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.     

Serum copper and zinc in industrial centers in Slovakia

The association between serum copper and zinc concentrations and age, sex, and other risk factors of cardiovascular disease in randomly selected adult volunteers aged 19–59 were investigated. There was a positive relationship between copper and age in both sexes, but zinc was negatively correlated with age in males only. Serum zinc was positively related to HDL-cholesterol in males. Serum copper was positively related to total cholesterol and LDL-cholesterol but negatively correlated to HDL-cholesterol in males. A positive relationship to body mass index was observed in females only. Subjects have been divided into a control group and a group with marked risk factors of cardiovascular disease. The levels of zinc were not different, whereas the levels of copper in both males and females were significantly higher in the risk group. Our results suggested a positive relationship between serum copper and cumulation of more factors of cardiovascular disease, however, their causal effect in humans has to be investigated further.     

The longitudinal distribution of cadmium,zinc, copper,iron, and metallothionein in the small-intestinal mucosa of rats after administration of cadmium chloride

Different routes of Cd intake may influence the intestinal distribution of Cd, metallothionein (MT), and trace metals differently. Therefore, we compared the effects of parenteral and enteral administration of Cd on the distribution of trace metals and MT along the small intestine. In a first experiment three groups of rats were employed: a control, one receiving CdCl₂ within the drinking water, and another receiving sc injections of CdCl₂. In a second experiment, rats were fed three different diets with either 0, 0.3, or 1 mmol CdCl₂/kg for one and two weeks to study the time- and dose-dependent effects of orally administered Cd. Metal concentrations (Cd, Zn, Cu, Fe) were measured by atomic emission spectrometry and MT was determined by radioimmunoassay. Intestinal MT levels did not show proximodistal gradients in controls or after sc administration of Cd, but orally administered Cd increased mucosal MT levels longitudinally from the duodenum to the ileum. Cd levels paralleled those of MT. Compared with the metal concentrations in the controls, sc administration of Cd did not change intestinal Zn, Cu, and Fe levels. Oral administration of Cd, however, increased Cu and decreased Fe levels in the intestinal mucosa significantly. The second experiment revealed that only high dietary concentrations of Cd increase intestinal Cd and MT levels longitudinally toward the distal parts, whereas at lower dietary concentration the longitudinal distribution was reversed. This shows that different routes and doses of Cd intake lead to a different trace metal and MT distribution and emphasizes the role of dietary Cd in the local induction of small-intestinal MT.     

Ascorbic acid feeding of rats reduces copper absorption,causing impaired copper status and depressed biliary copper excretion

The feeding of diets enriched with ascorbic acid (10 g/kg) to rats has previously been shown to lower plasma and liver copper concentrations. The present studies corroborate this. We hypothesized that ascorbic acid initially reduces copper absorption, this effect being masked later by the stimulatory effect on copper absorption of the impaired copper status. We also hypothesized that the impaired copper status as induced by ascorbic acid feeding is followed by a diminished biliary excretion of copper in an attempt to preserve copper homeostasis. Our hypotheses are supported by the present studies. Ascorbic acid feeding initially reduced apparent copper absorption, and in the course of the experiment this effect tended to turn over into a stimulatory effect. Copper deficiency, as induced by feeding a diet containing 1 mg Cu/kg instead of 5 mg Cu/kg, systematically increased copper absorption. Biliary excretion of copper in rats given ascorbic acid was unaffected initialy but became depressed after prolonged ascorbic acid feeding. A similar time course was seen for fecal endogenous copper excretion that was calculated as the difference between true and apparent copper absorption. Copper deficiency systematically reduced biliary copper excretion and fecal endogenous copper loss.     

The effect of various dietary zinc concentrations on the biological interactions of zinc,copper, and iron in rats

Three groups (14 rats each) were fed one of the following diets for 8 wks: a control purified basal diet containing 12 ppm zinc, 5 ppm copper, and 35 ppm iron; the basal diet with less than 2 ppm zinc; or the basal diet supplemented with 1000 ppm zinc. Rats fed the zinc-deficient diet had decreased weight gain, moderate polydipsia, and intermittent mild diarrhea. The zinc-supplemented rats had a cyclical pattern of food intake and weight loss from weeks 5 to 8. Tissue concentrations suggest that zinc and copper were not mutually antagonistic with chronic dietary imbalances. If tissue element concentrations reflected intestinal uptake, then competition and/or inhibition of intestinal uptake occurred between zinc and iron. The fluctuations in tissue element concentrations that occurred with increased duration of the study were at variance with previous studies of shorter time periods. The dietary proportions of zinc, copper, and iron appear to influence zinc, copper, and iron metabolism at the intestinal and cellular transport levels over a given period of time.     

Evaluation of zinc in the regulation of serum T3 and T4 levels and hepatic functions in carbontetrachloride-intoxicated rats

Circulating tri-iodothyronine (T₃) and thyroxine (T₄) concentrations were determined after 6 wk of zinc treatment to carbontetrachloride (CCl₄) intoxicated male albino rats. Concentrations of T₃ were observed to be significantly depressed following CCl₄ treatment alone. On the contrary, no significant change was noticed in the concentrations of T₄ when compared to controls. However, zinc administration to hepatotoxic animals resulted in restoring the T₃ activity to within normal limits, thus indicating the indirect effects of zinc on the regulation of thyroid hormone concentrations. The activities of all the serum and hepatic marker enzymes were found to be significantly elevated following CCl₄ treatment. However, following zinc supplementation to these intoxicated animals, the levels of the marker enzymes decreased significantly when compared to the CCl₄-treated animals. A similar trend was seen in the case of lipid peroxidation following zinc treatment.     

Copper metabolism in analbuminaemic rats fed a high-copper diet

Copper metabolism in male Nagase analbuminaemic (NA) rats was compared with that in male Sprague Dawley (SD) rats fed purified diets containing either 5 or 100 mg Cu/kg diet. Dietary copper loading increased hepatic and kidney copper concentrations in both strains to the same extent, but baseline values were higher in the NA rats. There was no strain difference in true and apparent copper absorption nor in faecal endogenous and urinary copper excretion. NA rats had higher levels of radioactivity in kidneys at 2 hr after intraperitoneal administration of ⁶⁴Cu. As based on the distribution of added ⁶⁴Cu, about 70% of plasma copper appeared to be in the non-protein compartment in the NA rats, whereas in SD rats, it was only about 1%. It is concluded that the NA rats are able to maintain a relatively normal metabolism of copper, even after dietary copper challenge. In the NA rats, zinc concentrations in kidneys, liver and urinary zinc excretion were elevated when compared with SD rats. The high-copper diet did not affect tissue zinc concentrations and apparent zinc absorption in both strains of rats.     

Serum copper and zinc levels and copper/zinc ratio in patients with breast cancer

Serum copper, zinc levels, and the Cu/Zn ratio were evaluated in 31 patients with breast cancer and 35 healthy controls. Copper and zinc were determined by atomic absorbtion spectrophotometry. The mean serum copper level and the mean Cu/Zn ratio in patients with breast cancer were significantly higher than the control group (p<0.001 andp<0.001). In addition, the mean serum zinc level in patients with breast cancer was significantly lower than the control group (p<0.001). Neither serum copper and zinc levels nor the Cu/Zn ratio were of value in discriminating of the disease activity and severity. Interestingly, the Cu/Zn ratio in premenopausal patients was higher than postmenopausal patients (p<0.05) and this was not related to age. The further combined biological and epidemiological studies are necessary to investigate the roles of copper and zinc in breast cancer.     

Pharmacokinetics and pharmacodynamics in copper deficiency I

The effect of nutritional copper (Cu) deficiency on the antiinflammatory activity and pharmacokinetics of aspirin (ASA) was investigated in rats. Male, weanling Sprague-Dawley rats were fed either a Cu-deficient (CuD) or Cu-sufficient (CuS) diet for 49–50 d. The antiinflammatory activity of ASA was studied using the carrageenan-induced paw edema (CPE) test. ANOVA analyses of edema volumes at 2, 3, 4, 5, and 21 h postcarrageenan indicated significant differences between groups. The percent inhibition of edema due to ASA treatment in CuS was lower than that in CuD rats at 5 h, AUC_5h, and AUC_21h. ASA was found to be significantly more effective in inhibiting the CPE in CuD rats when compared to the CuS rats. Thus, we hypothesized that the increase in ASA's antiinflammatory activity in CuD rats was a result of a decrement in its elimination during nutritional Cu deficiency. The elimination of ASA in CuD and CuS rats was studied using an iv dose of 200 mg/kg. Concentrations of ASA and salicylic acid (SA) were determined in blood; whereas the concentrations of SA, salicylic phenol-glucuronide (SPG), and salicyluric acid (SUA) were determined in urine by HPLC. The results of the pharmacokinetic analyses from blood and urinary data indicated no significant differences in the disposition of ASA between CuD and CuS rats. For instance, the total body clearance for ASA (mean±SD, mL/min/kg) was 37.9±9.4 and 38.5±13.9 (p>0.05); and the volume of distribution (Vd) for ASA (mean±SD, mL/kg) was 385.5±110.3 and 397.1.1±137.9 (p>0.05) for CuD and CuS groups, respectively. Thus, contrary to our hypothesis, the enhanced antiinflammatory activity of ASA in CuD rats does not appear to be mediated via a decrement in the elimination of the drug. In addition, plasma ASA-esterase activity was found to be independent of Cu nutritional status.     

High dietary aluminum affects the response of rats to silicon deprivation

Antagonistic interactions between silicon and aluminum occur in living organisms. Thus, an experiment was performed to ascertain whether high dietary aluminum would accentuate the signs of silicon deprivation in rats and conversely whether silicon deprivation would accentuate the response to high dietary aluminum. The experiment was factorially arranged with two variables: silicon as sodium metasilicate, 0 or 40 μg/g diet, and aluminum as aluminum citrate, 0 or 500 μg/g diet. After 9 wk, body weights and plasma urea nitrogen were higher and plasma concentrations of threonine, serine, glycine, cystine, and methionine were lower in silicon-adequate than silicon-deprived rats. High dietary aluminum significantly decreased plasma phenylalanine. An interaction between aluminum and silicon affected plasma triglyceride, cholesterol, and phosphorus concentrations. High dietary aluminum decreased these variables when silicon was absent from the diet, but increased them when silicon was present. Skull iron and silicon concentrations were decreased and iron and zinc concentrations in the femur were increased by the addition of 500 μg Al/g diet. High dietary aluminum decreased tibia density in silicon-adequate rats, but increased tibial density in silicon-deprived rats. The findings indicate that in rats, high dietary aluminum can affect the response to silicon deprivation and dietary silicon can affect the response to high dietary aluminum.     

Urinary excretion of microelements in endurance-trained volunteers during restriction of muscular activity and chronic rehydration

The objective of this investigation was to determine the effect of daily intake of fluid and salt supplementation (FSS) on increased urinary losses of microelements that developed during hypokinesia (decreased number of walking steps/d). The studies were performed on 30 endurance-trained male volunteers aged 23–26 yr, with an averaged maximum oxygen uptake of 65 mL/kg/min during 364 d of hypokinesia (HK). All volunteers were divided into three equal groups: Ten volunteers were placed continuously under an average of 10,000 running steps/d (14.2 km/d) (control subjects), ten volunteers subjected continuously to HK without the use of FSS (hypokinetic subjects), and ten volunteers were continuously submitted to HK and consumed daily FSS (hyperhydrated subjects). For the simulation of the hypokinetic effect the hypokinetic and hyperhydrated volunteers were kept under an average of 3,000 walking steps/d (2.7 km/d) for 364 d. Prior to their exposure to HK the volunteers were on an average of 10,000 running steps/d (14.2 km/d). During the prehypokinetic period of 60 d and during the hypokinetic period of 364 d were determined renal excretion of microelements responses of endurance-trained volunteers. In the hyperhydrated volunteers urinary excretion of iron, zinc, copper, manganese, cobalt, nickel, lead, tin, chromium, aluminum, molybdenum, and vanadium decreased, whereas in the hypokinetic volunteers it increased significantly. It was concluded that chronic hyperhydration may be used to attenuate urinary excretion of microelements in endurance-trained volunteers during prolonged restriction of muscular activity.     

Effects of albumin and adenosine phosphates on iron transfer from ferric lactate

Ferric lactate is known to modify Ca²⁺ uptake by the cells. To enlighten the role of protein and ATP in this phenomenon, iron transfer from ferric lactate to albumin and adenosine polyphosphates was determined by electrophoresis. The order of iron affinity was ATP>ADP>AMP for the polyphosphates, and albumin does not compete for iron binding with the polyphosphates. The iron transfer to ATP was also observed in vivo by adsorption chromatography of the adenosine polyphosphates fraction from blood plasma of mice injected with ferric lactate plus ATP. In vitro iron and calcium uptake by Ehrlich ascites tumor cells showed that albumin and ATP decreased iron uptake, whereas calcium incorporation is diminished by albumin but augmented by ATP. This difference might be explained by albumin binding of ferric lactate that is inhibited from reaching cell structures, whereas ATP, known to be an inhibitor of iron polimerization, facilitates it.     

Variations in plasma zinc in older men and women

The study evaluated the biological and analytical variance in plasma zinc from 36 adults 60–88 yr of age. Blood samples were taken by finger-prick from each subject on d 1, 2, 3, 8, and 15. Days 1, 2, and 3 were selected to describe daily variation; 1, 8, and 15 were selected to describe weekly variation. Plasma Zn was analyzed by flame atomic absorption using a microinjection technique. Variation was partitioned into analytical, intraindividual, and interindividual components using analysis of variance. The interindividual variability was generally greater than the intraindividual variability. The variability for plasma zinc was about 30% and was substantially greater than reported for younger populations. This variability could not be attributed to the covariates examined, including zinc intake from food and supplements, serum albumin, and C-reactive protein. The variability would affect the accuracy of plasma zinc status based on a blood sample collected on a single day. With the microtechnique used in this study, 8 sample days would be needed to estimate plasma Zn with 95% confidence level and 20% level of accuracy.     

Trace-elements status in camels

Data relating to trace-elements status in camels is scarce, from both a clinical and biochemical point of view. Clinical deficiency or toxicity has rarely been described in this species. However, there is a some evidence that camels are sensitive to trace element disorders in the same way as other ruminants. For example, copper deficiency in camels has been reported in East Africa. Normal plasma level is comparable to cattle (70–120 mg/100 mL). Camels appear to maintain zinc levels at a lower value than other domestic ruminants (<60μg/100 mL). Iron metabolism is more active in the liver than in the spleen. Data concerning manganese levels are possibly unreliable. Some cases of selenium deficiency (white muscle disease) have been reported. No data are available for cobalt status in camels. Finally, camels appear to be more sensitive to iodine deficiency than the other domestic ruminants.     

Interaction of trace elements in a longitudinal study of human milk from full-term and preterm mothers

Concentrations of 8 trace elements (Fe, Cu, Zn, Se, Br, Pb, Rb, and Sr) at different lactation time were measured by the PIXE multi-elemental technique. Time dependence and interelement correlations were studied. A total of 200 milk samples from 32 lactating mothers were supplied from 2 to 120 d after delivery of 26 full-term and 6 preterm infants. All elements showed a lognormal frequency-distribution. The Fe, Cu, Zn, and Se contents in preterm milk were found to be somewhat different with respect to full-term milk. Cu, Zn, Se, Br, Pb, and Rb concentrations declined with lactation time, both in pre- and full-term samples. Sr and Fe contents did not show any change with time. Detailed analysis of data by partial correlation and multiple regression methods was performed. No substantial differences between preterm and full-term samples were found in the results of partial correlation analysis. Cu and Zn were found to be correlated with lactation time, whereas the measured time dependence for the other elements has to be attributed to the effect of the existing interelement correlation. All the measured elements appeared to be correlated with at least one other element. In particular, Se was inversely correlated with Zn and directly with Cu. The zinc and copper contents in milk can therefore depend on the variation in the mother selenium intake.     

Endogenous excretion and true absorption of cobalt as affected by the oral supply of cobalt

At the end of a 49-d experiment with 32 growing male rats, a period of 8 d was used to determine endogenous excretion and true absorption as well as apparent absorption and retention of cobalt with the aid of the isotope dilution technique. For this purpose, a single im dose of⁵⁸Co was applied at d 35 of the experiment. After that, urine and feces were collected separately from d 8 to 15 after injection of the isotope. The specific cobalt activity of the liver was used as an endogenous reference source. The basal diet provided 5.9 ppb cobalt, the different treatment groups were obtained by supplementing the diet with 0, 10, 50, 250, or 1250 ppb cobalt. The different diets were offered from the beginning of the experiment. In the balance period, apparent and true absorption as well as fecal excretion behaved similar to cobalt intake, whereas urinary excretion increased more rapidly with increasing cobalt supply. Endogenous fecal excretion accounted for 3.5 ng Co/d in the groups fed the diets without and with 10 ppb cobalt. An increase was not observed until supplementing the diet with 50 ppb cobalt. This increase between 250 and 1250 ppb cobalt was higher than the corresponding increase in the dietary cobalt supply. This indicates that endogenous fecal excretion might be more important for homeostatic regulation at a higher dietary cobalt concentration. Endogenous renal excretion as calculated from the results of the isotope dilution technique showed a similar kind of response to increasing cobalt supply as endogenous fecal loss. Nevertheless, the elimination of excessive cobalt mainly took place by adjusting urinary excretion, whereas the variations in true absorption and endogenous fecal excretion had no quantitative importance. Apparent and true absorption were on average 28.0 and 29.8%, respectively, of the cobalt intake. In the case of retention, a marked decline was observed from 19% in the depletion group to 3% with 1250 ppb cobalt, again demonstrating the importance of urinary excretion for controlling the cobalt content of the organism.     

Managanese stimulates the oxidative brust of differentiated HL-60 cells

Incubation with manganese results in a twofold increase in the oxidative burst of differentiated HL-60 cells. This stimulation was characterized by examining the dose response, length of incubation time, and specifity of manganese. Managese only stimulated the burst in cells induced to differentiated with retinoic acid and not in undifferentiated HL-60 cells. Incubation with manganese did not result in a greater number of differentiated cells. The maximum stimulation occurred at 0.2 μmol/L manganese. Stimulation of the oxidative burst required 96 h of incubation with manganese, since cells incubated with the same levels of manganese for the last 24 h of culture did not result in any stimulation. Magnesium, present in the incubation medium at physiological serum levels (820 μmol/L) also stimulated the oxidative burst, whereas iron (0.3 μmol/L), zinc (18 μmol/L), and copper (12 μmol/L) had no effect. To determine whether manganese and magnesium stimulated the burst differently, the initial rates of superoxide anion production was determined. The initial rate of the reaction proceeded rapidly in cells incubated with managnese, whereas there appeared to be a lag before magnesiumtreated cells produced superoxide anion. Thus, manganese seems to stimulate the oxidative burst differently than magnesium.     

Cadmium-induced alterations in ocular trace elements

The present report demonstrates, for the first time, that feeding rats 50 ppm cadmium for just 7 wk results in detectable levels of cadmium in the eye of rats. Furthermore, these ocular cadmium concentrations affect significant alterations in the levels of the essential trace elements selenium, calcium iron, and copper in the eye. Rats were fed a low-selenium (<0.02 ppm selenium), high-copper basal diet (50 ppm copper) supplemented with 0, 0.1, and 0.5 ppm selenium. The animals were either untreated or treated with 50 ppm cadmium admixed with their feed. Cadmium treatment resulted in significant reductions (up to 50%) in ocular selenium. Furthermore, rats fed the basal diet and given 100 ppm cadmium via their feed for 6 wk exhibited a 69% reduction in the activity of the selenoenzyme, glutathione peroxidase, in the eye. Cadmium treatment also resulted in reductions of up to 50% in ocular calcium, irrespective of dietary selenium supplementation. Iron levels were increased by 30% in rats fed the low-selenium diet and decreased by as much as 40% in rats fed the selenium-supplemented diets, compared to animals fed identical levels of selenium without cadmium. Ocular copper levels were significantly increased only in rats fed the low-selenium diet and treated with cadmium. Ocular zinc levels were not significantly affected by dietary cadmium or selenium.     

Studies on lipid oxidation in fish phospholipid liposomes

Fish phospholipid liposomes were prepared and used as an artificial membrane system to study factors influencing-lipid oxidation. The extent of lipid oxidation was indexed by measuring the amount of thiobarbituric acid reactive substances (TBARS) produced. Fe²⁺, Fe³⁺, and Cu²⁺ were potent prooxidants in catalysing lipid oxidation. These metal ions induced lipid oxidation in a dose dependent manner. However, Zn²⁺, Ni²⁺, and Mn²⁺ did not significantly (p>0.05) affect lipid oxidation at all the concentrations (1, 10, or 100 μM) studied. Morin, luteolin (flavonoids), butein (chalcone), tannic acid, ellagic acid (polyphenols), butylated hydroxyanisole (BHA), and butylated hydroxytoluene (BHT) (synthetic antioxidants) were potent antioxidants (producing <50% TBARS compared to control) of Fe²⁺-catalyzed lipid oxidation. Morin, luteolin, and butein possess two hydroxyl substituents, a C₄ ketone structure and a 2–3 double bond, all of which contributed to their antioxidative potential. Fe²⁺ caused some losses of polyunsaturated fatty acids (PUFA), whereas tannic acid protected the oxidation of several of the PUFA including C 16∶1 (Palmitoleic acid), C 18∶3 (Linolenic acid), C 20∶4 (Arachidonic acid), C 20∶5 (Eicosapentaenoic acid), and C 22∶6 (Docosahexaenoic acid).     

The Effect of Peripheral Administration of Zinc on Food Intake in Rats Fed Zn-adequate or Zn-deficient Diets

Zinc deficiency induces a striking reduction of food intake in animals. To elucidate the mechanisms for this effect, two studies were connectedly conducted to determine the effects of peripheral administration of zinc on food intake in rats fed the zinc-adequate or zinc-deficient diets for a 3-week period. In study 1, two groups of male Sprague-Dawley rats were provided diets made either adequate (ZA; 38.89 mg/kg) or deficient (ZD; 3.30 mg/kg) in zinc. In study 2, after feeding for 3 weeks, both ZA and ZD groups received intraperitoneal (IP) injection of zinc solution with three levels (0.5, 1.0, and 2.0 mug zinc/g body weight, respectively) and cumulative food intake at 0.5, 1, 2, 4, and 24 h, and plasma hormones concentrations were measured. The results in study 1 showed rats fed the ZD diets revealed symptoms of zinc deficiency, such as sparse and coarse hair, poor appetite, susceptibility to surroundings, lethargy, and small movements. Zinc concentrations in serum, femur, and skeletal muscle of rats fed the ZD diets declined by 26.58% (P < 0.01), 27.32% (P < 0.01), and 24.22% (P < 0.05), respectively, as compared with ZA control group. These findings demonstrated that rat models with zinc deficiency and zinc adequacy had been fully established. The results in study 2 showed that IP administration of zinc in both ZA and ZD rats did not influence food intake at each time points (P > 0.05), although zinc deficiency suppressed food intake. Plasma neuropeptide Y (NPY) was higher, but insulin and glucagon were lower in response to zinc deficiency or zinc administration by contrast with their respective controls (P < 0.05). Leptin, T3, and T4 concentrations were uniformly decreased (P < 0.05) in rats fed the ZD diets in contrast to ZA diets; however, no differences (P > 0.05) were observed during zinc injection. Calcitonin gene-related peptide was unaffected (P > 0.05) by either zinc deficiency or zinc administration. The present studies suggested that zinc administration did not affect short-term food intake in rats even in the zinc-deficient ones; the reduced food intake induced by zinc deficiency was fprobably associated with the depression in thyroid hormones. The results also indicated that NPY and insulin varied conversely during the control of food intake.