• Journal of Nutrition and Health
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• v.51 no.5
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• pp.379-385
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• 2018

Purpose: Zinc (Zn) is an essential trace element for bone mineralization and osteoblast function. We examined the effects of Zn deficiency on osteoblast differentiation and mineralization in MC3T3-E1 cells. Methods: Osteoblastic MC3T3-E1 cells were cultured at concentration of 1 to $15{\mu}M$ $ZnCl_2$ (Zn- or Zn+) for 5, 15 and 25 days up to the calcification period. Extracellular matrix mineralization was detected by staining Ca and P deposits using Alizarin Red and von Kossa stain respectively, and alkaline phosphatase (ALP) activity was detected by ALP staining and colorimetric method. Results: Extracellular matrix mineralization was decreased in Zn deficiency over 5, 15, and 25 days. Similarly, staining of ALP activity as the sign of an osteoblast differentiation, was also decreased by Zn deficiency over the same period. Interestingly, the gene expression of bone-related markers (ALP, PTHR; parathyroid hormone receptor, OPN; osteopontin, OC; osteocalcin and COLI; collagen type I), and bone-specific transcription factor Runx2 were downregulated by Zn deficiency for 5 or 15 days, however, this was restored at 25 days. Conclusion: Our data suggests that Zn deficiency inhibits osteoblast differentiation by retarding bone marker gene expression and also inhibits bone mineralization by decreasing Ca/P deposition as well as ALP activity.

• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.4
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• pp.574-580
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• 1994

The effect of dietary zinc(Zn) levels on cadmium (Cd)-induced hepatotoxicity was studied in serum and liver of rats. Adult male Spraque-Dawley rats were fed on diets containing one of three levels of zinc carbonate(0, 56, $560\mu\textrm{g}/kg$ diet) and Cd-treated groups were administrated oral intubation with cadmium chloride 95.0 mg/kg of body weight) at the sametime once a week. Net weight gain (NWG), feed intake (FI) and feed effciiency ratio (FER) in Zn deficiency groups significantly decreased as compared to that of control and excessive groups. Cd oral intubation caused a decrease in NWG and FI but an increase in Zn deficiency group in FER. GSH-Px, GST and catalase activity showed significant decrease in Zn deficiency and Zn excessive group. LPO content in liver significantly increased in Zn deficiency group. Cd oral intubation increased the content of LPO in Zn deficiency group as compared to control. GSH content and GST activity of hepatic tissue significantly decreased in Zn deficiency and excessive group. The activity of AST and ALT in serum were markedly increased in Zn deficiency, Zn excessive and Cd-treated groups. LDH and ALP activities significantly increased in Cd-treated group while ALP activity decreased by Zn deficiency. It was observed that the livers of rats exposed to Cd and Zn excessive group showed a marked increase of hepatic enzyme as compare to only Cd-treated in rats.

• Nutritional Sciences
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• v.5 no.4
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• pp.190-196
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• 2002

Zinc deficiency has been shown to result in poor appetite, causing anorexia. However, the role of zinc in the regulation of food intake is not well understood. In the present study, we hypothesized that zinc deficiency dysregulates circulating leptin level and leptin mRNA gene expression, and that whether these changes were occuring as a direct result of, or as a compensatory effect of zinc deficiency in rats. After an adaptation period of 4 weeks, Sprague Dawley rats were provided with three different level of zinc, as one week of a Zn-adequate (30 mg/kg) diet, then two weeks of a Zn-depletion (1 mg/kg ), and finally by two weeks of a Zn-repletion (50 mg/kg) diet. At the end of each dietary experimental period, one third of the 26 rats were killed. Zinc levels of blood subfractions (plasma, yee blood cells and mononuclear cells) and in the liver were substantially decreased, despite the fact that food intake was not substantially decreased during the Zn-depletion period. Serum leptin concentration was significantly increased during the zinc depletion period. Leptin mRNA in adipose tissue was also shown to be highly expressed during the Zn-depletion period. Presumably, increased leptin level and leptin mRNA induction during Zn-depletion conditions may be the cause of lowered appetite which is the common symptom of Zn-deficiency. In conclusion, These increases in circulating leptin levels and in leptin gene expression would be the direct result of, rather than the compensatory effect of, zinc deficiency.

• Nutrition Research and Practice
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• v.1 no.2
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• pp.113-119
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• 2007

Zn is an essential nutrient that is required in humans and animals for many physiological functions, including immune and antioxidant function, growth, and reproduction. The present study evaluated whether Zn deficiency would negatively affect bone-related enzyme, ALP, and other bone-related minerals (Ca, P and Mg) in rats. Thirty Sprague Dawley rats were assigned to one of the three different Zn dietary groups, such as Zn adequate (ZA, 35 mg/kg), pair fed (PF, 35 mg/kg), Zn deficient (ZD, 1 mg/kg) diet, and fed for 10 weeks. Food intake and body weight were measured daily and weekly, respectively. ALP was measured by spectrophotometry and mineral contents were measured by inductively coupled plasma-mass, spectrophotometer (ICP-MS). Zn deficient rats showed decreased food intake and body weight compared with Zn adequate rats (p<0.05). Zn deficiency reduced ALP activity in blood (RBC, plasma) and the tissues (liver, kidney and small intestine) (p<0.05). Also, Zn deficiency reduced mineral concentrations in rat tissues (Ca for muscle and liver, and Mg for muscle and liver) (p<0.05). The study results imply the requirement of proper Zn nurture for maintaining bone growth and formation.

• Environmental Analysis Health and Toxicology
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• v.19 no.2
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• pp.191-200
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• 2004

Zinc (Zn) is an essential element in biological process, however inadequate Zn status in general population have been recognized. To update the knowledge for Zn-cadmium (Cd) interaction, we studied the intestinal uptake and transport, and the expression of metal transporter proteins (divalent metal transporter 1, DMT1 ; metal transporter protein 1, MTP1 ; zinc transporter 1, ZnTl ; metallothionein 1 , MT1) in duodenum after Cd exposure using Zn deficient animal model. Rats were led Zn deficient (ZnD, 0.5-1.0 mgZn/kg) or Zn supplemented (ZnS, 50mg Zn/kg) diet for 4 weeks, and followed single administration of $^{109}$ CdCl$_2$orally. The body Zn flatus and tissue Cd concentration were determined at 24 hrs after Cd administration. Total body burden of Cd and Cd absorption index (AI, %) were estimated based on the tissue Cd analyzed. DMT1, MTP1, ZnTl and MT1 mRNA were analyzed by using RT-PCR method. Feeding of Zn deficient diet for 4 weeks produced a reduced body weight gain and a depletion of body Zn. Tissue Cd concentration, body burden of Cd and Cd absorption index were higher in the ZnD diet fed rats than the ZnS diet red rats. Especially, Cd concentration in the small intestine (duodenum, jejunum and ileum) and the colon of FeD diet fed rats were higher markedly than in the FeS diet group. The expression levels of DMT1, MTP1 and ZnT1 mRNA in FeD diet fed rats were similar to the FeS diet. The level of MT1 mRNA expression was significantly lower in the FeD than the FeS diet fed rats. Taken together, theses results indicate that Zn deficiency in diet induce an increased intestinal absorption and tissue retention of Cd, and down -regulate the MT1 expression in the intestine which might be play a part of role in Cd absorption and transport in mammalian. These findings suggest that deficiency of essential metal could be enhanced the toxicity of toxic, non-esstial metals through the metal-metal interaction.

• Asian-Australasian Journal of Animal Sciences
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• v.10 no.5
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• pp.471-477
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• 1997

A study detennined whether certain biochemical and physiological variables were altered during marginal Zn deficiency. Ten weaned crossbred Hereford Angus heifer calves, weighing $163{\pm}2kg$, were utilized. Five calves were fed a Zn - deficient (- Zn) brome-alfalfa hay diet containing 17 mg Zn/kg diet DM, and five calves were fed a Zn-adequate (+Zn) diet with 23 mg Zn/kg diet DM from $ZnSO_4$ added to the - Zn diet (total diet, 40 mg Zn/kg diet DM), for 32 d. At 21 d the - Zn calves had a reduction (p < .05) in feed efficiency. By 25 d, plasma Zn and alkaline phosphatase concentrations were reduced (p < .05) in the - Zn calves. Blood urea nitrogen, glucose, insulin, IGF-I, Cu plasma concentration and Zn and Cu concentrations of red blood cell (RBC) and liver were not altered (p > .05) by the - Zn diet through 25 d. In response to a single i. m. injection of dexamethasone (20 mg) on d 25, calves fed the two dietary Zn amounts showed no changes (p > .05) in plasma or RBC Zn and Cu concentrations, serum IGF-I, insulin, and glucose when measured at 6, 12, 24, 48, 72, and 96 h after injection. In response to an intradermal injection of phytohemagglutinin on d 30, cell mediated immune (CMI) response was reduced (p < .05) in the - Zn calves. These observations indicate that during a marginal Zn deficiency in calves, there was a decrease in feed efficiency, plasma Zn, serum alkaline phosphatase, and CMI response.

• Nutritional Sciences
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• v.8 no.4
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• pp.242-249
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• 2005

It is well established that zinc plays an important role in bone metabolism and mineralization. The role of zinc in bone formation is well documented in animal models, but not much reported in cell models. In the present study, we evaluated zinc deficiency effects on osteoblastic cell proliferation, alkaline phosphatase activity and expression, and extracellular matrix bone nodule formation and bone-related gene expression in osteoblastic MC3T3-E1 cells. To deplete cellular zinc, chelexed-FBS and interpermeable zinc chelator TPEN were used. MC3T3-E1 cells were cultured in zinc concentration-dependent (0-15 ${\mu}M\;ZnCl_2$) and time-dependent (0-20 days) manners. MC3T3-E1 cell proliferation by MTT assay was increased as medium zinc level increased (p<0.05). Cellular Ca level and alkaline phosphatase activity were increased as medium zinc level increased (p<0.05). Alkaline phosphatase expression, a marker of commitment to the osteoblast lineage, measured by alkaline phosphatase staining was increased as medium zinc level increased. Extracellular calcium deposits measured by von Kossa staining for nodule formation also appeared higher in Zn+(15 ${\mu}M\;ZnCl_2$) than in Zn-(0 ${\mu}M\;ZnCl_2$). Bone formation marker genes, alkaline phosphatase and osteocalcin, were also expressed higher in Zn+ than in Zn-. The current work supports the beneficial effect of zinc on bone mineralization and bone-related gene expression. The results also promote further study as to the molecular mechanism of zinc deficiency for bone formation and thus facilitate to design preventive strategies for zinc-deficient bone diseases.

• Journal of Nutrition and Health
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• v.33 no.5
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• pp.517-523
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• 2000

The effect of dietary zinc deficiency and age on lipid peroxide level was investigaed in rats. Zinc level in serum and liver were also measured. Fifty Sprague-Dawly male rats aging 8 months(older rats) and 2 months(younger rats) were used as experimental animal. Zinc deficient diet(1.1ppm) and normal zinc diet(36.5ppm) were used as experimental diets. Rats in each age group were divided into zinc deficient(ZnDF), zinc pair-fed(ZnPF) and zinc ad-libitum(ZnAL) to remove the variances of food intake. After 4 weeks of experimetal period, rats were sacrificed. Thiobarbituric acid reactive substance(TBARS) levels in plasma and liver, lipofuscin and conjugated diene levels in liver were measured as lipid peroxide index. Food intakes of all groups were not different because zinc deficiency did not reduce food intake in ZnDF group. Younger rats gained weight continuously, while older rats lost weight in the begining of experiment and regained afterwards. In older rats, serum zinc level was decreaed while plasma TBARS. level was increased in ZnDF group. In younger rats, plasma TBARS concentration was increased in dietary zinc deficient rats although serum zinc concentration was not reduced. Liver zinc concentration was significantly higher in older rats comparing to younger rats. However, there was no difference among the three dietary groups. Liver TBARS level was not different by age or dietary zinc level. However it was tended to be higher in older rats. However there was no difference by the dietary zinc level. In both age groups, ZnDF group significantly increased plasma TBARS levels, which suggested dietary zinc deficiency could increase lipid peroxidation in part. Significantly higher levels of lipofuscin and conjugated diene in older rats suggested lipid peroxidation was accelerated by aging.

• Asian-Australasian Journal of Animal Sciences
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• v.1 no.2
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• pp.89-98
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• 1988

Three experiments were conducted to determine whether cobalt (Co) or nickel (Ni) could prevent zinc (Zn) deficiency signs in pigs fed a high calcium (Ca) corn-soybean diet. The basal diet contained 1.3% Ca, .93% phytic acid and means of 34 to 48 ppm Zn. After weanling, pigs in experiment I were fed the basal diet for 9 weeks, and was found that 50 ppm Co or Ni for 5 weeks increased average daily weight gain (ADG) and reversed skin lesions toward normal. These effects were similar to those of 100 ppm supplemental Zn. The Zn content and alkaline phosphatase activity of serum from pigs supplemented with Co or Ni were higher at 2 weeks and 4 weeks (P<.05) than those of the basal group. Zn content of bone, liver and kidney, and alkaline phosphatase activity in bone were increase after 5 weeks of supplementation with Co or Ni. In experiments 2 and 3, addition of 54 ppm and 27 ppm of either Co or Ni increased (P<.05) ADG and decreased incidence of skin lesions except in one group supplemented with 27 ppm Ni. Supplemental Co or Ni increased Zn in serum and alkaline phosphatase activity in serum and bone in both experiments. Over all experiments, supplemental Co or Ni decreased Zn deficiency signs in the following order of effectiveness: 54 ppm Co, 54 ppm Ni, 27 ppm Co and 27 ppm Ni. The alleviation of signs of Zn deficiency by Co or Ni may have been the result of increased availability of dietary Zn.

• Journal of Veterinary Science
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• v.24 no.1
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• pp.3.1-3.13
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• 2023

Background: Zinc (Zn) is an essential cofactor for physiological homeostasis in the body. Zn oxide (ZnO), an inorganic compound that supplies Zn, exists in various sizes, and its bioavailability may vary depending on the size in vivo. However, comparative studies on the nutritional effects of micro-sized ZnO (M-ZnO) and nano-sized ZnO (N-ZnO) supplementation on Zn deficiency (ZnD) animal models have not been reported. Objectives: This study investigated the nutritional bioavailability of N-ZnO and M-ZnO particles in dietary-induced ZnD mice. Methods: Animals were divided into six experimental groups: normal group, ZnD control group, and four ZnO treatment groups (Nano-Low, Nano-High, Micro-Low, and MicroHigh). After ZnD induction, N-ZnO or M-ZnO was administered orally every day for 4 weeks. Results: ZnD-associated clinical signs almost disappeared 7 days after N-ZnO or M-ZnO administration. Serum Zn concentrations were higher in the Nano-High group than in the ZnD and M-ZnO groups on day 7 of ZnO treatment. In the liver and testis, Nano-Low and Nano-High groups showed significantly higher Zn concentrations than the other groups after 14-day treatment. ZnO supplementation increased Mt-1 mRNA expression in the liver and testis and Mt-2 mRNA expression in the liver. Based on hematoxylin-and-eosin staining results, N-ZnO supplementation alleviated histological damage induced by ZnD in the testis and liver. Conclusions: This study suggested that N-ZnO can be utilized faster than M-ZnO for nutritional restoration at the early stage of ZnD condition and presented Mt-1 as an indicator of Zn status in the serum, liver, and testis.