The effect of magnesium deficiency on serum aldosterone in rats fed two levels of sodium.

Rats were fed 47 (deficient) and 606 ppm (adequate) magnesium with either 2,100 or 14,000 ppm sodium. Serum corticosterone and aldosterone levels were determined by randoimmunoassay in six rats from each treatment group killed on days 7, 14, and 28 of consumption of the experimental diets. Serum corticosterone levels were moderately, but not significantly, decreased in magnesium deficient animals. Serum aldosterone levels increased over time in the rats fed the lower sodium diet with adequate magnesium and were further elevated in magnesium deficient animals. In sodium loaded rats the increase in aldosterone levels in magnesium deficiency was less and occurred later. Retention and urinary excretion of sodium and potassium did not appear to be affected by magnesium status or the serum concentration of aldosterone. Possible mechanisms underlying the changes in aldosterone levels of magnesium depleted animals are discussed with reference to the known effects of magnesium deficiency on physiological functions.     

Effect of dietary carbohydrates and copper status on blood pressure of rats

Copper deficiency was induced in rats by feeding diets containing either 62% starch, fructose or glucose deficient in copper for 6 weeks. All copper deficient rats, regardless of the dietary carbohydrate, exhibited decreased ceruloplasmin activity and decreased serum copper concentrations. Rats fed the fructose diet exhibited a more severe copper deficiency as compared to rats fed either starch or glucose. The increased severity of the deficiency was characterized by reduced body weight, serum copper concentration and hematocrit. In all rats fed the copper adequate diets, blood pressure was unaffected by the type of dietary carbohydrate. Significantly reduced systolic blood pressure was evident only in rats fed the fructose diet deficient in copper. When comparing the three carbohydrate diets, the physiological and biochemical lesions induced by copper deprivation could be magnified by feeding fructose.     

Marginal copper deficiency and atherosclerosis

Copper is an essential trace element in the maintenance of the cardiovascular system. Copper-deficient diets can elicit, in animals, structural and functional changes that are comparable to those observed in coronary heart disease. In this study, the effect of dietary-induced copper deficiency on aortic lesion development was measured by quantitative image analysis in C57BL/6 mice that are susceptible to diet-induced aortic lesions. The diets administered were severely copper deficient (0.2 mg/kg diet), marginally deficient (0.6 mg/kg diet), or copper adequate (6.0 mg/kg diet). Similarly, increased aortic lesion areas and elevated serum cholesterol were demonstrated in both deficient groups, compared with the copper-adequate group. Evidence for graded differences in copper status among the dietary groups was shown by the dose-response increase in liver copper concentration, copper-zinc superoxide dismutase and cytochrome-c oxidase activities, together with serum caeruloplasmin oxidase with increasing intakes of dietary copper. Despite the difference in copper status between the copper marginal and severely deficient groups, similar lesions found in both groups of mice suggest a threshold effect of copper deficiency on lesion formation.     

The effect of dietary protein on the excretion of alpha2u, the sex-dependent protein of the adult male rat.

Adult male rats were maintained on normal (20% casein), protein-free (0% casein), high protein (50% casein), decicient protein (20% zein), and a supplemented, deficient protein (20% zein plus L-lysine and L-tryptophan) diets. Rats on a protein-free diet excreted approximately 1 mg alpha2u/24 h compared with a normal of 10-15 mg/24 h. Depleted rats placed on a 20% casein diet showed a rapid restoration of the normal alpha2u excretion as well as total urinary proteins. Accumulation of alpha2u in the blood serum was measured in nep-rectomized rats. Rats on a 0% casein diet accumulated only 30% of the alpha2u compared to normals. On a 50% casein diet, rats excreted 30-50 mg alpha2u/24 h. However, the accumulation was normal in the serum of nephrectomized rats. A high protein diet did not stimulate alpha2u synthesis but probably increased the renal loss of all urinary proteins. The excretion of alpha2u on a zein diet was reduced to the same degree as with the protein-free diet. Supplementation with lysine and tryptophan restored the capacity to eliminate alpha21 to near normal levels. Accumulation of alpha2u in the serum of nephrectomized rats kept on the zein diets showed that the effect to suppress the synthesis of the ahpha2u. Supplementation restored the biosynthesis of alpha2u. We conclude that the effect of dietary protein on the excretion of urinary proteins in the adult male rat is caused in large part by an influence on the hepatic biosynthesis of alphay2u. The biosynthesis of this protein, which represents approximately 30% of the total urinary proteins, is dependent on an adequate supply of dietary protein.     

Impaired translation initiation activation and reduced protein synthesis in weaned piglets fed a low-protein diet

Weanling mammals (including infants) often experience intestinal dysfunction when fed a high-protein diet. Recent work with the piglet (an animal model for studying human infant nutrition) shows that reducing protein intake can improve gut function during weaning but compromises the provision of essential amino acids (EAA) for muscle growth. The present study was conducted with weaned pigs to test the hypothesis that supplementing deficient EAA (Lys, Met, Thr, Trp, Leu, Ile and Val) to a low-protein diet may maintain the activation of translation initiation factors and adequate protein synthesis in tissues. Pigs were weaned at 21 days of age and fed diets containing 20.7, 16.7 or 12.7% crude protein (CP), with the low-CP diets supplemented with EAA to achieve the levels in the high-CP diet. On Day 14 of the trial, tissue protein synthesis was determined using the phenylalanine flooding dose method. Reducing dietary CP levels decreased protein synthesis in pancreas, liver, kidney and longissimus muscle. A low-CP diet reduced the phosphorylation of eukaryotic initiation factor (eIF) 4E-binding protein-1 (4E-BP1) in skeletal muscle and liver while increasing the formation of an inactive eIF4E.4E-BP1 complex in muscle. Dietary protein deficiency also decreased the phosphorylation of mammalian target of rapamycin (mTOR) and the formation of an active eIF4E.eIF4G complex in liver. These results demonstrate for the first time that chronic feeding of a low-CP diet suppresses protein synthesis in animals partly by inhibiting mTOR signaling. Additionally, our findings indicate that supplementing deficient EAA to low-protein diets is not highly effective in restoring protein synthesis or whole-body growth in piglets. We suggest that conditionally essential amino acids (e.g., glutamine and arginine) may be required to maintain the activation of translation initiation factors and optimal protein synthesis in neonates.     

Consequences of copper deficiency are not differentially influenced by carbohydrate source in young pigs fed a dired skim milk-based diet

Carbohydrates (CHO) such as fructose (FR) or sucrose, but not starch (ST), aggravate the consequences of dietary copper (Cu) deficiency in rats. To evaluate whether this Cu X CHO interaction is pertinent to human health, the pig was used as an animal model. In two studies, 66 weanling pigs were fed dried skim milk (DSM)-based diets for 10 wk with 20% of the total calories provided as either FR, glucose, or ST and containing either deficient (1.0-1.3 micrograms/g diet) or adequate (7.1 micrograms/g) levels of Cu. Plasma and tissue levels of Cu, the activities of plasma ceruloplasmin ferroxidase and erythrocyte Cu, Zn-superoxide dismutase, and hematocrits were lower (p less than 0.05) in animals fed Cu-deficient diets. The relative cardiac mass of all Cu-deficient groups was greater (p less than 0.05) than that of animals fed Cu-adequate diets. These effects were in general unaffected by type of CHO. For comparison, weaned male rats were also fed DSM-based containing diets ST or FR with adequate or deficient Cu for as long as 10 wk. Rats consuming the Cu-deficient diets were characterized by significantly lower hematocrits, decreased tissue Cu levels, and enlarged hearts, regardless of the CHO source. Together, these data demonstrate that DSM-based diets are not suitable for delineation of potential Cu X CHO interactions, and one or more components of DSM may exacerbate the consequences of dietary Cu deficiency.     

Effects of inadequate vitamin E and/or selenium nutrition on the release of arachidonic acid metabolites in rat alveolar macrophages

Effects of vitamin E and/or selenium (Se) deficiency on the secretion of arachidonic acid metabolites by zymosan-stimulated pulmonary alveolar macrophages (AM) were examined using cells from male Long-Evans hooded rats fed torula-yeast based diets with or without the supplementation of vitamin E (150 IU/kg) or Se (0.5 mg/kg). Alveolar macrophages obtained by lavage were purified by adherence and cultured for 4 h in Hank's balanced salt solution containing bovine serum albumin (0.1%) and zymosan (300 micrograms/ml). The arachidonic acid metabolites present in the culture supernatant were measured by radioimmunoassay. Altered vitamin E and Se nutrition had no effect on the number of cells or cell types recovered from the pulmonary airways. Alveolar macrophages derived from animals fed on diets deficient in vitamin E or Se or both nutrients secreted higher levels of prostaglandin E2 and thromboxane B2. Levels of both 5-hydroxyeicosatetraenoic acid and leukotriene B4 were significantly increased only in the group fed the diet adequate in Se but deficient in vitamin E. Our data suggest that vitamin E and Se might play an important role to control the levels of several physiologically and pathologically important arachidonic acid metabolites.     

Analysis of whole blood manganese by flameless atomic absorption spectrophotometry and its use as an indicator of manganese status in animals

To investigate the use of whole blood manganese (Mn) as an indicator of total body Mn, we measured Mn in whole blood and liver of rats fed purified diets containing adequate (45 micrograms Mn/g diet) or deficient (1 microgram Mn/g diet) Mn. The mean hepatic Mn concentration was significantly lower (P less than 0.001) in the Mn-deficient group compared to the control group, 0.36, microgram Mn/g and 1.73 micrograms Mn/g, respectively. Furthermore, whole blood Mn was significantly reduced (P less than 0.001) in the deficient group when compared to the control group, 4.0 ng Mn/ml and 8.6 ng Mn/ml, respectively. Hepatic Mn linearly regressed against whole blood Mn yielded a statistically significant (P less than 0.001) correlation coefficient of 0.775. These data suggest that whole blood Mn is a valid indicator of body Mn status and thus may be useful, in addition to the measurements of serum copper and zinc, for the diagnosis and prognosis of diseases in which the metabolism of trace elements is affected. In addition, this paper describes and delineates operational parameters for the measurement of whole blood Mn using the IL 551 atomic absorption spectrophotometer and the IL 555 B flameless atomizer.     

Zinc deficiency and the activities of lipoprotein lipase in plasma and tissues of rats force-fed diets with coconut oil or fish oil

The present study was performed to investigate the effect of zinc deficiency on the activities of lipoprotein lipase in postheparin serum and tissues of rats fed diets containing either coconut oil or fish oil as dietary fat, using a bifactorial experimental design. To ensure an adequate food intake, all the rats were force-fed by gastric tube. Experimental diets contained either 0.8 mg zinc/kg (zinc-deficient diets) or 40 mg zinc/kg (zinc-adequate diets). The effects of zinc deficiency on the activities of lipoprotein lipase in postheparin serum and postprandial triglyceride concentrations and distribution of apolipoproteins in serum lipoproteins depended on the type of dietary fat. Zinc-deficient rats fed the coconut oil diet exhibited a reduced activity of lipoprotein lipase in postheparin serum and adipose tissue, markedly increased concentrations of triglycerides in serum, and a markedly reduced content of apolipoprotein C in triglyceride-rich lipoproteins and high density lipoproteins compared with zinc-adequate rats fed coconut oil. By contrast, zinc-deficient rats fed the fish oil diet did not exhibit reduced activities of lipoprotein lipase in postheparin serum and adipose tissue and increased concentrations of serum lipids compared with zinc-adequate rats fed the fish oil diet. This study suggests that a reduced activity of lipoprotein lipase might contribute to increased postprandial concentrations of serum triglycerides observed in zinc-deficient animals. However, it also demonstrates that the effects of zinc deficiency on lipoprotein metabolism are influenced by dietary fatty acids.     

Alterations in plasma total and high density lipoprotein cholesterol levels in hyperlipidemic rats fed diets with varied content of selenium and vitamin E

The effect of dietary selenium and vitamin E on plasma total (TC) and high density lipoprotein cholesterol (HDLC) was evaluated in 54 Sprague Dawley rats fed cholesterol/cholic acid enriched diets. Diets 1, 2, and 3 had no added selenium (low Se) and 0 (low), 60 (adequate), and 600 (high) mg/kg dL alpha tocopheryl acetate added respectively. Sodium selenite at 0.2 mg/kg (adequate Se) was added to diets 4, 5, and 6 and at 4.0 mg/kg (toxic Se) to diet 7, 8, and 9 with the same pattern of vitamin E added to the diet as described above. TC and HDLC were measured using the Kodak Ectachem system. Rats in the low and adequate Se groups fed high vitamin E had lower TC values than rats fed lower vitamin E levels but differences were not significant. In the toxic Se groups, rats fed high vitamin E had significantly (p<0.05) higher plasma TC values than did lower Vitamin E groups. Rats on the high vitamin E diets with low or adequate Se had significantly (p<0.05) higher mean plasma HDLC values when compared to rats fed low or adequate vitamin E diets. HDLC values for animals on Se toxic diets were significantly (p<0.05) lower in rats fed a low vitamin E diet. In rats fed Se deficient and adequate diets, a high vitamin E intake resulted in a decrease in TC and an increase in HDLC. In Se toxic rats, TC was elevated by a high dietary intake of vitamin E as was HDLC with both values being significantly higher than values found in the vitamin E deficient rats. Vitamin E deficiency resulted in a plasma lipid pattern that has been associated with greater cardiovascular disease risk.     

Dietary deficiencies of single amino acids: whole-body amino acid composition of adult rats

To ascertain whether chronic amino acid deficiency alters the amino acid composition of the body, 44 adult female rats were randomly allocated to one of 11 treatments which included one control group, ingesting an adequate diet with balanced protein, and ten deficient groups in which one group received protein-deficient diets and the other groups consumed diets each deficient in a single essential amino acid. The degree of deficiency was adjusted to achieve a gradual decline in body weight to 85% of the initial weight and was then adjusted so that this weight was maintained until the end of the experiment at 93 days, when the rats were killed. Deficient rats had lower absolute weights of liver, gastrointestinal tract and muscle than animals given the adequate diet but greater relative weights (% of body weight) of heart and kidneys. There were no significant differences amongst groups in percentages of lipid, nitrogen, protein plus lipid or dry matter. Chronic marginal amino acid deficiencies did not selectively alter amino acid composition.     

Dietary deficiencies of single amino acids: Whole-body amino acid composition of adult rats

Abstract

To ascertain whether chronic amino acid deficiency alters the amino acid composition of the body, 44 adult female rats were randomly allocated to one of 11 treatments which included one control group, ingesting an adequate diet with balanced protein, and ten deficient groups in which one group received protein-deficient diets and the other groups consumed diets each deficient in a single essential amino acid. The degree of deficiency was adjusted to achieve a gradual decline in body weight to 85% of the initial weight and was then adjusted so that this weight was maintained until the end of the experiment at 93 days, when the rats were killed. Deficient rats had lower absolute weights of liver, gastrointestinal tract and muscle than animals given the adequate diet but greater relative weights (% of body weight) of heart and kidneys. There were no significant differences amongst groups in percentages of lipid, nitrogen, protein plus lipid or dry matter. Chronic marginal amino acid deficiencies did not selectively alter amino acid composition.     

Copper deficiency depresses rat aortae superoxide dismutase activity and prostacyclin synthesis

Prostaglandin synthesis shows dependence on lipid hydroperoxides and resultant oxygen derived radical formation. In view of the importance of dietary copper in cytosolic copper dependent superoxide dismutase (Cu/Zn SOD) activity and the role of SOD in oxygen radical formation, the influence of dietary copper on prostacylin (PGI2) synthesis and SOD activity in rat aorta was examined. Copper deficient (0.5 micrograms Cu/g diet) rats showed a significant 47% reduction in PGI2 synthesis rates by aortic ring incubations in comparison to copper adequate (6.0 micrograms Cu/g diet) animals. Aortic SOD activity was reduced by 46% in copper deficiency in comparison to copper adequate animals. Marginal dietary copper (1.6 micrograms Cu/g diet) significantly reduced aortic SOD activity by 32% but was without effect on aortic ring incubation PGI2 synthesis. These results indicate that dietary copper deficiency, and the resultant decrease in SOD activity, depresses aortic PGI2 synthesis.     

Zinc,iron, vitamin E,and erythrocyte stability in the rat

Previous studies have shown that deficiencies of zinc and vitamin E, as well as iron excess, contribute to peroxidative damage in several tissues in vivo. The present study reports on the sensitivity of red blood cells from young rats exposed to individual or concurrent imbalances of these three nutrients. For 21 d, rats were fed diets that were either deficient or replete in zinc and with or without excess iron or replete or deficient in vitamin E. When red blood cells from these rats were incubated in vitro, erythrocyte hemolysis, lipid peroxidation (assessed by MDA production), and hemoglobin degradation (assessed by alanine release), did not significantly increase unless vitamin E had been omitted from the diet. These results imply that either adequate tightly-bound zinc exists within the zinc-deficient cell to protect it from oxidative damage, or that other antioxidant defense mechanisms (including vitamin E) present within the plasma membrane and cytosol are sufficient to protect the cell from the otherwise damaging effects of zinc deficiency and/or iron excess.     

Effects of inadequate vitamin E and/or selenium nutrition on the release of arachidonic acid metabolites in rat alveolar macrophages

Effects of vitamin E and/or selenium (Se) deficiency on the secretion of arachidonic acid metabolites by zymosan-stimulated pulmonary alveolar macrophages (AM) were examined using cells from male Long-Evans hooded rats fed torula-yeast based diets with or without the supplementation of vitamin E (150 IU/kg) or Se (0.5 mg/kg). Alveolar macrophages obtained by lavage were purified by adherence and cultured for 4 h in Hankś balanced salt solution containing bovine serum albumin (0.1%) and zymosan (300 μg/ml). The arachidonic acid metabolites present in the culture supernatant were measured by radioimmunoassay. Altered vitamin E and Se nutrition had no effect on the number of cells or cell types recovered from the pulmonary airways. Alveolar macrophages derived from animals fed on diets deficient in vitamin E or Se or both nutrients secreted higher levels of prostaglandins E₂ and thromboxane B₂. Levels of both 5-hydroxyeicosatetraenoic acid and leukotriene B₄ were significantly increased only in the group fed the diet adequate in Se but deficient in vitamin E. Our data suggest that vitamin E and Se might play an important role to control the levels of several physiologically and pathologically important arachidonic acid metabolites.     

Protective role of selenium status on T3/T4 kinetics in rats under hyperlipidemia

The effect of high fat diet (HFD) on thyroid hormones (T3/T4) and protective role of selenium (Se) were studied in rats. Se levels in serum and liver decreased significantly, whereas glutathione peroxidase (GSH-Px) in liver and lipid levels (cholesterol and triglycerides) in serum increased after 1, 2 and 3 months of HFD feeding in comparison to controls in all the three Se status i.e. deficient (0.02 ppm), adequate (0.2 ppm) and excess (1 ppm) groups. Levels of T3/T4 decreased significantly on HFD feeding, as compared to respective controls in all the groups. Within the deficient group, as Se deficiency progressed, T3/T4 levels decreased after 2 and 3 months in comparison to 1 month. A significant increase was observed in T3/T4 concentration on feeding 1 ppm (excess) Se supplemented diet, in comparison to adequate group. Also, in 1 ppm Se supplemented group as the Se deposition increased i.e. after 2 and 3 months, levels of T3/T4 increased significantly. So, the present study indicates that Se supplementation up to 1 ppm normalizes the T3 and T4 concentrations or regulates the hypothyroidism induced by hyperlipidemia.     

Effect of biliary ligation on manganese accumulation in rat brain

Neurologic and radiologic disorders have been reported to occur in miners inhaling manganese (Mn)-laden dust and in humans receiving long-term parenteral nutrition. These abnormalities have been attributed to Mn intoxication because of elevated serum Mn concentrations. Because the liver, by way of the bile, is the major route of Mn excretion, it is possible that anything that decreases biliary excretion could increase accumulation of Mn in the brain. The purpose of this study was to determine whether biliary ligation would increase Mn accumulation in the brain of rats that were exposed to deficient or adequate amounts of dietary manganese. The first experiment had a 2 x 3 factorial design, two levels of Mn (0 or 45 μg/g diet) and three surgical treatments (control, sham, or bile-ligation). Animals were sacrificed 10 d after being fed⁵⁴Mn. In experiment 2, animals that had a sham operation or bile-ligation were sacrificed at 8 time points after being injected intraportally with⁵⁴Mn complexed to albumin. The biliaryligated animals had a significantly (p < 0.001) smaller percentage of the⁵⁴Mn in their brains (when expressed as a percentage of whole animal⁵⁴Mn) than the sham-operated animals. Mn deficiency had a similar effect. However, we did observe an increased accumulation of the radioisotope in the brain over time. Therefore, in short-term studies, biliary-ligated rats do not appear to be a good model for Mn accumulation in the brains of people with cholestatic liver disease. The U.S. Department of Agriculture, Agriculture Research Service, Northern Plains Area, is an equal opportunity/affirmative action employer and all agency services are available without discrimination.     

Metabolic effects of oral contraceptives in monkeys fed adequate protein & low proein diets

The effects of 2 oral contraceptives, Ovulen and Norlestrin, were studied in monkeys fed adequate protein and low protein diets. The experiment was carried out in parts. In the first one, the administration of contraceptives was cyclic and similar to that employed in human subjects. In the other experiments, the contraceptives were given continuously and an attempt was made to exaggerate the deleterious effects of the oral contraceptive on the liver by including small doses of a known hepatotoxic agent, aflatoxin (AT). In Experiment 1, 45 female monkeys were divided into 2 groups of 20 and 25 and received an adequate protein (16%) and low protein diet (4%) respectively. Each monkey was fed 1/5 of a tablet of Ovulen or Norlestrin orally for 3 weeks, and then administration was discontinued for 1 week. In Experiment 2, 35 female monkeys were divided into 7 groups of 5 each. All the animals recieved 4% protein diet. 5 groups were tube fed at the rate of 100 cal/kg body weight, while 2 groups were given diet ad libitum. Group I received the diet alone while groups II-V received 10 mcg AT, 25 mcg AT, 10 mcg AT plus 1/5 Ovulen tablets, and 25 mcg AT plus 1/5 Ovulen tablet respectively daily. Groups VI and VII received the diet ad libitum but were orally fed 75 mcg AT and 75 mcg AT plus 1/5 Ovulen tablet respectively. Serum glutamic-oxalacetic transaminase activity and alkaline phosphatase activity were studied at regular intervals after the administation of oral contraceptives in the experiments. Serum proteins and hemoglobin were also determined. Monkeys fed oral contraceptives showed increased serum glutamic-oxalacetic transaminase and alkaline phosphatase activities irrespective of the level of protein in the diet. Livers of animals receiving oral contraceptives were morphologically similar to the controls fed respective diets. The experiments were conducted for a period of almost 2 years.     

Dietary manganese suppresses alpha1 adrenergic receptor-mediated vascular contraction

We examined the effect of dietary manganese (Mn) on the vascular contractile machinery in rat thoracic aortas. Weanling male Sprague-Dawley rats were fed either an Mn-deficient (MnD), Mn-adequate (MnA) or Mn-supplemented (MnS) diet (<1, 10-15 and 45-50 ppm Mn, respectively). After 15 weeks on the diets the rats were sacrificed and 3-mm aortic rings were contracted in six cumulative doses of the alpha(1) adrenergic receptor agonist L-phenylephrine (l-Phe, 10(-8) to 3 x 10(-6) M) under 1.5-g preload and relaxed with one dose of acetylcholine (3 x 10(-6) M) to assess intact endothelium. The maximal force (F(max)) of contraction and relaxation, as well as the vessel sensitivity (pD(2)) were determined. Manganese deficiency, assessed by hepatic Mn content, significantly lowered the rate of animal growth. A two-way analysis of variance revealed that MnS animals developed lower F(max) when contracted with L-Phe compared with the MnD and MnA animals (P相似文献