The effects of magnesium and vitamin E co-supplementation on parameters of glucose homeostasis and lipid profiles in patients with gestational diabetes
Lipids in Health and Diseasevolume 17, Article number: 163 (2018)
Magnesium and vitamin E are known to exert multiple beneficial effects, such as anti-glycemic and anti-lipidemic properties. The aim of this study was to determine the effects of magnesium and vitamin E co-supplementation on metabolic status of women with gestational diabetes (GDM).
This randomized, double-blinded, placebo-controlled trial was conducted among 60 subjects diagnosed with GDM, aged 18–40 years. Subjects were randomly allocated into two groups to receive 250 mg/day magnesium oxide plus 400 IU/day vitamin E supplements or placebo (n = 30 each group) for 6 weeks. Participants’ blood samples were taken to determine their metabolic profiles.
Subjects who received magnesium plus vitamin E supplements had significantly lower fasting plasma glucose (β − 5.20 mg/dL; 95% CI, − 7.88, − 2.52; P = 0.002), serum insulin levels (β − 2.93 μIU/mL; 95% CI, − 5.68, − 0.18; P = 0.02) and homeostasis model of assessment-insulin resistance (β − 0.78; 95% CI, − 1.42, − 0.14; P = 0.01), and higher quantitative insulin sensitivity check index (β 0.01; 95% CI, 0.005, 0.02; P = 0.002) compared with placebo. In addition, magnesium plus vitamin E supplementation resulted in a significant reduction in serum triglycerides (β − 50.31 mg/dL; 95% CI, − 67.58, − 33.04; P < 0.001), VLDL- (β − 10.06 mg/dL; 95% CI, − 13.51, − 6.60; P < 0.001), total- (β − 26.10 mg/dL; 95% CI, − 41.88, − 10.33; P = 0.004), LDL- (β − 15.20 mg/dL; 95% CI, − 29.50, − 0.91; P = 0.03) and total-/HDL-cholesterol ratio (β − 0.46; 95% CI, − 0.72, − 0.19; P < 0.001) compared with placebo. Magnesium and vitamin E co-supplementation did not affect HDL-cholesterol levels.
Overall, magnesium and vitamin E co-supplementation for 6 weeks in women with GDM significantly improved glycemic control and lipid profiles, except for HDL-cholesterol levels.
Clinical trial registration number
Gestational diabetes mellitus (GDM) is defined as carbohydrates intolerance which first recognized at second or third trimester of pregnancy and has reported to increasing worldwide . It influences approximately 1 to 20% of all pregnancies worldwide as well as its prevalence among Iranian women is about 4 to 9% of all pregnancies . Both environmental risk factors and genetic background contribute to the development of GDM . In addition to maternal and fetal complications, GDM is associated with the elevated potential for metabolic disorder including type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD) in future life of both mother and offspring [4, 5]. In addition, insulin resistance and dyslipidemia are the hallmarks of GDM [6, 7].
There is evidence demonstrating that magnesium is required more during pregnancy . In addition, hypomagnesemia might lead to impaired glucose tolerance . Few studies have reported low circulating levels of magnesium and vitamin E in women with GDM [10, 11]. Furthermore, several human studies have demonstrated the beneficial effects of single magnesium  or vitamin E supplementation on metabolic profiles. In a meta-analysis, magnesium supplementation resulted in a significant reduction in insulin resistance, but did not affect fasting glucose and insulin levels . Earlier, we have shown that magnesium supplementation for 6 weeks to women with GDM led to a significant reduction in triglycerides and VLDL-cholesterol levels, but did not affect other lipid profiles . In addition, some studies have reported the beneficial effects of vitamin E supplementation on glucose metabolism and lipid profiles in patients with metabolic syndrome [15, 16]. Recently, it has been suggested that joint magnesium and vitamin E supplementation in diabetic rat was more beneficial to improve lipid profiles and blood viscosity rather than magnesium alone . In another study, combined vitamin E and magnesium supplementation could effectively improve triglycerides levels of obese rats, better than vitamin E alone .
This evidence might suggest the importance of magnesium and vitamin E co-supplementation on metabolic profiles in women with GDM. According to our best knowledge, data on the effects of magnesium and vitamin E co-supplementation on metabolic status of patients with GDM are scarce. Therefore, the aim of this study was to evaluate the effects of magnesium and vitamin E co-supplementation on metabolic status of patients with GDM.
This randomized, double-blinded, placebo controlled clinical trial, registered in the Iranian website for registration of clinical trials (no: IRCT20170513033941N24), was conducted among sixty women with GDM, aged 18–40 years and non-diabetic before pregnancy, diagnosed using American Diabetes Association guidelines  from December 2017 through March 2018. The study was approved by the ethics committee of Arak University of Medical Sciences (AUMS) and written informed consent was taken from all participants prior to the commencement of the study. Exclusion criteria were; taking magnesium and vitamin E supplements 3 months before the intervention insulin therapy required during the intervention, experiencing pre-eclampsia, eclampsia, hypo and hyperthyroidism, and being smokers.
To decrease the effects of potential confounders, stratified randomization was performed at the beginning of the study for all participants according to age and BMI. Then, participants in each block were randomly allocated into two treatment groups to take either 250 mg/day magnesium oxide (twenty-first Century, Arizona, USA) and 400 IU/day vitamin E (Zahravi, Tabriz, Iran) or placebo (Barij Essence, Kashan, Iran) (n = 30 each group) for 6 weeks. Randomization assignment was conducted using computer-generated random numbers. Randomization and allocation concealment for both researchers and participants were carried out by a trained staff at the gynecology clinic. Compliance to the magnesium and vitamin E intake was assessed through measuring serum magnesium levels. The consumption of magnesium supplements and placebos during the study was also checked by asking subjects to return the medication containers back and receiving brief daily cell phone reminders to take the supplements. All patients were advised to maintain their routine dietary habits without any changes in their other lifestyle factors such as physical activity during the study. All patients completed 3-day food records and three physical activity records presented as metabolic equivalents (METs) at weeks 0, 3, 6 of the treatment.
Assessment of anthropometric measures
Participants’ weight and height were measured using a standard scale (Seca, Hamburg, Germany) in a fasting status at baseline and after 6-weeks’ intervention. Body mass index (BMI) was calculated as weight in kg divided by height in meters squared.
Assessment of outcomes
In this study, glycemic control was considered as the primary outcome, and lipid profiles the secondary outcomes.
10 ml fasting blood samples were collected from participants at weeks 0 and 6 of the intervention. Commercial kits were used to measure serum magnesium, fasting plasma glucose (FPG), serum triglycerides, total-, VLDL-, LDL- and HDL-cholesterol concentrations (Pars Azmun, Tehran, Iran). Serum magnesium levels were measured by enzymatic method. The inter- and intra-assay coefficient variances (CVs) for magnesium, FPG, lipid profiles measurements were less than 5%. Serum insulin values were assessed using an ELISA kit (Monobind, California, USA) with the intra- and inter-assay CVs of lower than 6%. The homeostatic model of assessment for insulin resistance (HOMA-IR) and the quantitative insulin sensitivity check index (QUICKI) were determined according to suggested formulas . HOMA-IR was calculated according to the following formula: fasting insulin (μIU/mL) x fasting glucose (mmol/L)/22.5 . QUICKI was calculated as QUICKI = 1/[log(I0) + log(G0)], where I0 is the fasting insulin, and G0 is the fasting glucose .
Type one (α) and type two errors (β) were defined as 0.05, and 0.20, respectively to have the study power of 80%. Based on a previous published study , we used 1.05 as the mean difference of the HOMA-IR and 1.30 as SD. Calculating sample size, we required 25 patients in each treatment group; allowing for 20% dropouts in each group, the final sample size was considered to be 30 patients per treatment group.
Kolmogorov-Smirnov test was done to determine the normality of data. To detect the differences in anthropometric measures and dietary intakes between treatment groups, we used independent-samples t-test. To determine the effects of magnesium and vitamin E co-supplementation on parameters of glucose homeostasis and lipid profiles, we used general linear model and one-way repeated measures analysis of variance. In this analysis, treatment variable (magnesium plus vitamin E vs. placebo) was regarded as between-subject factor and time-points (baseline and week 6 of intervention) as within-subject factor. The effect sizes were presented as the mean differences with 95% confidence intervals. P-values < 0.05 were considered statistically significant. All statistical analyses were done using the Statistical Package for Social Science version 18 (SPSS Inc., Chicago, Illinois, USA).
During the enrollment phase of the study, 65 women with GDM were invited to participate in the trial; however, 5 participants were excluded from the study, due to not meeting the inclusion criteria. Finally, 60 participants [placebo (n = 30) and magnesium plus vitamin E (n = 30)] completed the trial (Fig. 1).
Mean age, height, weight and BMI at baseline and after the 6-week treatment were not statistically different between the two groups (Table 1).
Using 3-day dietary records, obtained during the intervention, there was no statistically significant difference in terms of dietary macro- and micro-nutrient intakes between magnesium plus vitamin E and placebo groups (Data not shown).
Subjects who received magnesium plus vitamin E supplements had significantly lower FPG (β − 5.20 mg/dL; 95% CI, − 7.88, − 2.52; P = 0.002), serum insulin levels (β − 2.93 μIU/mL; 95% CI, − 5.68, − 0.18; P = 0.02) and HOMA-IR (β − 0.78; 95% CI, − 1.42, − 0.14; P = 0.01), and higher QUICKI (β 0.01; 95% CI, 0.005, 0.02; P = 0.002) compared with placebo (Table 2). In addition, magnesium plus vitamin E supplementation resulted in a significant reduction in serum triglycerides (β − 50.31 mg/dL; 95% CI, − 67.58, − 33.04; P < 0.001), VLDL- (β − 10.06 mg/dL; 95% CI, − 13.51, − 6.60; P < 0.001), total- (β − 26.10 mg/dL; 95% CI, − 41.88, − 10.33; P = 0.004), LDL- (β − 15.20 mg/dL; 95% CI, − 29.50, − 0.91; P = 0.03) and total-/HDL-cholesterol ratio (β − 0.46; 95% CI, − 0.72, − 0.19; P < 0.001) rather than placebo group. Magnesium and vitamin E co-supplementation did not affect HDL-cholesterol levels.
In the present study, we examined the effects of co-supplementation of magnesium and vitamin E on parameters of glucose homeostasis and lipid profiles in women with GDM. We found that magnesium and vitamin E co-supplementation to women with GDM for 6 weeks improved glycemic control and lipid concentrations except for HDL-cholesterol values.
Gestational diabetes mellitus occurs because of altered glucose metabolism and peripheral insulin resistance . Our study indicated that magnesium and vitamin E co-administration to women with GDM lowered serum FPG, insulin levels and HOMA-IR, and led to a significant rise in QUICKI. Similar to our findings, a meta-analysis conducted by Simental-Mendia et al.  revealed that magnesium supplementation for at least 4 months improved FPG and HOMA-IR in both diabetic and non-diabetic individuals. In addition, our previous study indicated that a 6-week co-supplementation with magnesium and other nutrients in patients with GDM had beneficial effects on FPG, insulin levels, HOMA-IR and QUICKI . Moreover, Rafraf et al.  reported that vitamin E supplementation to people with T2DM for 8 weeks reduced serum FPG levels. However, some researchers failed to find the beneficial effects of magnesium  or vitamin E supplementation on glycemic control. For instance, in a meta-analysis conducted by Xu et al. , vitamin E supplementation did not affect parameters of insulin metabolism. In addition, a 3-month magnesium supplementation in hypomagnesic pre-diabetic patients with chronic kidney disease did not change FPG levels .
Maternal insulin resistance in GDM might increase placental size, though decrease placental efficiency, subsequently might affect fetal growth . It also has been demonstrated that well glycemic control may improve pregnancy outcomes . Magnesium is involved in glucose metabolism through its effects on tyrosine kinase activity of the insulin receptors . It also regulates glucose uptake via its influence on glucose transporte-4 activity , and regulates oxidative pathway of glucose metabolism through the activation of pyruvate dehydrogenas . Furthermore, the beneficial effects of vitamin E intake on insulin resistance may be explained through its effect on suppressing oxidative stress and gene expression of peroxisome proliferator activated-receptor (PPAR) alpha . Also, vitamin E can mediate glucose metabolism by stimulating glutathione and magnesium levels .
Gestational diabetes mellitus is accompanied by lipid profiles changes including an elevated triglyceride, total- and LDL-cholesterol levels . In the present study, we observed that magnesium and vitamin E co-supplementation to women with GDM reduced triglycerides, VLDL-, total-, LDL- and total-/HDL-cholesterol, but did not affect HDL-cholesterol levels. In agreement with our findings, the results of another clinical study indicated that magnesium supplementation for 4 months decreased triglycerides levels in pre-diabetic patients with hypomagnesemia . Consistent with our results, Ekhlasi et al.  reported that synbiotic and vitamin E co-supplementation reduced triglycerides, total- and LDL-cholesterol levels, but did not affect HDL-cholesterol concentrations. Moreover, a significant reduction in total cholesterol levels was reported after vitamin E supplementation to women with metabolic syndrome . In contrast, in a meta-analysis conducted by Xu et al.  there was no significant effects of vitamin E supplementation on lipid profiles. On the other hand, magnesium supplementation could not improve lipid levels in both diabetic and non-diabetic individuals . Hypertriglyceridemia during pregnancy worsen insulin resistance  and seems to be an independent predictor of fetal macrosomia . Recent studies have reported a positive association between maternal triglycerides levels and the risk of large for gestational age neonate, independent of glycemic controls . Magnesium acts as the cofactor of lipoprotein lipase which induces chylomicrone clearance and delays postprandial increase in triglycerides levels . Vitamin E, beside its antioxidant effects, modulates gene expression of PPAR gama, which involves in lipid metabolism .
Our study had a few limitations. Due to lack of enough funding, we could not evaluate the effects of magnesium and vitamin E co-supplementation on gene expression of insulin and lipid metabolism. We also did not measure vitamin E levels. In addition, further studies are necessary with single supplementation for each comparison with co-supplementation to assess the beneficial effects of each supplement on glycemic control and lipid profiles. Higher confidence interval of dependent variables found in some cases might make the findings difficult to be interpreted. Higher confidence interval might be explained by the small sample size in the included studies, which is another limitation of our study and thus more trials with larger sample size would be needed to confirm our findings.
Overall, magnesium and vitamin E co-supplementation for 6 weeks in women with GDM significantly improved glycemic control and lipid profiles except for HDL-cholesterol levels.
fasting plasma glucose
high density lipoprotein-cholesterol
homeostasis model of assessment-insulin resistance
low density lipoprotein-cholesterol
quantitative insulin sensitivity check index
very low density lipoprotein-cholesterol
American Diabetes Association. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-2018. Diabetes Care. 2018;41:S13–s27.
Takhshid MA, Haem Z, Aboualizadeh F. The association of circulating adiponectin and + 45 T/G polymorphism of adiponectin gene with gestational diabetes mellitus in Iranian population. J Diabetes Metab Disord. 2015;14:30.
Feng Y, Jiang CD, Chang AM, Shi Y, Gao J, Zhu L, et al. Interactions among insulin resistance, inflammation factors, obesity-related gene polymorphisms, environmental risk factors, and diet in the development of gestational diabetes mellitus. J Matern Fetal Neonatal Med. 2018:1–9.
Brown J, Alwan NA, West J, Brown S, McKinlay CJ, Farrar D, et al. Lifestyle interventions for the treatment of women with gestational diabetes. Cochrane Database Syst Rev. 2017;5:CD011970. https://doi.org/10.1002/14651858.CD011970.pub2.
Hiersch L, Yogev Y. Impact of gestational hyperglycemia on maternal and child health. Curr Opin Clin Nutr Metab Care. 2014;17:255–60.
Lambrinoudaki I, Vlachou SA, Creatsas G. Genetics in gestational diabetes mellitus: association with incidence, severity, pregnancy outcome and response to treatment. Curr Diabetes Rev. 2010;6:393–9.
Carpenter MW. Gestational diabetes, pregnancy hypertension, and late vascular disease. Diabetes Care. 2007;30(Suppl 2):S246–50.
Dalton LM, Ni Fhloinn DM, Gaydadzhieva GT, Mazurkiewicz OM, Leeson H, Wright CP. Magnesium in pregnancy. Nutr Rev. 2016;74:549–57.
Nair AV, Hocher B, Verkaart S, van Zeeland F, Pfab T, Slowinski T, et al. Loss of insulin-induced activation of TRPM6 magnesium channels results in impaired glucose tolerance during pregnancy. Proc Natl Acad Sci U S A. 2012;109:11324–9.
Goker Tasdemir U, Tasdemir N, Kilic S, Abali R, Celik C, Gulerman HC. Alterations of ionized and total magnesium levels in pregnant women with gestational diabetes mellitus. Gynecol Obstet Investig. 2015;79:19–24.
Grissa O, Ategbo JM, Yessoufou A, Tabka Z, Miled A, Jerbi M, et al. Antioxidant status and circulating lipids are altered in human gestational diabetes and macrosomia. Transl Res. 2007;150:164–71.
Jamilian M, Samimi M, Faraneh AE, Aghadavod E, Shahrzad HD, Chamani M, et al. Magnesium supplementation affects gene expression related to insulin and lipid in patients with gestational diabetes. Magnes Res. 2017;30:71–9.
Simental-Mendia LE, Sahebkar A, Rodriguez-Moran M, Guerrero-Romero F. A systematic review and meta-analysis of randomized controlled trials on the effects of magnesium supplementation on insulin sensitivity and glucose control. Pharmacol Res. 2016;111:272–82.
Asemi Z, Karamali M, Jamilian M, Foroozanfard F, Bahmani F, Heidarzadeh Z, et al. Magnesium supplementation affects metabolic status and pregnancy outcomes in gestational diabetes: a randomized, double-blind, placebo-controlled trial. Am J Clin Nutr. 2015;102:222–9.
Verma H, Garg R. Effect of magnesium supplementation on type 2 diabetes associated cardiovascular risk factors: a systematic review and meta-analysis. J Hum Nutr Diet. 2017;30:621–33.
Asemi Z, Soleimani A, Bahmani F, Shakeri H, Mazroii N, Abedi F, et al. Effect of the omega-3 fatty acid plus vitamin E supplementation on subjective global assessment score, glucose metabolism, and lipid concentrations in chronic hemodialysis patients. Mol Nutr Food Res. 2016;60:390–8.
Dou M, Ma AG, Wang QZ, Liang H, Li Y, Yi XM, et al. Supplementation with magnesium and vitamin E were more effective than magnesium alone to decrease plasma lipids and blood viscosity in diabetic rats. Nutr Res. 2009;29:519–24.
Chang W, Ma A, Wang Q, Mao R, Li C. Effects of vitamin E and magnesium on glucolipid metabolism in obese rats. Wei Sheng Yan Jiu. 2014;43:713–8.
Diagnosis and classification of diabetes mellitus. Diabetes Care. 2014;37(Suppl 1):S81–90.
Pisprasert V, Ingram KH, Lopez-Davila MF, Munoz AJ, Garvey WT. Limitations in the use of indices using glucose and insulin levels to predict insulin sensitivity: impact of race and gender and superiority of the indices derived from oral glucose tolerance test in African Americans. Diabetes Care. 2013;36:845–53.
Butte NF. Carbohydrate and lipid metabolism in pregnancy: normal compared with gestational diabetes mellitus. Am J Clin Nutr. 2000;71:1256s–61s.
Karamali M, Bahramimoghadam S, Sharifzadeh F, Asemi Z. Magnesium-zinc-calcium-vitamin D co-supplementation improves glycemic control and markers of cardiometabolic risk in gestational diabetes: a randomized, double-blind, placebo-controlled trial. Appl Physiol Nutr Metab. 2018:1–6.
Rafraf M, Bazyun B, Sarabchian MA, Safaeiyan A, Gargari BP. Vitamin E improves serum paraoxonase-1 activity and some metabolic factors in patients with type 2 diabetes: no effects on nitrite/nitrate levels. J Am Coll Nutr. 2016;35:521–8.
Razzaghi R, Pidar F, Momen-Heravi M, Bahmani F, Akbari H, Asemi Z. Magnesium supplementation and the effects on wound healing and metabolic status in patients with diabetic foot ulcer: a randomized, double-blind, placebo-controlled trial. Biol Trace Elem Res. 2018;181:207–15.
Xu R, Zhang S, Tao A, Chen G, Zhang M. Influence of vitamin E supplementation on glycaemic control: a meta-analysis of randomised controlled trials. PLoS One. 2014;9:e95008.
Toprak O, Kurt H, Sari Y, Sarkis C, Us H, Kirik A. Magnesium replacement improves the metabolic profile in obese and pre-diabetic patients with mild-to-moderate chronic kidney disease: a 3-month, randomised, double-blind, placebo-controlled study. Kidney Blood Press Res. 2017;42:33–42.
Tanaka K, Yamada K, Matsushima M, Izawa T, Furukawa S, Kobayashi Y, et al. Increased maternal insulin resistance promotes placental growth and decreases placental efficiency in pregnancies with obesity and gestational diabetes mellitus. J Obstet Gynaecol Res. 2018;44:74–80.
Cyganek K, Hebda-Szydlo A, Skupien J, Katra B, Janas I, Borodako A, et al. Glycemic control and pregnancy outcomes in women with type 2 diabetes from Poland. The impact of pregnancy planning and a comparison with type 1 diabetes subjects. Endocrine. 2011;40:243–9.
Grober U, Schmidt J, Kisters K. Magnesium in prevention and therapy. Nutrients. 2015;7:8199–226.
Pokusa M, Kralova Trancikova A. The central role of biometals maintains oxidative balance in the context of metabolic and neurodegenerative disorders. Oxidative Med Cell Longev. 2017;2017:8210734.
Yakaryilmaz F, Guliter S, Savas B, Erdem O, Ersoy R, Erden E, et al. Effects of vitamin E treatment on peroxisome proliferator-activated receptor-alpha expression and insulin resistance in patients with non-alcoholic steatohepatitis: results of a pilot study. Intern Med J. 2007;37:229–35.
Barbagallo M, Dominguez LJ, Tagliamonte MR, Resnick LM, Paolisso G. Effects of vitamin E and glutathione on glucose metabolism: role of magnesium. Hypertension. 1999;34:1002–6.
Ryckman KK, Spracklen CN, Smith CJ, Robinson JG, Saftlas AF. Maternal lipid levels during pregnancy and gestational diabetes: a systematic review and meta-analysis. BJOG. 2015;122:643–51.
Guerrero-Romero F, Simental-Mendia LE, Hernandez-Ronquillo G, Rodriguez-Moran M. Oral magnesium supplementation improves glycaemic status in subjects with prediabetes and hypomagnesaemia: a double-blind placebo-controlled randomized trial. Diabetes Metab. 2015;41:202–7.
Ekhlasi G, Kolahdouz Mohammadi R, Agah S, Zarrati M, Hosseini AF, Arabshahi SS, et al. Do symbiotic and vitamin E supplementation have favorite effects in nonalcoholic fatty liver disease? A randomized, double-blind, placebo-controlled trial. J Res Med Sci. 2016;21:106.
Wang Q, Sun Y, Ma A, Li Y, Han X, Liang H. Effects of vitamin E on plasma lipid status and oxidative stress in Chinese women with metabolic syndrome. Int J Vitam Nutr Res. 2010;80:178–87.
Simental-Mendia LE, Simental-Mendia M, Sahebkar A, Rodriguez-Moran M, Guerrero-Romero F. Effect of magnesium supplementation on lipid profile: a systematic review and meta-analysis of randomized controlled trials. Eur J Clin Pharmacol. 2017;73:525–36.
van de Woestijne AP, Monajemi H, Kalkhoven E, Visseren FL. Adipose tissue dysfunction and hypertriglyceridemia: mechanisms and management. Obes Rev. 2011;12:829–40.
Wang X, Guan Q, Zhao J, Yang F, Yuan Z, Yin Y, et al. Association of maternal serum lipids at late gestation with the risk of neonatal macrosomia in women without diabetes mellitus. Lipids Health Dis. 2018;17:78.
Vrijkotte TG, Krukziener N, Hutten BA, Vollebregt KC, van Eijsden M, Twickler MB. Maternal lipid profile during early pregnancy and pregnancy complications and outcomes: the ABCD study. J Clin Endocrinol Metab. 2012;97:3917–25.
Dibaba DT, Xun P, Fly AD, Yokota K, He K. Dietary magnesium intake and risk of metabolic syndrome: a meta-analysis. Diab Med. 2014;31:1301–9.
Bozaykut P, Karademir B, Yazgan B, Sozen E, Siow RC, Mann GE, et al. Effects of vitamin E on peroxisome proliferator-activated receptor gamma and nuclear factor-erythroid 2-related factor 2 in hypercholesterolemia-induced atherosclerosis. Free Radic Biol Med. 2014;70:174–81.
Research reported in this publication was supported by Arak University of Medical Sciences, Arak, Iran. We thanked Dr. Naghmeh Mirhosseini to scientifically review and revise the paper.
The present study was founded by a grant from the Vice Chancellor for Research, Arak University of Medical Sciences, in Iran.
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The primary data for this study is available from the authors on direct request.
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This study was considered exempt by the AUMS Institutional Review Board.
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