Magnesium deficiency affects plasma lipoprotein composition in rats

Weanling rats were pair-fed for 8 d with control and Mg-deficient diets containing 960 and 30 mg of Mg/kg, respectively. The marked reduction in plasma Mg levels indicated that the rats fed the Mg-deficient diet were indeed deficient. In the Mg-deficient rats the percent composition of triglycerides in VLDL, LDL and HDL was elevated and that of protein was reduced. Although the proportion of cholesterol was reduced in LDL and HDL, that of phospholipid was decreased only in HDL. Magnesium deficiency induced a decrease in the percent composition of apolipoprotein (apo) E and a relative increase in the apo C for VLDL. In HDL from Mg-deficient rats, the proportion of apo AI was higher than normal, apo AIV was lower than normal and apo E was virtually absent. The percent composition of oleic and linoleic acids was increased but that of stearic and arachidonic acids was depressed in both VLDL and HDL derived from Mg-deficient rats compared with pair-fed controls. Whether these alterations in lipoprotein profile contribute to hyperlipoproteinemia or are the results of the metabolic changes that produce hyperlipoproteinemia remain to be determined.     

Copper deficiency decreases plasma homocysteine in rats

The purpose of this study was to determine the effects of copper deficiency on key aspects of homocysteine metabolism that involve methionine recycling and transsulfuration. Male weanling Sprague-Dawley rats were fed AIN-93G-based diets containing <1 or approximately 6 mg Cu/kg. After 6 wk (Expt. 1) and 4 wk (Expt. 2) we found that plasma homocysteine was significantly decreased, and plasma glutathione significantly increased, in rats fed the low-Cu diet. Real-time RT-PCR was used to determine the expression of the subunits of glutamate-cysteine ligase (Gcl) in liver that catalyzes the rate-limiting step in glutathione biosynthesis. The expression of Gclc, the catalytic subunit of Gcl, was upregulated by Cu deficiency; Gclm, the modifier subunit, was not affected. Hepatic betaine-homocysteine methyltransferase (Bhmt), which catalyzes one of the two ways that homocysteine can be remethylated to methionine, was downregulated by Cu deficiency. Because Cu deficiency results in upregulation of Gclc and an increase in the biosynthesis of glutathione, it is plausible that the net flux of homocysteine through the transsulfuration pathway is increased. Furthermore, if Bhmt is downregulated, less homocysteine is available for remethylation (methionine recycling) and more is then available to irreversibly enter the transsulfuration pathway where it is lost. The net effect of increased Gclc and decreased Bhmt would be a decrease in homocysteine as a result of Cu deficiency.     

Dietary copper deficiency alters protein and lipid composition of murine lymphocyte plasma membranes

Protein and lipid analyses were conducted on isolated erythrocyte and lymphocyte plasma membranes from 7-wk-old male C57BL copper-deficient and copper-supplemented mice to investigate mechanisms for the altered immunity that accompanies dietary copper deficiency. Beginning at parturition, dams were fed a diet low in copper (0.5 mg/kg) and the offspring were weaned to this diet. Half the dams and their respective offspring received supplemental copper (20 mg/L) in the drinking water (+Cu) and served as controls. Unsupplemented offspring (-Cu) had lower activity of cuproenzymes serum ceruloplasmin, spleen and thymus cytochrome-c oxidase and copper, zinc-superoxide dismutase. The -Cu mice exhibited anemia, splenomegaly and thymic atrophy. Based on the marker enzyme alkaline phosphodiesterase I (APDE-I), lymphocyte plasma membranes were enriched 7- to 10-fold for spleen and thymus, respectively, after discontinuous sucrose density centrifugation. The activity of APDE-I was higher in spleen and thymus samples from -Cu mice than from those of +Cu mice for both crude homogenates and purified plasma membranes. Proteins were fractionated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by silver staining. A yellow-appearing band, Mr 74,000, present in all splenic membrane samples from +Cu mice was not evident in the samples from -Cu mice. Fatty acid methyl esters (FAME) were quantified by gas chromatography. Compared to splenic membranes from +Cu mice, the samples from -Cu mice demonstrated significant changes in all FAME (lower 16:0, 18:0 and 20:3n-6 and higher 18:1n-9, 18:2n-6 and 20:4n-6), including a higher unsaturation index. FAME composition of erythrocyte ghosts from -Cu mice demonstrated similar changes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Copper deficiency alters vasodilation in the rat cremaster muscle microcirculation.

The effects of copper deficiency on smooth muscle relaxation were studied in the cremaster muscle microcirculation. Male Sprague-Dawley rats were fed either a copper-adequate diet (CuA, 5 micrograms copper/g diet) or copper-deficient diet (CuD, no added copper) for 17-27 d before experimentation. In vivo television microscopy was used to quantify agonist-induced diameter changes in third-order arterioles. Endothelium-dependent relaxation, which is hypothesized to be mediated by nitric oxide, was attenuated by copper deficiency. Both receptor (acetylcholine, 10(-7) to 10(-4) mol/L) and nonreceptor (calcium ionophore A23187, 10(-8) to 10(-7) mol/L) relaxation was decreased. Nitric oxide-mediated dilation, which was endothelium-independent (10(-7) to 10(-5) mol/L sodium nitroprusside), was also attenuated by copper deficiency. Maximal responses were as follows: for acetylcholine, 136 +/- 16% CuA vs. 45 +/- 15% CuD; for A23187, 104 +/- 16% CuA vs. 21 +/- 11% CuD; and for nitroprusside, 125 +/- 12% CuA vs. 46 +/- 13% CuD. There was no difference in microvascular dilation between groups treated with 10(-6) to 10(-4) mol/L of the phosphodiesterase inhibitor papaverine (e.g., CuA 109 +/- 11% vs. CuD 133 +/- 21% with 10(-4) mol/L). These results suggest that copper deficiency inhibits the nitric oxide-mediated mechanism of vascular smooth muscle relaxation without altering the capacity of the smooth muscle to relax. We suggest that copper deficiency either decreases nitric oxide radical availability or disrupts the nitric oxide-guanylate cyclase interaction.     

Relative effects of dietary oleic- and linoleic-rich oils on plasma lipoprotein composition in rats

Plasma lipoprotein composition and hepatic lipid content were investigated in male Sprague-Dawley rats (104 +/- 2 g) fed diets containing 12% olive oil [OO, 70% 18:1(n-9)], 12% high oleic safflower oil [SO, 70% 18:(ln-9)] or 12% high linoleic safflower oil [SL, 73% 18:2(n-6)] for periods of up to 10 wk. Fasting plasma triglycerides were significantly higher after feeding oleic-rich diets than after feeding SL for 3, 5 and 6 wk. At 6 wk VLDL triglycerides were two- to threefold higher in rats fed OO or SO than in those fed SL, but by 10 wk both plasma and VLDL triglycerides were similar. A greater proportion of HDL2 (diameter 8.0-12.1 nm), a lower proportion of HDL1 (diameter 12.2-17.0 nm) and lower HDL apo E content occurred in rats fed OO and SO than in those fed SL at both 6 and 10 wk. LDL and HDL protein and cholesterol concentrations were not different with feeding SO or SL. After 10 wk of feeding the experimental diets, rats fed OO had significantly lower HDL protein, cholesterol and apo E concentrations and significantly higher hepatic triglyceride content compared to rats fed SO or SL, P less than 0.05. These data suggest that HDL and hepatic lipid content are determined by some property of the dietary oil other than its oleic acid content.     

Flaxseed oil supplementation does not affect plasma lipoprotein concentration or particle size in human subjects

alpha-Linolenic acid (ALA) is a major dietary (n-3) fatty acid. Some clinical trials with ALA supplementation have shown reduced cardiovascular risk; however the specific cardioprotective mechanism is not known. We studied the effects of daily supplementation with ALA derived from flaxseed oil on concentrations of plasma LDL cholesterol, HDL cholesterol, intermediate density lipoprotein cholesterol, and lipid particle sizes. In a randomized double-blind trial, 56 participants were given 3 g/d of ALA from flaxseed oil in capsules (n = 31) or olive oil containing placebo capsules (n = 25) for 26 wk. Changes in plasma HDL cholesterol, LDL cholesterol, and triglyceride concentrations did not differ between the 2 groups at 26 wk. The adjusted plasma total cholesterol concentration at 26 wk was 0.45 mmol/L higher in the flaxseed oil group (5.43 +/- 0.03 mmol/L) compared with the olive oil group (5.17 +/- 0.07 mmol/L) (P = 0.026). ALA did not affect LDL, HDL, or IDL particle size; however, the concentrations of the large, less atherogenic LDL1 (P = 0.058) and LDL2 (P = 0.083) subfractions tended to be greater in the ALA group. In conclusion, ALA does not decrease CVD risk by altering lipoprotein particle size or plasma lipoprotein concentrations.     

Copper deficiency in rats: the effect of clofibrate.

This study was undertaken to determine whether hepatic lipogenesis plays a role in the exacerbation of copper (Cu) deficiency. Forty-eight male rats were fed from weaning a Cu-deficient or adequate diet containing 62% carbohydrate as either starch or fructose with or without clofibrate for 5 weeks. Clofibrate was fed since it had been shown to possess hypolipidemic properties. Administration of clofibrate reduced the activity of the lipogenic enzyme glucose-6-phosphate dehydrogenase. Total hepatic lipid, however, was not reduced. Clofibrate did not affect hepatic lipid concentration and the pathology associated with Cu deficiency when fructose was fed was not prevented by the consumption of clofibrate.     

Selenium deficiency in Fisher-344 rats decreases plasma and tissue homocysteine concentrations and alters plasma homocysteine and cysteine redox status

The purpose of the present study was to determine the effect of graded amounts of dietary selenium on plasma and tissue parameters of methionine metabolism including homocysteine. Male weanling Fisher-344 rats (n = 7-8/group) were fed a selenium-deficient, torula yeast-based diet, supplemented with 0 (selenium deficient), 0.02, 0.05 or 0.1 microg (adequate) selenium (as selenite)/g diet. After 61 d, plasma total homocysteine and cysteine were decreased (P < 0.0001) and glutathione increased (P < 0.0001) by selenium deficiency. The concentrations of homocysteine in kidney and heart were decreased (P = 0.02) by selenium deficiency. The activities of liver betaine homocysteine methyltransferase, methionine synthase, S-adenosylmethionine synthase, cystathionine synthase and cystathionase were determined; selenium deficiency affected only betaine homocysteine methyltransferase, which was decreased (P < 0.0001). The ratios of plasma free reduced homocysteine (or cysteine) to free oxidized homocysteine (or cysteine) or to total homocysteine (or cysteine) were increased by selenium deficiency, suggesting that selenium status affects the normally tightly controlled redox status of these thiols. Most differences due to dietary selenium were between rats fed 0 or 0.02 microg selenium/g diet and those fed 0.05 or 0.1 microg selenium/g diet. The metabolic consequences of a marked decrease in plasma homocysteine and smaller but significant decreases in tissue homocysteine are not known.     

Effect of palm oil on plasma lipoprotein concentrations and plasma low-density lipoprotein composition in non-human primates

Palm oil (PO) contains ~43% of palmitic acid. It is the most abundant saturated fatty acid in the diet and it is generally considered the primary cholesterol (C)-raising fatty acid. However, the effect of palmitic acid on plasma cholesterol appears to depend on the cholesterol content of the diet. The aim of this study was to determine the effect of PO with either a high-fat, high-C or moderate-fat, moderate-C diet on lipoprotein C and low-density lipoprotein (LDL) composition. Fifty adult, male vervet monkeys were randomly assigned to the high-fat diet group (HFD: 35%E fat, ~0.106 mg C/kJ; n =20) and the moderate-fat diet group (MFD: 30%E fat, ~0.027 mg C/kJ; n =30). Baseline LDL-C, high-density lipoprotein (HDL)-C and body weight were used to stratify the vervets into comparable experimental groups within each dietary group. The HFD group was divided into two groups of 10 each: one group continued with the HFD in which 8.1%E was derived from lard (AF); in the other group, AF was substituted isocalorically with PO. The MFD group was divided into three groups of 10 each: one group continued with the MFD in which 11.8%E was derived from AF; in the other two groups, the AF was substituted isocalorically with either sunflower oil (SO) or PO. This article presents preliminary results on plasma lipoproteins and LDL composition after 6 months of dietary intervention. Plasma total and LDL-C was higher in all the groups, but the mean changes elicited by PO with either the HFD or MFD were no different from that observed with AF and SO. There was no difference in the mean change of LDL molecular weight within the HFD and MFD. It is concluded that PO is no different from AF (HFD and MFD) or SO (MFD) in its cholesterolaemic effect.     

Relationships among iron absorption, percent saturation of plasma transferrin and serum ferritin concentration in humans

The percent absorption of iron from four dietary sources was compared in 2018 human subjects with three indicators of iron status, serum ferritin concentration, percent saturation of plasma transferrin and iron absorption from a reference dose of ferrous sulfate. Higher correlation coefficients (r) were obtained by comparing dietary iron absorption with the reference dose absorption rather than with serum ferritin; for example, r = +0.61 and r = -0.38, respectively, for a meat and vegetable meal. However, in practice serum ferritin is almost as efficient as the reference dose absorption in estimating dietary iron absorption, because the 95% confidence limits calculated from the regression equations were very similar. The values of r calculated for iron absorption versus transferrin saturation were comparable to those obtained with the other indicators only in the range of transferrin saturation values below 25%, whereas in more iron-replete subjects (transferrin saturation greater than 25%), this correlation virtually disappeared. This indicates that, although both serum ferritin and transferrin saturation reflect iron status in iron-depleted subjects, the control of iron absorption in iron-replete subjects is more dependent on iron stores as reflected in the serum ferritin concentration than the percent saturation of transferrin.     

Protein deficiency impairs erythropoiesis in rats by reducing serum erythropoietin concentration and the population size of erythroid precursor cells.

Erythropoietin (EPO), a glycoprotein produced mainly by the kidney, is the major physiological regulator of erythropoiesis. We developed a sensitive and rapid ELISA for measurement of rat serum EPO with two monoclonal antibodies that recognize different epitopes. To understand the mechanism by which erythropoiesis is impaired in rats deficient in dietary protein, we investigated the levels of the immunoreactive EPO (iEPO) in serums and erythroid precursor cells in hemopoietic tissues during protein deprivation. The iEPO level of 32-d-old rats fed a protein-free diet was lowered to one-third that of rats fed 20% casein at 6 h after protein deprivation began. Protein deprivation decreased the number of EPO-responsive cells in spleen. These results indicate that the impairment of erythropoiesis during protein deficiency is caused by the decrease in serum EPO and the subsequent reduction of the population size of erythroid precursor cells in spleen.     

Alterations in plasma lipid, lipoprotein and apolipoprotein concentrations in copper-deficient rats

In the first experiment, 32 weanling male Sprague-Dawley rats were randomly divided into two treatment groups, namely, a copper-adequate (8 mg Cu/kg diet) or a copper-deficient (0.85 mg Cu/kg diet) group. These animals were used for the plasma lipoprotein determinations. In the second experiment, 20 similar rats were assigned to the two treatments and were used for plasma and blood volume determinations. Feed and distilled water were provided ad libitum. After 7 weeks, plasma was obtained by heart puncture. Plasma lipoproteins were partitioned and purified by ultracentrifugation and agarose-column chromatography into high, low and very low density lipoprotein fractions (HDL, LDL, VLDL). The apolipoprotein profile of HDL fraction was established by polyacrylamide gel electrophoresis. The markedly reduced liver copper content of rats fed the copper-deficient diet confirmed that they were indeed copper-deficient. Significant elevations in protein and cholesterol contents of HDL and LDL fractions and in triglyceride content of LDL fraction were observed in the copper-deficient rats. In addition, the apolipoprotein E concentration of the HDL fraction was significantly increased in the copper-deficient rats. In the second experiment, the hematocrit was markedly reduced and the plasma volume was significantly increased in the rats fed the copper-deficient diet. Data derived from this study and previous studies suggest that the hypercholesterolemia associated with copper deficiency was due mainly to an impairment in the cholesterol degradation process.     

Different effects of zinc and copper deficiency on composition of plasma high density lipoproteins in rats

Male Sprague-Dawley rats (six per group) were fed an egg white-based diet containing 0 or 5 micrograms/g Cu with 1, 10, 100 or 1000 micrograms/g Zn. After 6 wk of feeding, the rats were killed, and the tissues were processed for trace element, lipid and lipoprotein analysis. Copper deficiency was associated with a higher concentration of plasma free cholesterol, high density lipoprotein (HDL) cholesterol and HDL apolipoproteins. Plasma total cholesterol was not significantly affected. No significant differences were noted in HDL lipid composition. However, HDL apo E and apo A-I concentrations were higher with copper deficiency. Lecithin:cholesterol acyltransferase (LCAT) was not affected in a consistent manner by copper status. Varying the amount of zinc in the diet did not produce significant changes in plasma total cholesterol, plasma free cholesterol, HDL cholesterol, or HDL apolipoprotein concentrations. However, HDL from zinc-deficient rats were enriched in free cholesterol and depleted in triglycerides. Furthermore, the concentration of HDL apo C increased as the level of dietary zinc increased.     

Iron deficiency alters DMBA-induced tumor burden and natural killer cell cytotoxicity in rats.

Natural killer (NK) cell activity is impaired in iron-deficient rats. Natural killer cells destroy tumor cells; therefore, iron-deficient rats may be less able to combat cancer growth. Natural killer cell cytotoxicity, both basal and interferon gamma (IFN gamma)-stimulated, was studied in moderately and severely iron-deficient rats challenged with the carcinogen 7,12-dimethylbenz[a]anthracene (DMBA). Female weanling rats were fed ad libitum semipurified diets containing 8, 13 or 42 mg Fe/kg. A pair-fed group was fed the 42 mg Fe/kg diet at the level consumed by the 8 mg Fe/kg group. Following 6 wk of dietary treatment, DMBA-treated rats received a single intragastric dose of DMBA. Dietary treatment was continued. Rats were killed at 1, 4, 8, 14 and 20 wk post-DMBA treatment. Natural killer cell cytotoxicity (both basal and IFN gamma-stimulated) was analyzed. Feeding the 13 mg Fe/kg diet resulted in lower NK cell activity (P = 0.006) and greater tumor burden (P = 0.045) and tumor incidence. Interferon gamma treatment relieved the lower NK cell cytotoxicity observed in moderate iron deficiency. Feeding the 8 mg Fe/kg diet impaired NK cell activity (P = 0.006), but tumor burden and incidence were less than in moderate iron deficiency. In this model, iron deficiency, particularly moderate iron deficiency, contributed to cancer development and compromised NK cell cytotoxicity.     

Interrelationship of plasma triglycerides and HDL size and composition in rats fed different dietary saturated fats

We investigated the relative effects of different dietary saturated fats on the size distribution, apolipoprotein (apo) and chemical composition of HDL in fasted rats. Male Sprague-Dawley rats (174 +/- 2 g) were fed diets containing 0.035% cholesterol and 16% fat (wt/wt) from corn oil (CO diet) or from 2% CO plus 14% butterfat (BF diet), beef tallow (BT diet), palm oil (PO diet) or coconut oil (CN diet) for 6 wk. Apparent lipid digestibility was significantly lower with the PO and BT diets vs. the CO, BF and CN diets. Plasma total cholesterol levels were significantly higher in rats fed the PO and BT diets than in rats fed the BF and CN diets but were not different among the PO-, BT- and CO-fed groups. Nondenaturing gradient gel electrophoresis immunoblot analysis indicated that HDL apo A-I and E resided on particles with significantly smaller modal diameters in rats fed all saturated fats compared with those fed the CO diet. Chemical analyses indicated that HDL generally contained proportionately less protein and more triglyceride, free cholesterol and apo E with saturated fat feeding than with CO diet feeding. Significantly higher plasma and VLDL triglyceride levels were noted with ingestion of the BT, PO or CN diet than with the CO diet. Butterfat feeding resulted in lower plasma triglycerides and HDL-esterified cholesterol than did feeding the other saturated fats. Very low density lipoprotein triglyceride concentrations were inversely correlated with HDL modal diameter of apo E containing lipoproteins (P less than 0.005). These data provide further evidence of the interrelationship of triglyceride and HDL metabolism and suggest that mechanisms independent of cholesterol ester transfer protein may mediate this response in rats.     

Iron deficiency in young rats alters the distribution of vitamin A between plasma and liver and between hepatic retinol and retinyl esters.

We assessed whether iron deficiency alters the concentration of vitamin A (VA) in plasma or liver and the chemical distribution between hepatic unesterified and esterified retinol. Weanling male Sprague-Dawley rats (n = 10/group) were allocated to one of four diet groups: low iron (ID3, 3 mg of elemental iron/kg diet), marginal iron (ID15, 15 mg/kg), control diet food-restricted to the ID3 group (FR, 35 mg/kg), and control diet ad libitum consumption (AD, 35 mg/kg). Both ID3 and FR rats grew less than AD and ID15 rats. At the end of 5.5 wk, plasma retinol concentrations of the ID3 and FR rats were reduced >40% compared to ID15 and AD rats [Kruskal-Wallis test (K-W), P < 0.0042)]. Paradoxically, the hepatic VA concentration was greater in FR rats, with accumulation of more retinyl esters and retinol compared to the other dietary groups. Concentrations of hepatic retinyl esters and retinol did not differ among the other groups, but the molar ratio of hepatic retinyl esters to retinol was greater in ID3 rats (20.1 +/- 1.4) compared to ID15 rats (13.8 +/- 1.6, P = 0.02), AD (11.3 +/- 2.1, P < 0.0042) and FR (9.5 +/- 1.1, P < 0.0042). Iron deficiency may cause changes in liver and plasma VA that are refractory to VA intake, and thus a benefit may be derived from combining iron and VA supplements during nutrition interventions.     

Early iron deficiency alters sensorimotor development and brain monoamines in rats

Iron deficiency in human infancy reportedly leads to developmental delays and changes in neurobiology that may be irreversible. Using a rodent model, the present study examined whether dietary iron deficiency late in pregnancy and during lactation alters sensorimotor development and brain monoaminergic systems. Rats were assigned to 1 of 4 dietary treatments during gestation and lactation: 1) iron sufficient control; 2) prenatal iron deficiency beginning on gestational d 15 (G15); 3) postnatal iron deficiency beginning on postnatal d 4 (P4); 4) iron deficiency beginning on G15 followed by an iron sufficient diet on P4. Developmental milestones, open field behavior, brain iron and proteins, monoamines, and their transporters were evaluated between P6 and P21. Only G15 iron deficient rats had greater dopaminergic activity than controls as indicated by increased tyrosine hydroxylase levels, phosphorylated tyrosine hydroxylase levels, and cellular dopamine in prefrontal cortex and striatum at P15. These rats also showed delayed eye opening, ear development, and reduced locomotor activity. Iron repletion at P4 returned most measures to control levels by the time of weaning. Postnatal iron deficiency reduced striatal and ventral midbrain iron as well as cellular dopamine levels in prefrontal cortex and striatum at P21. Developmental delays in ear development and achievement in bar holding and surface righting also resulted from postnatal iron deficiency. These results indicate that iron deficiency begun at G15 affects early dopamine neurobiology, the development of specific developmental milestones, and behavior in preweaned rats.     

Carbohydrate restriction alters lipoprotein metabolism by modifying VLDL, LDL, and HDL subfraction distribution and size in overweight men

To determine the effects of carbohydrate restriction (CR) with and without soluble fiber on lipoprotein metabolism, 29 men participated in a 12-wk weight loss intervention. Subjects were matched by age and BMI and randomly assigned to consume 3 g/d of either a soluble fiber supplement (n=14) or placebo (n=15) with a macronutrient energy distribution of approximately 10% carbohydrate, approximately 65% fat, and approximately 25% protein. Because the groups did not differ in any of the variables measured, all data were pooled and comparisons were made between baseline and 12 wk. After 12 wk, subjects had a mean weight loss of 7.5 kg (P<0.001), and abdominal fat was reduced by 20% (P<0.001). Plasma LDL cholesterol and triglycerides (TG) were significantly reduced by 8.9 and 38.6%, respectively. Similarly, apolipoproteins C-I (-13.8%), C-III (-21.2%) and E (-12.5%) were significantly lower after the intervention. In contrast plasma HDL-cholesterol concentrations were increased by 12% (P<0.05). Changes in plasma TG were positively correlated with reductions in large (r=0.615, P<0.01) and medium VLDL particles (r=0.432, P<0.05) and negatively correlated with LDL diameter (r=-0.489, P<0.01). Changes in trunk fat were positively correlated with medium VLDL (r=0.474, P<0.0) and small LDL (r=0.405, P<0.05) and negatively correlated with large HDL (r=-0.556, P<0.01). We conclude that weight loss induced by CR favorably alters the secretion and processing of plasma lipoproteins, rendering VLDL, LDL, and HDL particles associated with decreased risk for atherosclerosis and coronary heart disease.     

Copper deficiency in rats: the effect of type of dietary protein.

The present investigation was conducted to determine whether type of dietary protein can exacerbate the pathology induced by the combination of fructose feeding and copper (Cu) deficiency. Weanling male Sprague-Dawley rats were assigned to three different groups differing in the nature of dietary protein. The proteins used were egg-white, casein or lactalbumin. All diets contained 62.5% carbohydrate as fructose and were low in Cu (0.6-0.72 microgram Cu/g diet). Although the lowest concentration of Cu was found in the livers of rats fed egg-white, the pathology associated with Cu deficiency was more severe in rats fed lactalbumin. The highest concentration of hepatic Cu was found in rats fed casein. The data show that the type of dietary protein can exacerbate signs associated with Cu deficiency. The concentrations of hepatic Cu do not reflect accurately the pathology associated with Cu deficiency.     

Fish protein improves blood pressure but alters HDL2 and HDL3 composition and tissue lipoprotein lipase activities in spontaneously hypertensive rats

Summary The two-month effects of dietary fish protein and casein on VLDL, HDL₂ and HDL₃ compositions and hepatic lipase (HTGL) and tissue lipoprotein lipase (LPL) activities were examined in spontaneously hypertensive rats (SHR) at 4 wk of age. After 2 mo of experiment, the fish protein diet induced lower blood pressure (–14 %) as compared to casein. Liver triacylglycerol and total cholesterol concentrations were 1.37- and 1.71-fold lower in the fish protein group than in the casein group, respectively. Total cholesterol concentration in plasma was also diminished by fish protein (–21 %) and was reflected in HDL₂ fraction (–44 %). SHR fed the fish protein diet as compared with those fed casein, showed a significantly low HDL₃ particle number, as measured by diminished HDL₃ mass and apo A-I. The consumption of fish protein did not affect VLDL particle number, but significantly decreased VLDL-triacylglycerol (–32 %) and adipose tissue total lipid concentrations as compared to casein. This was accompanied by diminished HTGL and adipose tissue LPL activities (–10%, –91%, respectively). These data demonstrate that fish protein plays an antihypertensive role and reduces plasma and tissue lipid concentrations. Thus, a fish protein intake might be beneficial for patients with hypertension.