The effect of zinc supplementation on plasma lipids and low-density lipoprotein oxidation in males. Effects of zinc and multimineral vitamin supplementation on glycemic and lipid control in adult diabetes Zinc decreases C-reactive protein, lipid peroxidation, and inflammatory cytokines in elderly subjects: a potential implication of zinc as an atheroprotective agent. Disturbed zinc homeostasis in diabetic patients by in vitro and in vivo analysis of insulinomimetic activity of zinc. Effects of zinc supplementation on the anthropometric measurements, lipid profiles and fasting blood glucose in the healthy obese adults. Short-term zinc supplementation in women with non-insulin-dependent diabetes mellitus: effects on plasma 5'-nucleotidase activities, insulin-like growth factor I concentrations, and lipoprotein oxidation rates in vitro. Effect of zinc supplementation on serum leptin levels and insulin resistance of obese women Effect of zinc supplementation on plasma high-density lipoprotein cholesterol and zinc. Effect of zinc supplementation on body mass index and serum levels of zinc and leptin in pediatric hemodialysis patients Antioxidant effect of zinc in humans. Plasma zinc concentrations during the first 2 years after diagnosis of insulin-dependent diabetes mellitus: a prospective study. Lipid peroxidation in insulin-dependent diabetic patients with early retina degenerative lesions: effects of an oral zinc supplementation. The effect of five-year zinc supplementation on serum zinc, serum cholesterol and hematocrit in persons randomly assigned to treatment group in the age-related eye disease study: AREDS Report No. 7. Zinc supplementation in prediabetes: A randomized double‐blind placebo‐controlled clinical trial† Effects of zinc supplementation on serum zinc and leptin levels, BMI, and body composition in hemodialysis patients. Effect of vitamin C and zinc on osmotic fragility and lipid peroxidation in zinc‐deficient haemodialysis patients Dietary Intervention Causes Redistribution of Zinc in Obese Adolescents
Recent studies in animals and in vitro support the hypothesis that zinc , an essential micronutrient , possesses antioxidant properties . The aims of this study were to determine whether zinc provides antioxidant protection in humans by decreasing low-density lipoprotein ( LDL ) oxidizability and to determine the effect of zinc supplementation on plasma lipid and its distribution among lipoproteins . Ten healthy male volunteers were recruited to participate in a r and omized crossover trial . Subjects were asked to consume 50 mg zinc as 220 mg zinc sulphate ( equivalent to 4 x recommended dietary intake , or RDI ) daily for 4 weeks , followed by placebo , and vice versa . Venous blood sample s were collected at 2-week intervals for the determination of plasma lipids and the in vitro oxidizability of LDL in the presence of copper ions . No changes in the oxidizability of LDL or the plasma concentrations of total cholesterol , high-density lipoprotein ( HDL ) cholesterol and its subfractions , LDL cholesterol , or triacylglycerol were observed following zinc supplementation compared to placebo .  Plasma zinc concentrations were increased significantly , indicating that the lack of effect was not due to poor compliance . The antioxidant effect of  zinc  in relation to LDL was not demonstrated in humans at this dose , and higher doses are unlikely to be effective given the adverse interaction with copper metabolism and the potential decrease in the activity of superoxide dismutase , a free radical quenching enzyme . The findings of this study suggest that zinc provides little , if any , antioxidant protection against LDL oxidation in humans Aims : To evaluate the effects of zinc with or without other antioxidants on blood glucose , lipid profile , and serum creatinine in adult diabetics on long-term follow-up . Material s and methods : Patients ( n = 96 ) were r and omly allocated to three groups : group A ( n = 29 ) was supplemented with oral zinc sulfate ( 22 mg/day ) and multivitamin/mineral ( zinc+MVM ) preparation ; group B ( n = 31 ) was given the same preparation without zinc ( MVM ) ; and group C ( n = 36 ) was given a matching placebo for a period of 4 months in a single-blinded study . Blood sample s were taken at baseline and after 4 months of supplementation to assess blood glucose ( fasting and postpr and ial ) and glycosylated hemoglobin ( HbA1C% ) and serum levels of zinc , creatinine , and lipids . Results : The zinc+MVM group had a mean change of fasting blood sugar −0.33 mmol/L ( st and ard error of the mean 0.21 mmol/L ) and was significant ( P = 0.05 ) when compared with the other two groups ( mean change in the MVM group + 0.19 ( 0.31 ) mmol/L and + 0.43 ( 0.23 ) mmol/L in the control group , respectively ) . The HbA1C% level reduced significantly , irrespective of the baseline level , in zinc+MVM-supplemented individuals . In the other two groups , the change of HbA1C% level was not significant . Serum lipid levels reduced significantly in the zinc+MVM and MVM groups . Conclusions : Zinc+MVM supplementation showed beneficial effects in the metabolic control of adult diabetics in addition to elevating their serum zinc level . Zinc supplementation  improved glycemic control measured by HbA1C% and fasting and postpr and ial glucose . Furthermore , zinc supplementation  lowered serum cholesterol and cholesterol/high-density lipoprotein ratio BACKGROUND Chronic inflammation and oxidative stress are common risk factors for atherosclerosis . Zinc is an essential micronutrient that can function as an antiinflammatory and antioxidative agent , and as such , it may have atheroprotective properties . OBJECTIVE We hypothesized that zinc down-regulates the production of atherosclerosis-related cytokines/molecules in humans . DESIGN To examine these effects , we conducted a r and omized , double-blinded , placebo trial of zinc supplementation  in elderly subjects . We recruited 40 healthy elderly subjects ( aged 56 - 83 y ) and r and omly assigned them to 2 groups . One group was given an oral dose of 45 mg zinc/d as a gluconate for 6 mo . The other group was given a placebo . Cell culture models were conducted to study the mechanism of zinc as an atheroprotective agent . RESULTS After 6 mo of supplementation , the intake of zinc , compared with intake of placebo , increased the concentrations of plasma zinc and decreased the concentrations of plasma high-sensitivity C-reactive protein ( hsCRP ) , interleukin (IL)-6 , macrophage chemoattractant protein 1 ( MCP-1 ) , vascular cell adhesion molecule 1 ( VCAM-1 ) , secretory phospholipase A2 , and malondialdehyde and hydroxyalkenals ( MDA+HAE ) in elderly subjects . Regression analysis showed that changes in concentrations of plasma zinc were inversely associated with changes in concentrations of plasma hsCRP , MCP-1 , VCAM-1 , and MDA+HAE after 6 mo of supplementation . In cell culture studies , we showed that zinc decreased the generation of tumor necrosis factor-alpha , IL-1beta , VCAM-1 , and MDA+HAE and the activation of nuclear transcription factor kappaB and increased antiinflammatory proteins A20 and peroxisome proliferator-activated receptor-alpha in human monocytic leukemia THP-1 cells and human aortic endothelial cells compared with zinc-deficient cells . CONCLUSION These findings suggest that zinc may have a protective effect in atherosclerosis because of its antiinflammatory and antioxidant functions Disturbances of zinc homeostasis have been observed in several diseases , including diabetes mellitus . To further characterize the association between zinc and diabetes , we recruited 75 patients with type 1 or type 2 diabetes and 75 nondiabetic sex-/age-matched control subjects in order to analyze differences concerning human zinc transporter 8 ( hZnT-8 ) expression , single nucleotide polymorphisms ( SNPs ) in the genes of hZnT-8 as well as metallothionein 1A and serum/intracellular zinc . Furthermore , we investigated the relation between insulin and zinc homeostasis in type 2 diabetic subjects and consoli date d our results by in vitro analysis of the effect of insulin on cellular zinc status and by analysis of the modulation of insulin signal transduction by intracellular zinc homeostasis . Concerning the expression of hZnT-8 and the SNPs analyzed , we did not observe any differences between diabetic and control subjects . Serum zinc was significantly lower in diabetic patients compared to controls , and intracellular zinc showed the same tendency . Interestingly , type 2 diabetes patients treated with insulin displayed lower serum zinc compared to those not injecting insulin . In vitro analyses showed that insulin leads to an increase in intracellular zinc and that insulin signaling was enhanced by elevated intracellular zinc concentrations . In conclusion , we show that type 1 and type 2 diabetic patients suffer from zinc deficiency , and our results indicate that zinc supplementation may qualify as a potential treatment adjunct in type 2 diabetes by promoting insulin signaling , especially in zinc-deficient subjects UNLABELLED Purpose : The aim of this study was to assess the effects of zinc supplementation on anthropometric measures , improving lipid profile biomarkers , and fasting blood glucose level in obese people . METHODS This r and omized , double- blind clinical trial was carried out on 60 obese participants in the 18 - 45 age range for one month . The participants were r and omly divided into the intervention group , who received 30 mg/d zinc gluconate , and the placebo group who received 30mg/d starch .  Anthropometric measurements ( body mass index ( BMI ) , weight and waist circumference ) were recorded before and at the end of study . Lipid profile biomarkers and fasting blood glucose were determined using enzymatic procedure . Analysis of Covariance ( ANCOVA ) test was run to compare the post-treatment values of the two groups , and t-test was conducted to compare within group changes . RESULTS Serum zinc concentration was increased significantly in intervention group ( p=0.024 ) . BMI and body weight was significantly decreased ( p=0.030 and p=0.020 , respectively ) . Lipid profile biomarkers and fating blood glucose did not change significantly but triglyceride level was significantly decreased ( p=0.006 ) in the intervention group . CONCLUSION The obtained results indicate that zinc supplementation  improves BMI , body weight , and triglyceride concentration without considerable effects on lipid profile and glucose level .  Zinc can be suggested as a suitable supplementation therapy for obese people , but more studies are needed to verify the results Non-insulin-dependent diabetes mellitus ( NIDDM ) may cause vulnerability to moderate zinc deficiency . In this study , short-term zinc supplementation ( 30 mg/d as amino acid chelate for 3 wk ) elevated plasma zinc and activities of 5'-nucleotidase , a zinc-dependant enzyme , in 20 postmenopausal women with NIDDM .  Placebo , given to 20 other women with NIDDM , had no effects on these indexes nor on any others taken in this study . Although zinc supplementation doubled the mean value for 5'-nucleotidase activity , values were still significantly lower than those of age-matched control subjects . Plasma insulin-like growth factor I concentrations increased with zinc treatment if starting concentrations were < 165 microg/L but were unchanged if they were > 165 microg/L. Lipoprotein oxidation in vitro , which has abnormal lag times and propagation rates for subjects with NIDDM and for moderately zinc-deficient rats , were unchanged by zinc supplementation . Possibly , this lack of effect occurred because the zinc treatment did not normalize zinc status . In conclusion , this study supports the contention that moderate zinc deficiency occurs frequently in subjects with NIDDM Leptin is thought to be a lipostatic signal that contributes to body weight regulation . Zinc might play an important role in appetite regulation and its administration stimulates leptin production . However , there are few reports in the literature on its role on leptin levels in the obese population . The present work asseses the effect of zinc supplementation on serum leptin levels in insulin resistance ( IR ) . A prospect i ve double-blind , r and omized , clinical , placebo-controlled study was conducted . Fifty-six normal glucose-tolerant obese women ( age : 25–45 yr , body mass index [ BMI ] = 36.2 ±2.3 kg/m2 ) were r and omized for treatment with 30 mg zinc daily for 4 wk . Baseline values of both groups were similar for age , BMI , caloric intake , insulin concentration , insulin resistance , and zinc concentration in diet , plasma , urine , and erythrocytes . Insulin and leptin were measured by radioimmunoassay and IR was estimated by the homeostasis model assessment ( HOMA ) . The determinations of zinc in plasma , erythrocytes , and 24-h urine were performed by using atomic absorption spectrophotometry . After 4 wk , BMI , fasting glucose , and zinc concentration in plasma and erythrocyte did not change in either group , although zinc concentration in the urine increased from 385.9±259.3 to 470.2±241.2±μg/24 h in the group with zinc supplementation ( p<0.05 ) . Insulin did not change in the placebo group , whereas there was a significant decrease of this hormone in the supplemented group . HOMA also decreased from 5.8±2.6 to 4.3±1.7 ( p<0.05 ) in the zinc-supplemented group but did not change in the placebo group . Leptin did not change in the placebo group . In the zinc group , leptin was 23.6±12.3 μg/L and did not change . More human data from a unique population of obese individuals with documented insulin resistance would be useful in guiding future studies on zinc supplementation ( with higher doses or longer intervals ) or different measures The recent report by Hooper PL , et al. ( JAMA 1980;244:1960 - 1 ) that pharmacological doses ( 160 mg ) of zinc lowered high-density lipoprotein (HDL)-cholesterol in men and that zinc might be an atherogenic agent prompted this report of the effect of zinc supplementation on HDL-cholesterol in women . Four levels of zinc supplements ( 0 , 15 , 50 , or 100 mg/day ) were given to 32 women for 8 wk . Fasting plasma HDL-cholesterol and zinc  were measured at biweekly intervals . Plasma zinc increased in the supplemented groups , peaked at wk 4 , then decreased toward initial values . The decline in plasma zinc regardless of continuing zinc administration may reflect a homeostatic response . No significant differences were seen in HDL-cholesterol over the 8 wk except in the 100 mg group at wk 4 when a transient decrease , -8.4 % ( 57 to 48 mg/dl , p less than 0.04 ) was observed . Thus we conclude that in women the reduction in HDL-cholesterol in response to the pharmacological doses of zinc used in this study was transient and not dose-related Introduction Zinc is an essential trace element for human nutrition , and its deficiency is associated with anorexia , poor food efficiency , growth retardation , and impaired neurological and immune systems . The zinc-deficiency rate is particularly high in many disease states , such as with end-stage renal disease patients undertaking hemodialysis . The aim of this study was to determine the effect of zinc supplementation on body mass index ( BMI ) and serum levels of zinc and leptin in pediatric hemodialysis patients . Patients and methods This was a prospect i ve clinical trial study in which 60 hemodialysis patients were r and omly divided into two groups : group I received 50–100 mg zinc sulfate ( equivalent to 11–22 mg elemental zinc ) according to age , sex , and nutritional status of the child ; and group II received placebo ( cornstarch ) twice daily for 90 days . Anthropometric measurements were taken , and serum zinc and leptin levels were determined by colorimetric test with 5-Br-3′-phosphoadenosine-5′-phosphosulfate and enzyme-linked immunosorbent assay , respectively , at days 0 and 90 of the study . Results Zinc supplementation result ed in a significant increase in mean serum zinc level and BMI . Serum leptin decreased significantly after supplementation in children under hemodialysis . A significant negative correlation was observed between serum zinc and leptin levels as a result of zinc supplementation . Conclusion There was an increase in serum zinc level and BMI and decreased serum leptin  after zinc supplementation in children under hemodialysis Oxidative stress is known to be an important contributing factor in many chronic diseases . We tested the hypothesis that in healthy normal volunteers zinc acts as an effective anti-inflammatory and antioxidant agent .  Ten normal volunteers were administered daily  oral zinc supplementation ( 45 mg zinc as gluconate ) and 10 volunteers received placebo for 8 weeks . Plasma zinc , MDA , HAE , and 8-OHdG levels ; LPS-induced TNF-alpha and IL-1beta mRNA ; and ex vivo TNF-alpha-induced NF-kappaB activity in mononuclear cells ( MNC ) were determined before and after supplementation . In subjects receiving zinc , plasma levels of lipid peroxidation products and DNA adducts were decreased , whereas no change was observed in the placebo group . LPS-stimulated MNC isolated from zinc-supplemented subjects showed reduced mRNA for TNF-alpha and IL-1beta compared to placebo . Ex vivo , zinc protected MNC from TNF-alpha-induced NF-kappaB activation . In parallel studies using HL-60 , a promyelocytic cell line , we observed that zinc enhances the upregulation of mRNA and DNA-specific binding for A20 , a transactivating factor which inhibits the activation of NF-kappaB. Our results suggest that zinc supplementation may lead to downregulation of the inflammatory cytokines through upregulation of the negative feedback loop A20 to inhibit induced NF-kappaB activation . Zinc administration to human subjects with conditions associated with increased oxidative stress should be explored Studies of  zinc  status in insulin-dependent diabetes mellitus ( IDDM ) have shown contradictory results . Zinc is essential for many enzymes involved in the human metabolism and may play a role in the bio synthesis and storage of insulin in the B-cell . We therefore prospect ively followed 26 patients ( 14 males and 12 females ) with newly diagnosed IDDM in order to determine the plasma zinc variation at the time of diagnosis and after 1 , 3 , 6 , 12 and 24 months . Seventy-two healthy persons ( 36 males and 36 females ) served as controls . Only minor differences in plasma zinc were demonstrated during the first 2 years of IDDM . A sex difference was found in healthy controls but only after 24 months in the diabetics . Quantitative changes of the B-cell function , development of insulin antibodies , age , body weight and serum albumin did not correlate with the course of plasma zinc DESIGN Placebo for 3 months , followed by 30 mg/day zinc gluconate in identical capsules . SETTING Diabetic out patients clinic at the University Hospital , Grenoble . SUBJECTS Diabetic patients cared for type I diabetes mellitus . 22 patients began the study , 4 dropped out . 10 patients suffered of an early retinopathy , 8 patients had no retinopathy . INTERVENTIONS In this order : T0 biological measurements , 3 months placebo treatment , T1 biological measurements , 3 months zinc gluconate treatment , T2 biological measurements . Plasma Zn , Cu , Se , thiobarbituric acid reactants and antioxidant enzymes were measured [ plasma and red glutathione peroxidase ( Se-GPx ) , red cell superoxide dismutase ( Cu-Zn-SOD ) ] . RESULTS Lower plasma zinc level in the two groups . An increase in zinc level was observed and was more important in diabetic patients with no retinopathy ( P = 0.05 ) . The thiobarbituric acid reactants were above the reference values in all the patients , and were decreased at T2 ( P < 0.05 ) . Increase of GPx activity after zinc supplementation in patients with retinopathy . CONCLUSIONS Zinc deficiency in insulin-dependent diabetic patients is corrected by a zinc supplementation . Moreover this supplementation decreases lipid peroxidation . The effects of zinc are different in diabetic patients with or without retinopathy . The increase in Se-GPx activity observed in patients with retinopathy could be linked to the protective effect of zinc on the protein itself The effects of long-term supplementation with pharmacologic doses of zinc oxide on serum levels of zinc , lipids and hematocrit have not been studied systematic ally to date . Eleven Clinical Centers enrolled 4757 participants from 1992 to 1998 as part of the Age-Related Eye Disease Study ( AREDS ) . Of these , 3640 participants , aged 55 - 80 y , who had early-to-late age-related macular degeneration ( AMD ) were r and omly assigned to daily supplementation with or without 80 mg of zinc as zinc oxide plus 2 mg of copper as cupric oxide to study the effects of zinc supplementation on the progression to late AMD . This paper reports on the effect of a 5-y supplementation with zinc oxide and cupric oxide on serum zinc , copper , lipids , and hematocrit for 717 participants from three clinical centers . At the 5-y exam , the median increase in serum zinc levels for participants assigned to zinc formulations was 17 % compared with a 2 % increase for participants not assigned to zinc ( P < 0.001 ) . The differential effect on serum zinc was observed at 1 y and remained fairly constant over the 5-y period . After 5 y , no significant differences in changes in serum hematocrit , copper or lipids were found between participants assigned to formulations containing zinc and copper , and those assigned to formulations without zinc and copper . Estimates from a modified Block Food-Frequency Question naire suggest the AREDS population at baseline had a zinc intake from diet similar to that of the general population BACKGROUND This study evaluated the effects of zinc supplementation on glycemic control , other cardiometabolic and anthropometric parameters , and  disease progression in prediabetes . METHODS A r and omized double-blind placebo-controlled Phase 2 clinical trial was conducted over a 12-month period in 200 subjects ( 43 % male ; mean [ ± SD ] age 51.8 ± 7.3 years ) , r and omly assigned ( 1 : 1 ) to the treatment or control group . The treatment group received zinc ( 20 mg daily ) . Subjects were evaluated at baseline and at 1 , 3 , 6 , and 12 months . The primary outcome was the change in glycemic control from baseline . Multiple regression analyses were performed , with change in outcome variables after intervention from baseline used as continuous dependent variables . RESULTS In both groups , mean serum zinc concentrations prior to the trial were below normal ( 15.29 - 21.41 μmol/L ) . During the 12-month follow-up , a significantly higher percentage of participants developed type 2 diabetes in the control compared with zinc-treated group ( 25.0 % vs 11.0 % respectively ; P = 0.016 ) . Fasting plasma glucose ( FPG ) , 2-h glucose levels in the oral glucose tolerance test ( OGTT ) , homeostasis model assessment of insulin resistance ( HOMA-IR ) , total cholesterol ( TC ) , and low-density lipoprotein cholesterol ( LDL-C ) were significantly lower in the treated group , with significant improvement in β-cell function . In all four regression models , the best predictor of the dependent variables ( i.e. change in FPG , 2-h glucose in the OGTT , HOMA-IR , and homeostatic model assessment of β-cell function ) was zinc treatment . CONCLUSIONS Zinc supplementation reduced blood glucose and insulin resistance while improving β-cell function . Furthermore , supplementation reduced disease progression to diabetes and had beneficial effects on TC and PROJECT The 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 . PROCEDURE In this r and omized , double-blind , and placebo-controlled trial , sixty HD patients were r and omly 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 st and ard calibrated instruments . Serum zinc and leptin levels were determined by atomic absorption and ELISA method respectively before and after intervention . RESULTS Zinc supplementation result ed 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 . CONCLUSIONS More studies are needed to clarify the mechanisms by which serum leptin level is influenced as a result of zinc supplementation in HD patients Peroxidation of the membrane lipid structure of red blood cell leads to haemolysis and anaemia in haemodialysis patients . Dietary constituents of antioxidant vitamins and trace elements may play an important role in protecting against oxidant damage . In this study , the effects of supplementation of vitamin C and zinc on osmotic fragility and lipid peroxidation of erythrocytes were investigated in 34 zinc‐deficient haemodialysis patients . Sixteen sex‐ and age‐matched normal volunteers acted as controls . Patients were r and omized to receive vitamin C ( 250 mg day−1 ) , zinc ( 20 mg day−1 ) or a placebo treatment for 3 months . The levels of vitamin C , zinc , malondialdehyde ( MDA ) and osmotic fragility were measured initially and 3 months after supplementation . Mean serum concentration of vitamin C and zinc increased significantly in the groups at the end of the respective study periods . Supplementation with vitamin C and zinc improved osmotic fragility , and decreased the level of MDA in the groups , but some side‐effects ( i.e. nausea , vomiting , fever , muscle pain , weakness ) were observed during the zinc treatment . The results showed that the supplementation of both treatments decreased osmotic fragilty and MDA in zinc‐deficient haemodialysis patients . However , vitamin C treatment was found to be safer than zinc supplementation . Copyright © 2001 John Wiley & Sons , Obese people tend to have low zinc circulation levels ; this is not always related to zinc intake but can reflect the distribution of zinc in relation to the proportion of body fat and factors related to the inflammatory processes that cause obesity . The purpose of this study was to assess zinc distribution in 15 obese adolescent girls before and after a nutritional orientation program . Participants ranged from 14 to 18 years old ( postpubescent ) and had a body fat percent ( BF% ) of > 35 % .  Zinc nutritional status and other zinc-dependent parameters , such as superoxide dismutase ( SOD ) and insulin levels , were assessed by biochemical analysis of plasma and erythrocytes , salivary sediment , and urine . Sample s were collected before and after 4 months of dietary intervention . Dual energy X-ray absorptiometry ( DXA ) was used to verify BF% both at the beginning and at the end of the study . Food consumption was assessed in ten individual food question naires throughout the study ; food groups were separated on the question naires in the same way as suggested by some authors to develop the Healthy Eating Index ( HEI ) but with the addition of zinc . After 4 months of nutritional orientation , 78 % of the participants showed a decrease in BF% . Intraerythrocytic zinc increased over the study period , while salivary sediment zinc , SOD , insulin , and Zn urinary24 h/creatinine all decreased ( p < 0.05 ) . There was no difference in zinc intake throughout the study but participants did increase their consumption of fruits , dairy , and meats during the study ( p < 0.05 ) . There were inverse and statistically significant correlations between the increased levels of intraerythrocytic zinc and decreased levels of SOD . There was also a statistically significant correlation between BF% and Zn urinary 24h/creatinine , and SOD . All these parameters were diminished at the end of the study . The dietary intervention for obese adolescent girls is effective with decrease of BF that led to the redistribution of zinc in the body as shown by the changes in erythrocytes , plasma , salivary , urine zinc , as well as the complementary parameters of insulin and SOD . These changes were not affected by zinc intake
In conclusion , Zinc supplementation  has favourable effects on plasma lipid parameters .
Zinc supplementation  significantly reduced total cholesterol , LDL cholesterol and triglycerides .
Therefore it may have the potential to reduce the incidence of atherosclerosis related morbidity and mortality
Zinc is a mineral that plays a vital role in many biological processes and plays an important role in insulin action and carbohydrate metabolism .
It may also have a protective role in the prevention of atherogenesis .
Numerous studies have evaluated the effects of Zinc supplementation on serum lipids in humans and have demonstrated varying results .
We systematic ally evaluated the literature and performed a meta- analysis on the effects of Zinc supplementation on serum lipids .