Dietary Zinc Levels Research Articles

Interrelationship of Dietary Vitamin D3 with Zinc and Iron in Young Turkeys ,

Three experiments were conducted with Large White turkeys to four weeks of age. The interrelationship of zinc and vitamin D3 was studied in two experiments. Iron and vitamin D3 were involved in one experiment. One group of ten male and one group of ten female poults were randomly assigned to each treatment within an experiment. All experiments involved a factorial arrangement of two dietary variables, D3 and either zinc or iron. For example, all possible combinations of four zinc levels; 31, 46, 76 and 106 p.p.m. and three vitamin D3 levels; 600, 1200, and 3600 I.C. units/kg. were fed in the second zinc experiment. Significant (P < 0.05) weight gain differences occurred among both zinc and D3 levels in this experiment. Four week body weights were 356, 436, 459 and 444 g., respectively, for Zn levels; and 409, 410 and 452 g., respectively, for D3 levels. Significant (P < 0.05) interactions occurred between dietary zinc and D3 levels, and between iron and D3 levels relative to body weight gain. Vitamin D3 tended to increase tibia zinc levels in poults receiving higher zinc levels; the opposite occurred with lower levels of the element. Zinc level in feces was decreased with vitamin D3. Hemoglobin level was not influenced by D3 but was increased by iron.

Effect of Dietary Copper, Manganese, and Zinc on Nitrogen Equilibrium and Mineral Distribution Subsequent to Trauma in Mature Rats

Following fracture of the femur, changes in nitrogen retention and mineral tissue concentrations in response to graded levels of dietary copper, manganese, and zinc were investigated. Retained nitrogen and liver copper, manganese, zinc, nitrogen and glycogen were determined prior to trauma and at 48-hour intervals for 8 days posttrauma. The excretion of nitrogen increased, and liver copper,manganese, and zinc decreased, as did liver nitrogen and glycogen in response to fracture. Increasing dietary copper, manganese, or zinc increased liver copper, manganese, or zinc, respectively, and decreased nitrogen loss by traumatized rats. The data suggest that trauma induced a change in the concentrations of liver copper, manganese, and zinc which coincided with changes in liver nitrogen and glycogen. The results indicated that subsequent to femoral fracture, the nutritional requirement for copper, manganese, and zinc for minimal nitrogen loss were higher than the NRC requirements for the mature male rat.

Oral contraceptives, norethindrone and mestranol: effects on tissue levels of minerals.

The study involved three levels of dietary zinc (deficient, marginal, and adequate) and four hormonal conditions; namely, no steriods, norethindrone, mestranol, and norethindrone plus mestranol. The steroids were incorporated into diets and fed to 11-wk-old female Sprague-Dawley rats. After 10 wk of treatment, various tissues were excised for mineral assays by atomic-absorption spectrophotometry. Both steroids, reduced weight gain. Mestranol depressed plasma zinc, tibia copper and magnesium, and liver iron, but elevated the zinc levels in liver and erythrocytes, plasma copper, liver magnesium and calcium, and iron content of tibia and heart. In general, the effect was most prominent with adequate zinc but diminished in magnitude with the reduction of zinc intake. In addition, norethindrone increased heart iron and tibia calcium. Mestranol appeared to be the main causative factor and may have induced a possible shift of minerals from one pool to another. As expected, zinc deficiency resulted in the reduction of zinc concentrations of plasma, tibia, kidney, and pancreas, and the elevation of copper, iron, magnesium, and calcium concentrations of various tissues.

Zinc metabolism and homeostasis in rats fed a wide range of high dietary zinc levels.

Zinc metabolism and homeostasis were studied in young growing rats fed a 38 ppm zinc diet with added zinc levels ranging from 0 to 8400 ppm for 21 days. High dietary zinc did not cause toxicity symptoms. Stable zinc in feces increased linearly with dietary zinc intake but fecal 65Zn, from a single oral dose, did not increase above the 1200 ppm dietary level. Stable zinc in liver, kidney, and tibia increased two to three times with 2400 ppm added zinc, but was not further elevated until 8400 ppm was fed. Stable zinc in muscle and heart was not affected appreciably by dietary zinc level. In all tissues, 65Zn retention was drastically reduced with 1200 ppm added dietary zinc. Additional dietary zinc reduced 65Zn in muscle and heart but had little effect on liver and kidney 65Zn. The data indicate that rats have fairly effective homeostatic control mechanisms for tissue zinc below about 7200 ppm dietary zinc. Whereas, with dietary zinc up to about 1200 ppm, decreasing absorption is the main route of homeostatic control, above this level, more rapid zinc turnover rates and increasing endogenous zinc excretion appear to have major importance.

Precipitation of a selenium deficiency by high dietary levels of copper and zinc.

High mortality and a high incidence of exudative diathesis and muscular dystrophy were observed in chicks fed a diet supplemented with either 800 or 1600 ppm copper. Adding 0.5 ppm selenium to a basal diet containing 0.2 ppm prevented mortality and selenium deficiency signs. Dietary zinc levels of 2100 to 4100 ppm also resulted in high mortality, exudative diathesis, and muscular dystrophy. A selenium supplement of 0.5 ppm completely prevented the deficiency signs and markedly reduced mortality. The results demonstrate that both copper and zinc can induce a selenium deficiency in chicks when a diet relatively low in this element is fed.

Effect of Zinc Deficiency in Rats on Insulin Release from the Pancreas

To explain impaired intravenous glucose clearance in zinc-deficient rats, various parameters of insulin metabolism were measured. Three levels of dietary zinc were fed ( 1, 20, 1,200 ppm). To help distinguish between effects caused by zinc deficiency per se and inanition which accompanies zinc deficiency, a pair-fed control group (20 ppm) was included in some studies. Feeding of high or low zinc diets did not alter the insulin content of the pancreas, but immunoreactive serum insulin and total serum insulin-like activity measured by an in vitro adipose tissue assay were significantly reduced in the zinc-deficient group compared with ad libitum controls. The pair-fed control group also showed significantly reduced circulating immunoreactive insulin but not total serum insulin-like activity. High zinc diets did not affect serum insulin levels. In vitro studies of the release of pancreatic insulin during short incubation periods with glucose as a stimulant indicated that significantly less immunoreactive insulin as well as insulin-like activity was released by pancreata from zinc-deficient rats compared with pair-fed and ad libitum control rats. The pair-fed group, however, showed a significantly decreased release of pancreatic insulin compared with ad libitum-fed controls. Feeding of a high zinc diet did not affect the release of immunoreactive insulin but the release of total insulin-like activity was significantly increased above the ad libitum control value. The response of epididymal adipose tissue to insulin was significantly increased in zinc-deficient rats compared with ad libitum controls but not affected in rats fed the high zinc diet. J. Nutr. 103: 1739-1744, 1973.

Zinc-DDT Interrelationships in Growth and Reproduction in the Rat

Female rats were fed diets containing low levels of DDT, para- thion and carbaryl for 4 months while subjected to the added stresses of preg nancy and moderately low (8 to 10 ppm) or very high (7,000 ppm) levels of dietary zinc. No measurable effects of pesticides or of the low intake of zinc were noted on growth, reproduction, or enzyme activities. The high zinc diet re sulted in slower growth, death of some fetuses and an increase in zinc and DDT in maternal livers. Hemoglobin levels in both maternal and fetal bloods were unaffected by either pesticides or high zinc alone, but were reduced when pesti cides were fed with the high zinc diet. DDT and metabolites were found in the livers of full-term fetuses, demonstrating the transfer of these chlorinated hydro carbon compounds across the placenta. J. Nutr. 102: 523-528, 1972.

Endogenous Zinc Excretion and 65Zn Metabolism in Holstein Calves Fed Intermediate to High but Nontoxic Zinc Levels in Practical Diets

Zinc and 65Zn metabolism, from a single intravenous dose (given 7 days after diets were initiated) were studied in Holstein bull calves fed a practical diet containing 38 ppm zinc or the same diet with 200 or 600 ppm supplemental zinc (zinc oxide). The supplemental zinc increased endogenous fecal 65Zn excretion by 30% with 200 ppm added zinc having as much influence as 600 ppm. The supplemental zinc had a very variable effect on 65Zn distribution in different tissues 14 days after dosing. With some tissues including testicle, rumen wall and abomasum (fundic) each increase in dietary zinc reduced 65Zn content. In muscle, dietary zinc level had no effect on 65Zn concentration. Adding 200 ppm zinc to the diet increased 65Zn and stable zinc in pancreas, liver and kidney; however, a further increase to 638 ppm caused very large increases in these tissues indicating a breakdown in homeostatic control for both injected and absorbed zinc. With the 638 ppm diet smaller increases in 65Zn occurred in bone and small intestine. Serum 65Zn increased with the high zinc diet. Except for muscle, where there was no change, specific activity in every tissue studied decreased with each increase in dietary zinc.

Effect of Supplementary Zinc on the Intracellular Distribution of Hepatic Copper in Rats

Thirty weanling rats were divided into five groups and were fed a ration containing 6 ppm copper or this ration supplemented with 1,000, 2,000, 4,000, or 8,000 ppm zinc as zinc carbonate. After 10 weeks on these diets, the rats were killed for determination of zinc and copper levels in the whole livers and in the intracellular fractions. There was a significant correlation between liver zinc levels and the dietary levels. The accumulation of zinc in the liver resulted in a two-phase depression of hepatic copper. The addition of up to 2,000 ppm dietary zinc resulted in a linear decrease in liver copper levels, but the addition of zinc above 2,000 ppm resulted in a further decrease at a slower rate. Increasing dietary zinc levels had no influence on the hepatic copper content of the nuclei and debris, and mitochondria, but this element significantly depressed the copper levels in the microsomes and the soluble fraction. Likewise, elevated dietary zinc did not affect the zinc levels in the nuclei and debris, and mitochondria, but the levels of this element were significantly increased in the microsomes and the soluble fraction. The percentage dialyzable copper in the soluble fraction decreased with each level of increase in dietary zinc.

EFFECT OF CAFFEINE ON GROWTH, FEED EFFICIENCY AND LEANNESS OF GROWING PIGS AND ITS INTERACTION WITH CALCIUM, ZINC AND CORN OIL

A series of four experiments was conducted to determine the effectiveness of caffeine in promoting increased leanness and feed efficiency in self-fed pigs. A level of 1.5 g of caffeine per kg of feed was one of the most effective levels tested in increasing carcass leanness, but some pigs developed a skin rash which restricted growth rate and reduced feed efficiency. This was accentuated by high levels of dietary zinc or calcium and, in one of two experiments, by a level of 3% corn oil. When a level of 1.0 g/kg of caffeine was used, there was no skin rash, little or no reduction in growth rate, and a slight but nonsignificant increase in feed efficiency. Depth of backfat was significantly reduced (P &lt; 0.01) and the carcass protein: fat ratio was 14–16% higher than in controls. No advantage was found in gradually increasing the caffeine content of the ration from 0.5 g/kg at weaning to 1.5 g/kg eight weeks later, compared with feeding 1.0 g/kg throughout the entire growing, finishing period.

Early tissue 65 Zn distribution after duodenal dosing in calves fed zinc-deficient and control diets.

SummaryFollowing duodenal dosing, 65Zn was rapidly accumulated by several calf tissues, with a considerable amount in the liver and other tissues within 1 hr. With adequate dietary zinc, liver contained a substantial quantity of labile zinc which was greatly depleted in calves fed a zinc-deficient diet for 2 weeks. Other soft tissues had a very limited amount of labile zinc. Zinc turnover rate was much slower in muscle than in the softer tissues, and was not greatly affected by dietary zinc level. Transfer of zinc from the intestinal mucosa to the blood appeared to be the rate-limiting step in zinc absorption. This step was accelerated by feeding a zinc-deficient diet for 2 weeks. However, 65Zn uptake by the mucosa from the intestinal contents was vastly increased by the zinc-deficient diet.

65Zn Absorption Rate Following Single Duodenal Dosing in Calves Fed Zinc-deficient or Control Diets

Effects of dietary zinc level on 65Zn absorption and its movement in the intestinal tract were studied in calves fed zinc-deficient (5 ppm Zn) and control (37 ppm Zn) purified diets for 2 weeks. The calves were killed at 1, 4, 8, and 24 hours after dosing via duodenal catheter. Absorption, defined as 65Zn unrecovered in intestinal contents and feces, was very rapid during the first hour for both dietary treatments. After 1 hour, absorption progressively diminished with little absorption after 8 hours. The deficient diet substantially increased 65Zn absorption. Blood 65Zn levels increased sharply during the first 0.5 hour and tended to decline from 1 to 24 hours. Liver and kidney 65Zn values reflected absorption and in conjunction with blood data indicated that 65Zn, following removal from the intestinal contents, was rapidly transferred to the blood and transported to body tissues. Passage of 65Zn down the small intestine was rapid and substantially faster for control than for deficient-fed calves. In controls at 4 hours, most of the unabsorbed 65Zn was beyond the small intestine. Relating intestinal movement data to 65Zn absorption suggested that little absorption occured in the cecum or beyond.

Influence of Dietary Phosphorus and Zinc Levels on Whole Body Mineral, Liver Mineral, and Liver Vitamin-C Contents of Fingerling Rainbow Trout, &lt;I&gt;Oncorhynchus mykiss&lt;/I&gt;

A laboratory based 2 × 2 factorial experiment was conducted to investigate the influence of dietary phosphorus and zinc levels on whole body mineral, liver mineral, and liver vitamin-C contents of fingerling rainbow trout for 21 weeks. Two levels of phosphorus (19 and 30 mg g-1) and two levels of zinc (55 and 100 μ g g-1) in the dry diets were tested. Duplicate tanks of 30 rainbow trout (average weight 1.56 ± 0.24 g) per 60L glass tank were fed experimental diets three times a day to satiation level in 15 to 24oC water temperature. The result of the present study demonstrated that dietary zinc supplementation significantly influenced the whole body zinc and liver copper contents in fingerling rainbow trout where as additional phosphorus did not show any significant difference. Zinc supplementation significantly influenced the liver vitamin-C contents of the fish. Hence it is clear that zinc supplementation is necessary in fingerling rainbow trout feed. Further studies in this area are needed broadly. Key words: Phosphorus, zinc, whole body, liver mineral, liver vitamin-C, rainbow trout DOI = 10.3329/jard.v5i1.1470 J Agric Rural Dev 5(1&amp;2), 135-142, June 2007

Zinc Requirement of Baby Pigs on Casein Diets

In 2 trials to determine their zinc requirement 27 baby pigs were fed diets in which casein supplied the protein. Casein was treated with disodium ethylenediaminetetraacetate to remove zinc and insure a subrequirement dietary level in the first trial. Since deficiency symptoms appeared in pigs on the untreated basal casein diet, in trial 1, this procedure was discontinued in trial 2. Levels of dietary zinc used were 4, 10 and 14 ppm in trial 1 and 10, 14 and 20 ppm in trial 2. All pigs receiving 10 ppm or less of dietary zinc in either trial exhibited symptoms of zinc deficiency, including parakeratotic lesions and a reduction of growth rate, food utilization, serum zinc, calcium and alkaline phosphatase levels, bone size and strength, allometric weight of thymus, tissue zinc level and zinc and calcium balance. The pigs which received 14 ppm or more of dietary zinc in either trial showed no parakeratotic lesions, and rate of growth and food utilization were normal. Pigs receiving 14 ppm of dietary zinc gave evidence of zinc repletion with serum zinc and alkaline phosphatase slowly returning to near normal values for nursing pigs of this age. Values of serum zinc and alkaline phosphatase were more readily restored to normal in pigs receiving 20 ppm of dietary zinc. Zinc retention data indicated that a dietary zinc level of between 14 and 20 ppm was required to maintain total body tissue levels similar to those of the nursing pig.

The Effects of High Levels of Dietary EDTA, Zinc or Copper on the Mineral Contents of Some Tissue of Turkey Poults

ANTAGONISTIC effect of high levels of dietary zinc on uptake of copper has been established for rats (Smith and Larson, 1946; Van Reen, 1953; Grant-Frost and Underwood, 1958; McCall and Davis, 1961; Van Campen and Scaife, 1967), chickens (Hill and Matrone, 1962), and pigs (Ritchie et al., 1963; Suttle and Mills, 1966a,b). High levels of zinc also interfere with storage of iron for rats (Cox and Harris, 1960; Magee and Matrone, 1960; Kinnamon, 1966; Settlemire and Matrone, 1967), and pigs (Cox and Hale, 1962).No definite information about the antagonism between zinc, copper and iron is available for turkey poults. A level of 30.8 mmoles ethylenediaminetetraacetic acid (EDTA) or about 2 gm. zinc per kg. of a practical type turkey starter diet caused no deleterious effects on the growth of poults. A level of 0.9 gm. copper per kg. diet caused a depression in growth of poults and this was .

65Zn and Stable Zinc Absorption, Excretion and Tissue Concentrations as Affected by Type of Diet and Level of Zinc in Normal Calves

The effects of dietary zinc level (2 vs. 38 ppm) in a purified diet and of a practical versus a purified diet with the same zinc level (38 ppm) on 65Zn metabolism were determined following a single oral dosing in 2.5- and 4.5-month-old male Holstein calves. The 12 animals were killed 14 days after 65Zn dosing and before those given the zinc-deficient diet developed any clinical indication of a deficiency. Calves fed the low zinc purified diet absorbed considerably more 65Zn, but there was little overall difference between groups fed the practical-type diet and the purified diet with added zinc. Those given the practical diet had a higher fecal endogenous 65Zn excretion the second week after dosing. Younger calves in the first experiment absorbed a much higher percentage of 65Zn from diets with adequate zinc than older ones in the later experiment. There was no difference in net 65Zn retention due to age among those given the zinc-deficient diet, suggesting that differences associated with age were not caused by reduced ability of animals to absorb zinc but rather to effects of other factors on the homeostatic control mechanism. Tissue samples from calves given the deficient diet retained much more of the administered 65Zn dose in all tissues than those given zinc-adequate diets. When results were calculated relative to net absorbed dose, the more active metabolic tissues including liver, heart, lung, kidney, spleen, testicles and digestive tract sections from calves fed the zinc-deficient diet still retained much more 65Zn than comparable tissues of the other calves: this effect was greater in the younger calves. As percentage of absorbed dose, diet did not have marked effects on 65Zn in tissues which metabolize 65Zn more slowly, including hair, scrotum, muscle and bone. Most tissues from calves fed the zinc-deficient diet contained somewhat less stable zinc than those from animals fed adequate zinc. Dry matter content of tissues was not affected by the diets.

Effects of level of dietary copper, molybdenum, sulfate and zinc on bodyweight gain, hemoglobin and liver copper storage of growing pigs.

Effects of level of dietary copper, molybdenum, sulfate and zinc on bodyweight gain, hemoglobin and liver copper storage of growing pigs.

The effect of different levels of dietary zinc and calcium upon the zinc concentration of the rat femur and incisor

Weanling rats were maintained for either 8 or 11 weeks on purified diets containing normal (0.0047%) and high (0.424%) zinc concentrations. These levels of zinc were associated with either normal (0.56%) or low (0.03%) calcium in the diet. The zinc content of the femora and of the incisor dentine and enamel was determined polarographically and the ash content of the femora and dentine was also measured. Both calcium deficiency and excessive intake of zinc significantly increased the concentration of zinc in bone and dentine while a similar trend was observed in enamel. The high zinc diets depressed the ash content of bone and raised that of dentine, this effect being more significant at the normal level of dietary calcium.

Effects of Zinc Deficiency per se and of Dietary Zinc Level on Urinary and Endogenous Fecal Excretion of 65Zn from a Single Intravenous Dose by Ruminants

Following single intravenous doses of 65Zn, rate of excretion was studied in experiments designed to separate the physiological effects of a zinc deficiency per se from those of level of dietary zinc. Fecal excretion of 65Zn was higher in normal animals fed a normal diet containing 46 ppm zinc then in comparable animals fed a zinc-deficient diet containing 6 ppm zinc. Specific activity of fecal zinc from animals fed the deficient diet was much higher, reflecting the much lower level of total fecal zinc. When fed the same diets, normal animals excreted more 65Zn in the feces than did zinc-deficient animals. However, the deficient animals excreted more 65Zn in the urine, suggesting a possible pathological effect of the deficiency on the kidneys. Level of dietary zinc per se did not affect urinary excretion in normal animals. Urinary excretion of 65Zn was highest the first day, decreased sharply the second day, and decreased gradually thereafter. Excretion of 65Zn via urine was low, with the total for 13 days being less than 0.3% of the dose. Fecal excretion was highest the second and third days after dosing and decreased gradually thereafter. Level of 65Zn in the blood declined very rapidly immediately following dosing and very slowly after the first day. These studies indicate that both a low zinc diet and a zinc deficiency per se cause reduced endogenous fecal excretion of 65Zn for at least 2 weeks after the zinc enters the blood, thus contributing to homeostasis of this element.

Zinc Toxicity in Ruminants. I. Effect of High Levels of Dietary Zinc on Gains, Feed Consumption and Feed Efficiency of Lambs

Zinc Toxicity in Ruminants. I. Effect of High Levels of Dietary Zinc on Gains, Feed Consumption and Feed Efficiency of Lambs