Changes in serum leptin levels in strenuous exercise and its relation to zinc deficiency in rats

This study aimed to investigate the possible changes in serum leptin concentration caused by acute exercise and the effects of zinc deficiency on these changes. Forty male rats were divided into control-control, control-elercise, zinc-deficient-control, and zinc-deficient-exercise groups (10 rats in each). Control-exercise and zinc-deficient-exercise groups performed exercisse at 6 m/min speed on a rodent treadmill for 60 min or until exhaustion. All rats were decapitated 48h after the exercise, and blood samples were collected to determine serum leptin and zinc levels. Serum leptin levels in the zinc-deficient-control group were lower than in the control-control group. The mean exercise time of control-exercise group was significantly longer than the zinc-deficient-exercise group. We conclude that serum leptin levels significantly decrease both 48 h after strenuous exercise and in the zinc-deficient rats, and there is a further decrease in leptin levels when rats fed on a zinc-deficient diet performed exercise.     

Daily zinc supplementation effect on zinc deficiency in rats during prolonged restriction of motor activity

The objective of this investigation was to evaluate the effect of 47 mg zinc supplementation on deficiency of zinc in rats during 98 d of restriction of motor activity (hypokinesia), which appeared by higher plasma zinc concentration. One Hundred 13-week-old Sprague-Dawley male rats weighing 360–390 g were used to perform the studies: They were equally divided into four groups: 1. Unsupplemented control animals (UCA); 2. Unsupplemented hypokinetic animals (UHA); 3. Supplemented control animals (SCA); and 4. Supplemented hypokinetic animals (SHA). For the simulation of the effect of hypokinesia (HK), the UHA and SHA were kept in small individual cages made of wood, which restricted their movements in all directions without hindering food and water intake. The SCA and SHA received daily with their food an additional amount of zinc. Before and during the experimental period of 98 d, plasma, urinary and fecal zinc, balance of zinc, food intake, and body weight were determined at different intervals. In the SHA and UHA, the concentration of zinc in plasma, and the elimination of zinc in urine and feces increased significantly when compared with the SCA and UCA, whereas the balance of zinc was negative. The body weight and food intake decreased significantly in the SHA and UHA when compared with the SCA and UCA. The increased plasma concentration of zinc in both the SHA and UHA groups was in contrast to the observed hypozincnemia during prolonged immobilization as during prolonged hospitalization. This reaction suggests that there may be some other mechanisms that are affecting the process of control and regulation of zinc metabolism during prolonged HK. It was concluded that exposure to prolonged restriction of motor activity of rats induces significant increases in plasma concentration, fecal and urinary elimination of zinc in the presence of negative zinc balance and regardless the daily intake of large amounts of zinc with their food, leading to zinc deficiency.     

Effect of zinc deficiency and supplementation on lipid peroxidation of renal tissue in ovariectomized rats

The aim of this study was to investigate how zinc deficiency and supplementation affects lipid peroxidation in the renal tissue in ovariectomized rats. Four study groups were formed with 10 Spraque-Dawley rats each. Two of the groups served as normal and ovariectomized controls; the other two were ovariectomized rats that were zinc deficient and zinc supplemented, respectively. The zinc-deficient ovariectomized rats showed greater renal and plasma lipid peroxidation, as indicated by higher malondialdehyde levels than all other groups (p<0.05). These values were higher in the ovariectomized controls than those of the normal controls and of the ovariectomized, zinc-supplemented groups (p<0.05), which, in, turn, showed no significant differences of their respective renal and plasma malondialdehyde values. The renal and erythrocyte glutathione levels in the zinc-supplemented rats were higher than those in all other groups (p<0.05). The zinc-deficient group had the lowest renal and erythrocyte glutathione levels (p<0.05). The renal tissue zinc levels in the ovariectomized rats were higher than those in the zinc-deficient animals, but lower than in the normal controls and zincsupplemented rats (p<0.05). The zinc-supplemented animals had the highest renal tissue zinc levels (p<0.05). The results of this study suggest that zinc deficiency increases renal tissue damage in ovariectomized rats and that zinc supplementation can be used to prevent this condition.     

Effects of zinc deficiency and supplementation on malondialdehyde and glutathione levels in blood and tissues of rats performing swimming exercise

The aim of the study was to investigate the effects of zinc deficiency and supplementation on lipid peroxidation and glutathione levels in blood and in some tissues of rats performing swimming exercise. Forty adult male Sprague-Dawley rats were divided into four groups: group 1, zinc-deficient consisted of swimming rats; group 2 consisted of zinc-supplemented swimming rats; groups 3 and 4 were the swimming and nonswimming controls, respectively. The levels of malondialdehyde and glutathione were measured after 4 wk of zinc-deficient or zinc-supplemented diet and 30 min of swimming exercise daily. The erythrocyte glutathione levels of groups 2 and 4 were significantly higher than those of groups 1 and 3 (p<0.01). The plasma malondialdehyde level of group 1 was significantly higher than all other groups. The glutathione levels in liver, kidney, striated muscle, and testes of group 2 were higher than in the other groups (p<0.01) and higher in kidney and striated muscle of group 3 than in groups 1 and 4 (p<0.01). The tissue malondialdehyde levels of striated muscle, liver, kidney, and testes of group 1 were significantly higher than for all other groups (p<0.01). Our findings suggest that both swimming exercise and zinc deficiency result in an increase of lipid peroxidation in tissues and that zinc supplementation prevents these alterations by the activation of the antioxidant system.     

Blood levels of copper, iron, zinc, and lead in adults in India and Pakistan and the effect of oral zinc supplementation for six weeks

Deficiency in the intake of trace elements, such as copper (Cu), iron (Fe), selenium (Se), and zinc (Zn), is very common in the general population of most developing countries. A preliminary study in India and Pakistan showing the plasma levels of Zn and Fe indicates that approx 50% of the subjects who participated have low levels of both Fe and Zn, suggesting a marginal deficiency. The low plasma levels of these elements are more pronounced in females. The mean levels of Ze, Cu, and Fe in the plasma of 83 subjects were 0.71 ± 0.11, 0.96 ± 0.10, and 0.80 ± 0.12 mg/L, respectively. The Cu:Zn ratio in the plasma was 1.43 ± 0.16. Three groups of 15 subjects each were given three different levels of oral supplements of Zn (15, 30, and 45 mg of Zn as Zn gluconate) for 6 wk, and blood samples were analyzed during various intervals. Plasma concentration of Zn increased significantly (p < 0.001) in all the groups after 4 wk of supplementation and reached almost normal levels after 6 wk. Along with the increase in Zn, there was a significant decrease(p < 0.001) in plasma Cu levels. There were no changes in the concentration of Fe during the supplementation period. The supplementation was well tolerated by most subjects. The results of this pilot study indicate that Zn supplementation is a practical possibility comparable to that of Fe supplementation in order to prevent marginal Zn deficiency in vulnerable groups in the general population of developing countries.     

Effects of zinc supplementation on serum zinc and leptin levels,BMI, and body composition in hemodialysis patients

ProjectThe aim of this study was to determine the effects of zinc supplementation on serum zinc and leptin levels as well as on anthropometric status and some biochemical parameters in hemodialysis (HD) patients.ProcedureIn this randomized, double-blind, and placebo-controlled trial, sixty HD patients were randomly divided into groups to receive a daily supplement of 100 mg elemental Zn (supplemented group) or placebo (control group) for 60 days. Anthropometric measurements were taken using standard calibrated instruments. Serum zinc and leptin levels were determined by atomic absorption and ELISA method respectively before and after intervention.ResultsZinc supplementation resulted in significant increase in the mean serum zinc level in the experimental group while changes observed in the placebo group were not significant. The mean serum leptin in women part of the experimental group was decreased significantly after supplementation. After adjusting for age, BMI, body fat (%), serum zinc and dietary Zn intake, a negative and significant association was observed between serum zinc and leptin levels in all subjects (β = −0.33, P = 0.03) as a result of Zn supplementation.ConclusionsMore studies are needed to clarify the mechanisms by which serum leptin level is influenced as a result of zinc supplementation in HD patients.     

Both zinc deficiency and supplementation affect plasma melatonin levels in rats

At physiological levels, zinc and various hormones affect each other reciprocally. Reduction in zinc levels in pinealectomized rats suggests the relation between zinc and melatonin. The effect of both zinc deficiency and supplementation on plasma melatonin levels in rats were investigated in this study. The study was done in Sel?uk University, Experimental Medicine Research and Application Center. Twenty-four adult male Sprague Dawley rats were divided into 3 groups. Eight rats were fed with zinc-deficient diet. Zinc supplementation was administered intaperitoneally to 8 rats. The remaining 8 rats were used as controls. All rats sacrificed 3 weeks later. Plasma melatonin and zinc levels were determined. The plasma zinc levels of the zinc-supplemented group were higher than those of the other groups as expected (P<0.01). Similarly, the melatonin levels in the zinc-supplemented group were higher than those in the other groups. A significant decrease was observed in melatonin levels of the zinc-deficient group compared to the control and zinc-supplemented group (P<0.01). The results of this study suggest that zinc deficiency decreases the melatonin levels and zinc supplementation may increase the plasma melatonin levels in rats.     

Effects of zinc and/or iron deficiency on rectal temperature in rats

O'Dell et al. reported that rectal temperature was decreased by zinc deficiency in rats. However, it is not known whether a combined deficiency of zinc and iron affects rectal temperature. Forty 4-wk-old male Sprague-Dawley rats were assigned into four dietary treatment groups of 10 rats each for the 4-wk study: zinc-deficient group (4.5 mg Zn and 35 mg Fe/kg diet; −Zn), iron-deficient group (30 mg Zn/kg diet, no supplemental iron; −Fe), zinc/iron-deficient group (4.5 mg Zn/kg diet, no supplemental iron; −Zn−Fe), and control group (AIN-93G; Cont). At d 24–27, the rectal temperature was determined. The rectal temperature of the −Zn group was significantly lower than the Cont group. The rectal temperature of the −Zn−Fe group was similar to that of the Cont group, although thyroid-stimulating hormone and total thyroxin concentrations were the lowest in the −Zn−Fe group among all groups. The pattern of the plasma nitrate/nitrite concentrations across groups was similar to rectal temperature. Although observation of the rectal temperature is not conclusive, the balance between zinc and iron intake seems to determine the body temperature set point. These results suggest that the thermogenic effect of thyroid hormones is not throught to influence the paradoxical maintenance of rectal temperature in combined deficiency of zinc and iron.     

Effects of zinc deficiency on the fatty acid composition and metabolism in rats fed a fat-free diet

The effects of dietary zinc deficiency (ZD) on the composition and metabolism of the fatty acyl chains of phospholipids in rat liver were investigated with a fat-free diet. The levels of (n−9) fatty acids such as 18∶1 and 20∶3(n−9) in liver phospholipids (PL) were significantly lower in ZD-rats (19.4% and 5.4%, respectively) than in PF-rats (25.2 and 8.3%). On the other hand, the level of (n−6) acids such as 18∶2 and 20∶4 were higher in ZD-rats (3.3 and 19.1%, respectively) than in PF-rats (2.1 and 14.9%). In order to study the metabolism of fatty acids in vivo,¹⁴C-18∶0 or¹⁴C-18∶2 was intravenously injected, and then the conversion to the respective metabolite was examined. After the injection of¹⁴C-18∶0, the radioactivity was found in 18∶0 (49.3% of the total), 18∶1 (33.2%), and 20∶3 (n−9) (9.1%) in liver PL in PF-rats at 24h. In ZD-rats, the radioactivity was dramatically lower in 18∶1 (23.5%) and 20∶ (n−9) (3.6%), suggesting that the conversion of 18∶0 to 18∶1 and 20∶3 (n−9) was strongly inhibited in ZD-rats. When¹⁴C-18∶2 was injected, the radioactivity was mainly found in 18∶2, 20∶3(n−6), and 20∶4. The radioactivity in 20∶4 in ZD-rats was slightly higher than that in control rats. These results indicate that zinc deficiency affects the fatty acid metabolism in liver, in particular, it causes a reduction in δ9 desaturase activity, when rats are fed a fat-free diet.     

Effects of zinc supplementation in patients with type 1 diabetes

The purpose of this study was to identify the effect of oral zinc supplementation in patients with type 1 diabetes (T1DM) on metabolic control and zinc blood concentrations. The sample consisted of 20 patients with T1DM and a control group (n=17). Metabolic control was evaluated by glycemia at fast, 24 h glycosuria, and HbA1c. Zinc concentrations were measured in plasma and erythrocytes. After the first collection of biological material, oral zinc supplementation was initiated and continued for 4 mo in T1MD patients (T1). Daily dosages were established based on Dietary Recommended Intakes (DRIs), considering zinc intake based on data from other studies previously performed with this population. All analyses were repeated after supplementation (T2). Metabolic control was unsatisfactory, with an HbA1c increase at T2. There was no difference in zinc concentrations in plasma and erythrocytes between patients with T1DM and control. Zinc concentrations in plasma were within the normal range in T1MD before and after supplementation and the control. Zinc concentrations in erythrocyte presented lower than normal values for all groups. A zinc increase in erythrocyte after supplementation was observed in T1DM patients, although without statistical significance. More studies are needed to confirm oral zinc supplementation as nutritional management in diabetes.     

Dietary phytate,zinc and hidden zinc deficiency

Epidemiological data suggest at least one in five humans are at risk of zinc deficiency. This is in large part because the phytate in cereals and legumes has not been removed during food preparation. Phytate, a potent indigestible ligand for zinc prevents it's absorption. Without knowledge of the frequency of consumption of foods rich in phytate, and foods rich in bioavailable zinc, the recognition of zinc deficiency early in the illness may be difficult. Plasma zinc is insensitive to early zinc deficiency. Serum ferritin concentration ≤ 20 μg/L is a potential indirect biomarker. Early effects of zinc deficiency are chemical, functional and may be “hidden”. The clinical problem is illustrated by 2 studies that involved US Mexican-American children, and US premenopausal women. The children were consuming home diets that included traditional foods high in phytate. The premenopausal women were not eating red meat on a regular basis, and their consumption of phytate was mainly from bran breakfast cereals. In both studies the presence of zinc deficiency was proven by functional responses to controlled zinc treatment. In the children lean-mass, reasoning, and immunity were significantly affected. In the women memory, reasoning, and eye-hand coordination were significantly affected. A screening self-administered food frequency questionnaire for office might help caregiver's identify patients at risk of zinc deficiency.     

Relationship between plasma leptin and zinc levels and the effect of insulin and oxidative stress on leptin levels in obese diabetic patients

Leptin is thought to be a lipostatic signal that contributes to body weight regulation. Zinc plays an important role in appetite regulation also. Our aim is to evaluate the relationship between leptin and zinc in obese and nonobese type 2 diabetic patients and its relationship with oxidative stress and insulin. We studied 25 nonobese nondiabetic women (controls); 35 nonobese diabetic women; and 45 obese diabetic women. Plasma leptin concentration was determined by immunoradiometric assay. Thiobarbituric acid reactive substances (TBARS), markers of oxidative stress, were assayed by the spectrofotometric method. Plasma levels of zinc and insulin were measured by atomic absorption spectrophotometer and electrochemiluminescence methods, respectively. We found that nonobese diabetic patients had significantly lower zinc and higher TBARS levels than control subjects (P<0.01). There was no difference in plasma leptin levels between nonobese diabetic subjects and controls. Obese diabetic subjects had significantly higher plasma leptin, TBARS, and insulin levels and significantly lower plasma zinc levels than nonobese diabetic subjects (for each comparison; P<0.01). The univariate and multivariate analyses demonstrated a significant positive correlation between leptin and body mass index (P<0.01) and insulin (P<0.01), and a significant negative correlation between leptin and zinc in obese subjects. Additionally, TBARS levels was positive correlated with insulin and negative correlated with zinc in obese diabetic subjects. We conclude that zinc may be a mediator of the effects of leptin, although the detailed mechanism is still unknown and requires further investigation. Free radical induced mechanism(s) may be involved in this process.     

The effect of zinc deficiency on the body composition of rats

Body composition and the levels of some plasma metabolites were measured in zinc deficient and control rats with the aim of assessing the nature of the metabolic defects resulting from zinc deficiency. Two experiments, lasting 15 and 20 d, were carried out using 52 immature rats. Zinc deficient animals were fed a diet of 1–2 mg Zn/kg. Pair fed andad libitum control rats received the same diet with 100 ppm zinc added to the drinking water. Feed intake and growth rate were measured, and the carcasses were analyzed for protein, fat, and ash. In each experiment, a group of rats were killed on d 1 to provide pretreatment values and to allow for estimates of net deposition of carcass components. Lactate, urea, and zinc were assayed in plasma, as well as zinc concentration in carcasses and liver. The main effect of zinc deficiency was to reduce feed intake and efficiency of feed conversion, resulting in a reduced proportion of carcass wat because of the reduced feed efficiency, zinc deficiencyper se resulted in an increase in the proportion of fat in the carcass. Plasma lactate concentration was unchanged, but urea concentration increased in both pair fed and zinc deficient rats relative toad libitum fed control animals. The results indicate that a defect in protein synthesis and an increase in energy expenditure, perhaps resulting from increased protein turnover, underlies the reduced growth and efficiency of feed conversion of zinc deficiency.     

Testosterone and zinc supplementation in castrated rats: Effects on plasma leptin levels and relation with LH, FSH and testosterone

The present study aims to examine how zinc and testosterone supplementation, in combination and separately, affect plasma LH, FSH and leptin levels in castrated rats. Eighty experimental animals used in the study were allocated to 8 groups, each containing an equal number of rats. Group 1, control group; Group 2, castration group; Group 3, testosterone group (5 mg/kg/day); Group 4, zinc-supplemented group (3 mg/kg/day); Group 5, testosterone and zinc-supplemented group; Group 6, zinc-supplemented castration group; Group 7, testosterone and castration group; and Group 8, zinc-supplemented, testosterone and castration group. Plasma zinc, leptin, LH, FSH and free and total testosterone levels were determined in the blood samples collected from the animals by decapitation. Group 2 had the highest leptin levels and together with group 6, it also showed the highest LH and FSH levels (p<0.01). The lowest leptin levels were observed in groups 3 and 7 (p<0.01). Leptin levels in groups 4 and 6 were higher than those in groups 1, 5 and 8 (p<0.01). LH levels in group 4 were lower than those in groups 2 and 6 and higher than those in all other groups (p<0.01). Free and total testosterone levels in groups 7 and 8 were lower than those in groups 3 and 5, but higher than those in all other groups (p<0.01). Plasma LH levels may be more effective than testosterone on plasma leptin and zinc may be an important mediator of the effect LH has on leptin.     

Effects of zinc supplementation to ration on some hematological parameters in broiler chicks

The aim of the study was to examine the effects of zinc supplementation on some hematological parameters. Sixty newborn male broiler chicks were utilized in the study. Zinc (Zn) was added into drinking water at levels of 0, 125, 500, and 1000 mg/kg. In the study, there was no significant difference between control and Zn-supplemented groups in erythrocyte count, hemoglobin amount, hematocrit levels, total leukocyte count, and differential leukocyte % levels, but the α-naphthyl acetate esterase ANAE(+) lymphocyte rate significantly (p<0.05) increased in the 125-ppm Zn-supplemented group compared with the control group. In conclusion, the data obtained may be beneficial in demonstrating the effects of zinc on, at least, these parameters.     

Effects of zinc deficiency and pinealectomy on cellular immunity in rats infected with Toxoplasma gondii

The effects of zinc and/or melatonin deficiencies on cellular immunity were investigated in rats infected with Toxoplasma gondii. A total of 50 adult male Sprague-Dawley rats were divided into 5 groups of 10 rats each. In group I, the rats were infected with T. gondii and fed a zinc-deficient diet; in group II, the rats were infected and their pineal gland was surgically removed. Group III included rats that were infected, pinealectomized, and fed a zinc-deficient diet. Group IV consisted of T. gondii-infested rats that received no treatment of any kind, and group V were normal controls. After 3 wk of treatment, all rats were sacrificed and the percentages of CD3, CD4, and CD8 lymphocytes, zinc, and melatonin levels in plasma and the percentage of lymphocyte in blood smears were analyzed. The CD3 ratios of groups I–III were significantly lower than those of groups IV and V (p<0.01). The CD4 lymphocytes were significantly higher in group IV than that in all other groups (p<0.05). In group IV, the CD8 lymphocytes were higher than in groups I–III (p<0.01) and those in group V were higher than for groups I and III (p<0.01). Lymphocyte incidence in group IV was higher than in the other four groups (p<0.01). The plasma zinc and plasma melatonin levels in groups I–III were significantly lower than those in the controls (p<0.01, both cases). These results suggest that zinc and/or melatonin deficiency have a negative influence on cellular immunity in rats with toxoplasmosis.     

Soil-sodicity-induced zinc deficiency in maize

Summary Maize (Zea mays L. cv. Ganga-2) plants were grown in pot culture on a loamy alluvial soil of Lucknow district (India) alkalinized to graded levels of ESP (Exchangeable Sodium Percentage) ranging from 15.5 to 55.3. Before sowing maize seeds the soil was fertilised with NPK, Fe, Mn and Cu. At and above ESP 34 Zn-deficiency symptoms first appeared at 30 days. The symptoms gradually became pronounced with increase in age and at 60 days they were found even at ESP 15.5. The severity of symptoms was related to increase in sodicity. Alkalinization of soils depressed available soil Zn and tissue Zn and increased tissue ratios of Na/Zn and P/Zn. It also decreased the total plant content of Zn, Fe, Mn, Cu and even Na. Increase in soil sodicity increased both tissue concentration and total content of P in plants upto ESP 34 beyond which it decreased it. Among different extractants, 0.1N HCl, DTPA pH 7.3 and EDTA-(NH₄)₂ CO₃ pH 8.6, for measuring available soil Zn the latter showed best correlations with soil ESP (−), tissue P (−), P/Zn ratio (−), dry matter yield (+) and tissue Zn (+). Tissue Zn was related to yield (+), tissue Na (−) and soil ESP (−). Mild, moderate, severe and very severe Zn deficiency in maize was induced by soil ESP levels, 18, 25, 33 and 45, respectively.     

Effect of zinc deficiency and zinc supplementation on adrenals,plasma steroids and thymus in rats

Weanling rats were given diets deficient in or supplemented with zinc. Within a few weeks there were increases in the weight of the adrenal glands and in the concentration of cholesterol and 11-hydroxycorticosteroids in the adrenal glands of the zinc deficient animals. The decrease in cholesterol concentration due to ACTH administration was greater in zinc-deficient than in supplemented rats. After four weeks on the zinc-deficient diet rats had smaller thymus glands than zinc-supplemented rats but zinc-deficient diets had no such effect on adrenalectomised rats. The addition of 2 mg zinc/ml drinking water had no effect on adrenal weight or thymus weight but increased plasma 11-hydroxysteroids after 30 days. The possible connection between zinc intake and resistance to injury and disease is discussed.     

Effects of zinc and melatonin deficiency on testicular tissue of rats

The present study was designed to investigate the effects of zinc and/or melatonin deficiency on rat testes. A total of 24 adult male Sprague-Dawley rats were used in this study. The rats were divided into four groups of six rats each, as follows: (I) controls, (II) zinc deficient, (III) pinealectomized, zinc normal, and (IV) pinealectomized, zinc deficient. The plasma zinc levels in the control group were higher than in all the other groups (p<0.01), and those of the zinc-deficient groups II and IV were significantly lower than for group III (p<0.01). The melatonin levels in the controls were also significantly higher than for all other groups (p<0.01) There was no significant difference in sperm production between the controls and the group of animals that had no epiphysis. A significant suppression was observed in the spermatogenetic activity of the zinc-deficient groups (p<0.01). The suppression was higher in group II than in group IV. These results indicate that testicular damage caused by zinc deficiency may be reduced by melatonin deficiency.