to clarify the effects of dietary oils on physiological and metabolic changes induced by a stress, using one-time or repetitive water-immersion of restrained rats (single or repetitive stress) as an experimental stress load. In rats fed any test diets containing 20%) of the mixture of tripalmitin, tristearin, and corn oil (PSC), olive oil (OLI). safflower oil (SAF), and linseed oil (LIS) with repetitive stress loading, body weight gains and food intakes were generally reduced. The weights of the thymus and spleen also declined, but the adrenal weights were enhanced. Particularly, the increase in the adrenal weight of rats given the OLI diet was greater than of rats supplied with other diets. When the rats were loaded with the single or repetitive stress, the concentrations of urea, lipid peroxide, and corticosterone in the plasma were increased in rats fed any of dietary oils. The rise of plasma corticosterone level was especially great in rats fed the OLI diet. The concentrations of total cholesterol (T-CHOL) and triglyceride (TG) in the plasma and liver generally tended to be higher in rats fed the OLI diet than in rats given the other diets with and without stress exposure. Plasma corticosterone concentration was correlated to the adrenal weight (r=0.87, p<0.05). This study showed that OLI especially enhanced the adrenal weight in rats exposed to the repetitive stress and further raised the increased secretion of adrenal corticosterone in rats loaded with the single or repetitive stress compared with the other oils. The mechanism explaining these actions of OLI was inferred to be related to the levels of T-CHOL and TG in the plasma and liver generally enhanced by stress.     

Influence of dietary fats and vitamin E on plasma and hepatic vitamin A and beta-carotene levels in rats fed excess beta-carotene

Effects of different dietary lipids and excess vitamin E on plasma and hepatic concentrations of beta-carotene were evaluated in rats fed diets containing a large excess (0.2%) of beta-carotene. Male weanling Wistar Kyoto rats were fed beta-carotene-supplemented diets containing various dietary lipids as follows: Group I, a saturated fat (coconut oil); Group II, a monounsaturated fat (olive oil); Group III, a polyunsaturated fat rich in omega-6 fatty acids (safflower oil); Group IV, same as Group III plus vitamin E; and Group V, a polyunsaturated fat rich in omega-3 fatty acids (menhaden oil). All diets contained 2% safflower oil to provide sufficient amounts of linoleic acid (an essential fatty acid). Rats were killed after six weeks of feeding the various diets, and the concentrations of beta-carotene and vitamin A were determined in plasma and liver. Plasma vitamin A levels were not altered by any of the dietary lipids or by an excess of vitamin E. The concentrations of beta-carotene in plasma were the lowest in rats fed the diet containing menhaden oil. The feeding of the diet containing an excess of vitamin E also resulted in a significant decrease in plasma beta-carotene concentration. Similarly, the hepatic beta-carotene concentration was also reduced to about one-half in rats fed the diet containing an excess of vitamin E. Liver beta-carotene concentration was higher in Groups II and III than in the other three dietary groups. Hepatic vitamin A concentrations were also affected by the type of dietary fat.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of tristearin, triolein and safflower oil diets on cholesterol balance in rats

Diets containing relatively homogeneous triglycerides composed of 18-carbon chain saturated, monounsaturated or polyunsaturated fatty acids were fed to rats. Cholesterol absorption and turnover were studied. Cholesterol absorption was significantly less in rats fed tristearin than in animals fed triolein or safflower oil. Cholesterol removal from plasma was fastest in rats fed tristearin and slowest with safflower oil and triolein. Plasma cholesterol levels were lowest with tristearin and highest with safflower oil. Increased cholesterol in high density lipoproteins was observed with tristearin and triolein. Lymph and hepatic cholesterol, and lymph triglycerides were highest with safflower oil, suggesting endogenous mobilization. Cholesterol production was least with triolein. Sterol synthesis was greatest with tristearin, perhaps attributable to decreased negative feedback analogous to effects of cholestyramine. Differences in lipoprotein composition observed with the various diets are important since effects on particle size and shape may influence removal mechanisms. The mechanisms underlying the different effects of dietary triglycerides on sterol absorption and metabolism remain to be elucidated.     

Regulation of plasma and liver total cholesterol levels by dietary oleic acid in rats fed a high-cholesterol diet.

The effects of diets containing fats and oils or fatty acids on the lipid metabolism were investigated in male rats of the Wistar strain fed hypercholesterolemic diets, especially focusing our attention on the correlation between dietary oleic acid (OLE) contents and the levels of plasma and liver total cholesterol (T-CHOL) or the fatty acid profiles in plasma and liver CHOL-ester. In the rats fed the free (FR)-type fatty acids, the concentrations of plasma and liver T-CHOL were high and the amounts of neutral steroids excreted into the feces were low when compared with those of rats given the triacylglycerol (TG)-type fatty acids, showing that TG-type fatty acids suppress the intestinal CHOL absorption more than the FR-type fatty acids do. The concentrations of plasma T-CHOL were highest in rats fed the oleic acid (OLE)-rich diets, followed in order by rats supplied with the palmitic acid (PAL)-rich diets, the hydrogenated coconut oil (HCO) diet, and the linoleic acid (LIN)-rich diets; the lowest was in rats given tristearin (TSTE) and linseed oil (LIS) diets. A positive correlation was obtained between the dietary OLE contents and the levels of plasma and liver T-CHOL or OLE in the plasma and liver CHOL-ester, and an inverse correlation between dietary OLE contents and the amounts of excreted neutral steroids. These results suggest that the dietary OLE contents regulate the levels of plasma and liver T-CHOL in CHOL-loaded rats.     

Manganese, iron and lipid interactions in rats

The interactive effects of manganese, iron and lipid on mineral status, manganese-dependent superoxide dismutase (MnSOD) activity and lipoprotein composition were investigated by feeding weanling rats two levels of manganese (0.4 or 56 micrograms Mn/g diet), two levels of iron (29 or 109 micrograms Fe/g diet) and either 12% high-linoleic acid safflower oil or 12% high-oleic acid safflower oil for 8 wk. Rats fed the manganese-deficient diets had decreased heart MnSOD activity; depressed tibia and kidney manganese concentrations; lowered plasma and high density lipoprotein (HDL) cholesterol, HDL protein and HDL apo E concentrations; and elevated HDL protein/cholesterol ratios. Ingestion of supplemental iron slightly decreased heart MnSOD activity and tibia and kidney manganese concentrations but had no effect on hematocrits or on plasma and HDL cholesterol levels. Rats fed the linoleic acid-rich rather than the oleic acid-rich oil had increased heart MnSOD activity but had unchanged plasma and HDL cholesterol levels. The decrease in plasma and HDL cholesterol levels with manganese deficiency appeared not to be a result of increased lipid peroxidation but may have resulted from decreased cholesterol synthesis and/or secretion.     

ApoE distribution among lipoproteins of rhesus monkeys is modulated by dietary fat and cholesterol

The effect of dietary saturated fat and cholesterol on plasma cholesterol and apolipoprotein E (apoE) distribution among lipoproteins was studied in rhesus monkeys. Two groups of four monkeys had been fed diets containing 31% energy as either corn oil or coconut oil for 5 yr from birth. Each group was then fed short-term their respective diet with a 0.2% cholesterol supplement, the opposite fat without cholesterol, the opposite fat +0.2% cholesterol, followed by their original fat without cholesterol for 5 to 8 wk periods. Plasma was assayed for total cholesterol, total triglyclerides, and the distribution of apoE within lipoproteins (VLDL, IDL, LDL, HDL) separated by gradient-density electrophoresis. When coconut oil was fed, plasma cholesterol and triglyceride concentrations were 134% and 157%, respectively, of the levels when corn oil was fed. Cholesterol supplementation of corn oil also elevated the plasma cholesterol (141%), whereas cholesterol supplementation of coconut oil appeared to induce a synergistic increase (198%). Both groups of monkeys responded similarly to a given diet. The distribution of apoE in lipoproteins differed according to dietary treatment, with cholesterol feeding causing a major shift from HDL to IDL, whereas coconut oil caused a modest shift from HDL to VLDL. The relative amount of apoE in LDL was unchanged by diet. We conclude that dietary saturated fat or cholesterol can modulate the apoE distribution within lipoproteins in rhesus monkeys in conjunction with the previously noted expansion of the cholesteryl ester pool in VLDL and IDL.     

Copper requirement of baby pigs fed purified diets.

Three experiments involving 52 baby pigs were conducted to determine the minimum copper requirement of baby pigs fed purified diets. Diets were supplemented with anhydrous cupric sulfate to yield the following copper concentrations (ppm, by analysis) when the three experiments were combined: 0.6, 0.9, 1.3, 1.9, 2.0, 2.8, 3.2, 4.0, 4.9, 5.6 and 9.3. Parameters examined include weight gain, hematocrit, hemoglobin concentration, mean corpuscular hemoglobin concentration, plasma ceruloplasmin activity, plasma copper concentration, copper balance, brain and erythrocyte superoxide dismutase activity, copper concentration of liver, kidney, spleen, heart, brain, femur and hair, liver ferritin-iron and total iron concentration, strength characteristics of the femur, and gross and histological appearance at necropsy. Weight gains were subnormal at dietary copper concentrations below 1.9 ppm; plasma ceruloplasmin activities, and plasma and tissue copper concentrations were depressed at dietary copper levels below 2.8 ppm. Bone histopathology was evident at dietary copper levels below 3.2 ppm, and copper balance was low at dietary copper levels below 4.9 ppm. Some evidence of anemia was present at dietary copper levels below 5.6 ppm. Under the conditions of this study, the copper requirement of the baby pig fed a purified diet was judged to be approximately 5.6 ppm (6 ppm copper, dry basis).     

Variable effects of iron status on the concentration of ferritin in rat plasma, liver, and spleen

The present studies were conducted to determine the relationships between iron status and ferritin levels in plasma, liver, and spleen of rats. Rats were fed either iron-adequate or iron-deficient purified diets, and measurements of hemoglobin and plasma and tissue ferritin levels were made at various times during iron depletion and iron repletion. Although mean plasma ferritin concentrations of iron-deficient rats were directionally less than those of iron-adequate rats, these differences were not statistically significant due to high variability among similarly treated animals. During iron repletion plasma ferritin concentrations again were so variable that no significant effect of iron repletion on plasma ferritin concentrations was observed. On the other hand, liver and spleen ferritin concentrations of similarly treated rats were much less variable. Ferritin liver and spleen stores decreased more rapidly than hemoglobin during iron deficiency and were restored more slowly than hemoglobin during iron repletion. There was no evidence of correlation between liver and plasma ferritin concentration. Because of the variable responses of plasma ferritin concentration to iron depletion and repletion and the lack of relationship between plasma and liver ferritin concentrations, it is concluded that plasma ferritin concentration is not a good indicator of iron status in rats.