• Korean Journal of Community Nutrition
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• v.5 no.2
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• pp.152-160
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• 2000

The purpose of this study was to investigate zinc and copper metabolism and risk factors of chronic diseases in 20 normal adults women. The daily intake, excretions in urine and feces, and serum levels of zinc and copper were determined by 24-hr food records and chemical analysis. The results were summarized as follows. mean age, body weight and BMI were 22.88 years, 54.65kg and 21.28kg/$m^2$ respectively. Mean daily intakes of energy and protein were 1578.84㎉(79% of RDA) and 52.05g (87% of RDA). The zinc and copper intake, excrestion in urine and feces were 7093.23$\mu\textrm{g}$(59% of RDA/2093.87$\mu\textrm{g}$, 203.50$\mu\textrm{g}$/39.87$\mu\textrm{g}$ and 3416.41$\mu\textrm{g}$/857.62$\mu\textrm{g}$, respectively. The serum levels of fasting glucose, insulin, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglyceride, zinc and copper were 76.60mg/㎗, 15.66IU/㎗, 160.30mg/㎗, 50.95mg/㎗, 89.80mg/㎗, 89.79mg/㎗, 95.65$\mu\textrm{g}$/㎗ and 73.28$\mu\textrm{g}$/㎗ respectively. Dietary ratio of Zn to Cu was shown to have significant positive correlations with serum insulin, total cholesterol, LDL-cholesterol. The urinary ratio of Zn to Cu was shown to have significant positive correlations with triglyceride. The serum copper level was shown to have significant negative correlations with serum total cholesterol and LDL-cholesterol. In summary, Zn consumption of adult women in their normal diet does not meet the Zn requirement for Koreans. Also, intakes of Zn and Cu may effect the glucose metabolism and cardiovascular diseases. Therefore, to increase the Zn intake and to maintain an appropriate intake ratio of Zn to Cu, nutrition education needs to be implemented.

• 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.

• Journal of the Korean Society of Food Science and Nutrition
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• v.19 no.5
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• pp.411-417
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• 1990

To compare the dietary and urinary minerals with serum lipid and minerals this study was carried out on 30 rural housewives in Kyunggi area. Mean intake of energy was 1770.3Kcal and protein 55.5g per day. Mineral intakes per day were measured; sodium 4330mg phos-phorus 485.7mg calcium 388.0mg zinc 8.99mg and copper 2.23mg Urinary minerals were analy-sed ; sodium 4379mg phosphorum 371.3mg calcium 190.0mg zinc 328.0mg and copper 49.6mg. Serum contents of lipid and minerals were : cholesterol 169.0mg% triglyceride 70.6mg% $\beta$-lipoprotein 304.9mg% sodium 142.3mM phosphorus 3.94mg% calcium 9.06mg% zinc 1215.7 ppb and cooper 620.0ppb. Eietary sodium and zinc urinary copper were significantly related with serum lipids.

• Journal of Preventive Medicine and Public Health
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• v.31 no.2 s.61
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• pp.265-274
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• 1998

To investigate the change of nitric oxide(NO), copper, and zinc in serum on smoking and alcohol ingestion in young adults, this study was performed in a cross-sectional study in 127 healthy men in Korea who had HBsAg(-), HCVAb(-), and no symptomatic liver, heart, gastrointestinal, chronic diseases, and inflammatory sign(lower than 10,000 white blood cell count in CBC). At the men's entry into the study, blood samples were drawn from each subject and immediately centrifuged for analysis of NO, copper, and zinc. Each man completed a questionnaire that provided information on smoking, alcohol intake and present and past medical history NO was analyzed by HPLC(Green et al., 1982), copper and zinc by atomic absorption spectrophotometer with air-acetylene flame and total cholesterol(TC) by Spectrum EPX. Smoking(number of cigarettes per day and pack-year) and alcohol intake was grouped fertile. Copper was adjusted for age and zinc and for age and TC. NO, copper, and zinc on smoking and alcohol ingestion were analyzed in general linear models, respectively. NO, copper and zinc in serum did not show statistical differences between non-smoking and high-smoking group and no-alcohol intake and high-alcohol intake group. This study suggested that copper, zinc, and NO was not. good biological marker for early effect by smoking and alcohol intake in young adults. However, selection bias should be considered in evaluation of this result. A large prospective study will be needed in advance on usefulness of copper, zinc, and NO as a marker for risk factors and early change of atherosclerosis.

• Biotechnology and Bioprocess Engineering:BBE
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• v.5 no.1
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• pp.40-43
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• 2000

Pyrrolidinedithiocarbamate (PDTC) and N-Acetylcysteine (NAC) are metal and nonmetal-chelating antioxidant which can induce rat and human smooth muscle cell death. When the smooth muscle cells from mouse aorta (MASMC) that we successfully cultured recently was exposed to PDTC and NAC in a normal serum state, the cells were induced to death by these compounds. However, PDTC did not induce the cell death in a serum depleted medium. This data suggests that certain factors in the serum may mediate the cytotoxic effect of PDTC. The metal chelator, Ca-EDTA blocked PDTC-induced cell death, but Cu-, Fe-, and Zn-EDTA did not block the PDTC-induced cell death. This data indicated that copper, iron, and zinc in the serum may lead to the cytotoxic effect of PDTC. Investigation of the intracellular zinc level in PDTC-induced smooth muscle cell death using the zinc probe dye N-(6-methoxy-8-quinolyl)-p-toluenesulfonamide shows that only the muscle-containing layers of the arteries have higher level of zinc. As expected, PDTC increased the intracellular fluorescence level of the zinc. In agreement with these results, the addition of an exogenous metal, zinc, induced the vascular aortic smooth muscle cell death which led to an increased intracellular zinc level. We concluded that PDTC induced mouse aortic smooth muscle cell death required not only zinc level but also intracellular copper and iron level. The mechanism of this antioxidant to induce vascular smooth muscle cell death may provide a new strategy to prevent their proliferation in arteriosclerotic lesions.

• Biotechnology and Bioprocess Engineering:BBE
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• v.5 no.1
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• pp.44-47
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• 2000

Cell growth and DNA synthesis were studied from a cultured early- and late- pas- sage mouse aorta smooth muscle cell (MASMC) because the proliferation of vascular smooth muscle cell (VSMC) is a key factor in development of atherosclerosis. In this study, the cells were cultured in fetal bovine serum (FBS) and stimulated by growth factors such as thrombin and platelet-derived growth factor-BB (PDGF-BB). Compared to the number of early-passage MASMC (passage 3 to 9) the number of late-passage MASMC (passage 30 to 40) in a normal serum state was increased 2 fold at Day 1, 3 and 6 in culture, respectively. Incorporation of $[^3H]$ thymidine into DNA induced by serum, PDGF and thrombin in late-passage MASMC was greater than those in early-passage MASMC. We also examined whether intracellular zinc levels would be an aging factor or not. The intracellular zinc level in early- and late-passage MASMC was monitored by using the zinc probe dye N-(6-methoxy-8-quinolyl)-p-toluenesulfonamide. It is interested that late-passage MASMC increased the intracellular fluorescence level of zinc, more than the early passage MASMC did. The alterations of intracellular zinc level occur concurrently with changes in MASMC proliferation rate during aging. This data suggest that the age-associated changes in zinc concentrations may provide a new in vitro model for the study of smooth muscle cell differentiation.

• Nutrition Research and Practice
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• v.6 no.3
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• pp.221-225
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• 2012

Zinc deficiency is known to be associated with insulin resistance in obese individuals. This study was performed to evaluate the effect of zinc supplementation on insulin resistance and metabolic risk factors in obese Korean women. Forty obese women (body mass index (BMI) ${\geq}25kg/m^2$) aged 19-28 years were recruited for this study. Twenty women of the study group took 30 mg/day of supplemental zinc as zinc gluconate for 8 weeks and 20 women of control group took placebo. Usual dietary zinc intake was estimated from 3-day diet records. Insulin resistances were measured using Homeostasis model assessment (HOMA) indices, and insulin sensitivities Matsuda indices, which were calculated using oral glucose tolerance test data. Metabolic risk factors, such as waist circumference, blood pressure, fasting glucose, triglyceride, high density lipoprotein (HDL) cholesterol, and adipocyte hormones such as leptin, and adiponectin were also measured. At the beginning of study, dietary zinc averaged 7.31 mg/day and serum zinc averaged $12.98{\mu}mol/L$ in the study group. Zinc supplementation increased serum zinc by 15% and urinary zinc by 56% (P < 0.05). HOMA values tended to decrease and insulin sensitivity increased slightly in the study group, but not significantly so. BMI, waist circumference, blood pressure, blood glucose, triglyceride, HDL cholesterol, and adipocyte hormones did not change in either the study or control group. These results suggest that zinc status may not affect insulin resistance and metabolic risk factors in obese Korean women. Further research is required on a larger cohort with a longer follow-up to determine the effects of zinc status on insulin resistance and metabolic variables.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.10
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• pp.5043-5046
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• 2012

The role of Helicobacter pylori status and serum zinc value in gastric disease patients and healthy controls were investigated. Cases used in this work were 45 gastric cancer patients, 44 with peptic ulcers, 52 suffering gastritis and 64 healthy controls, all diagnosed histologically with the controls undergoing medical checkups. Helicobacter pylori status and serum levels of Zn were determined by 13C-urea breath test and flame atomic absorption spectrophotometer, respectively. Our study showed that Helicobacter pylori infection has no change in gastritis, peptic ulcer and gastric cancer group, on the contrast, serum levels of Zn were significantly reduced in gastritis, peptic ulcer and gastric cancer group, compared with healthy controls, and the higher the Zn levels are, the more increased risk of gastric cancer. Helicobacter pylori infection is a cause of gastritis, peptic ulcers and even gastric cancer, while serum zinc level is an indicator of protection of gastric membranes against damage.

• Journal of Veterinary Clinics
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• v.14 no.2
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• pp.361-364
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• 1997

The paper is to report a case of zinc-deficient parakeratotic hyperkeratosis in a dog. In this dermatosis, although an available diagnosis of zinc-deficient dermatosis is to analyse the serum or hair zinc Bevels, exact analysis of zinc is difficult and unreliable due to contamination of zinc by various environmental, physiologic and disease-related factors. Diagnosis may be performed by history, physical examination and blood chemical analysis. Laboratory evaluation revealed hypercholesterolemia and low activities of serum alkaline photophatase and total protein. The dog showed thick crusts at the elbows joint, stifle joint and testis. Zinc sulfate is administered per oral to patient with application of salicylic acid added vaseline ointment on hyperkaratic lesions. The dog is successfully cured.

• Nutrition Research and Practice
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• v.2 no.4
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• pp.283-288
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• 2008

This study was carried out to determine whether a short-tenn zinc supplementation contributes to beneficial changes in glycemic control among type 2 diabetic patients. Seventy-six diabetic subjects and 72 normal adults participated in this study. Subjects were divided into supplemented and control groups. Forty-four diabetic patients and 34 normal subjects were supplemented with 50 mg zinc daily as zinc gluconate for 4 weeks. Zinc status was assessed from fasting plasma levels and urinary excretion. The effects of zinc supplementation on fasting blood glucose, $HbA_{1c}$, insulin, and C-peptide were measured at the beginning of the study and after 4 weeks of supplementation. The changes in glycemic control indicators were compared between diabetic groups, classified by baseline $HbA_{1c}$ levels, and by diabetic duration. At baseline, the incidence of marginal zinc deficiency in the diabetic group, as determined by plasma zinc level, was approximately twice as high as in the normal adult group. The changes of $HbA_{1c}$ concentration, and fasting blood glucose following supplementation were not statistically significant in diabetic subjects. In normal subjects, a significant decrease of $HbA_{1c}$ occurred only in the zinc supplemented group. No significant changes were observed for serum insulin and C-peptide in diabetic as well as normal subjects. However, when the changes were compared by baseline $HbA_{1c}$ level, we found that diabetic subjects with $HbA_{1c}\;{\geq}\;7.5%$ showed significantly improved levels of $HbA_{1c}$ and fasting glucose after Zn supplementation. While such improvement in fasting blood glucose was significant among diabetics with shorter diabetic duration, significant levels of increase in serum insulin and C-peptide were observed in zinc supplemented subjects with longer diabetic duration. Fasting blood glucose was significantly decreased, whereas serum insulin and C-peptide were increased in diabetics with marginal zinc status. Therefore, we suggest that Zn supplementation for a short-term period may improve glycemic control in diabetic patients with higher $HbA_{1c}$ levels and marginal zinc status.