Effects of magnesium oxide on the lipid profile of healthy volunteers

Marken, Patricia A.; Weart, C. Wayne; Carson, Deborah Stier; Gums, John G.; Lopes‐Virella, Maria F.

doi:10.1016/0021-9150(89)90007-5

Cited by 30 publications

(17 citation statements)

References 24 publications

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“…Some (13-15) but not all (16,17) randomized trials indicated that magnesium supplementation can improve dyslipidemia and lower fasting insulin and glucose concentrations. A meta-analysis of 9 randomized trials in diabetes patients reported that 4-16 wk of magnesium supplementation was effective in reducing fasting glucose concentrations and raising HDL cholesterol concentrations but reported 1 Hb A 1c , glycated hemoglobin; hs-CRP, high-sensitivity C-reactive protein; IL-6, interleukin-6; TNF-a, tumor necrosis factor-a; sICAM-1, soluble intercellular adhesion molecule-1; sVCAM-1, soluble vascular cell adhesion molecule-1.…”

Section: Discussionmentioning

confidence: 99%

“…Because of limited and conflicting data from randomized clinical trials (13)(14)(15)(16)(17), whether magnesium supplementation can be effective in improving metabolic and inflammatory profiles in apparently healthy individuals at risk of metabolic abnormalities remains uncertain. Moreover, none of the few randomized studies have applied a systems-biology approach to examine the mechanistic effects of magnesium supplementation on gene expression and protein profiling.…”

Section: Introductionmentioning

confidence: 99%

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Magnesium supplementation, metabolic and inflammatory markers, and global genomic and proteomic profiling: a randomized, double-blind, controlled, crossover trial in overweight individuals

Chacko

Sul²,

Song³

et al. 2011

The American Journal of Clinical Nutrition

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Background: Dietary magnesium intake has been favorably associated with reduced risk of metabolic outcomes in observational studies; however, few randomized trials have introduced a systemsbiology approach to explore molecular mechanisms of pleiotropic metabolic actions of magnesium supplementation. Objective: We examined the effects of oral magnesium supplementation on metabolic biomarkers and global genomic and proteomic profiling in overweight individuals. Design: We undertook this randomized, crossover, pilot trial in 14 healthy, overweight volunteers [body mass index (in kg/m 2 ) 25] who were randomly assigned to receive magnesium citrate (500 mg elemental Mg/d) or a placebo for 4 wk with a 1-mo washout period. Fasting blood and urine specimens were collected according to standardized protocols. Biochemical assays were conducted on blood specimens. RNA was extracted and subsequently hybridized with the Human Gene ST 1.0 array (Affymetrix, Santa Clara, CA). Urine proteomic profiling was analyzed with the CM10 ProteinChip array (Bio-Rad Laboratories, Hercules, CA). Results: We observed that magnesium treatment significantly decreased fasting C-peptide concentrations (change: 20.4 ng/mL after magnesium treatment compared with +0.05 ng/mL after placebo treatment; P = 0.004) and appeared to decrease fasting insulin concentrations (change: 22.2 lU/mL after magnesium treatment compared with 0.0 lU/mL after placebo treatment; P = 0.25). No consistent patterns were observed across inflammatory biomarkers. Gene expression profiling revealed up-regulation of 24 genes and down-regulation of 36 genes including genes related to metabolic and inflammatory pathways such as C1q and tumor necrosis factorrelated protein 9 (C1QTNF9) and pro-platelet basic protein (PPBP). Urine proteomic profiling showed significant differences in the expression amounts of several peptides and proteins after treatment. Conclusion: Magnesium supplementation for 4 wk in overweight individuals led to distinct changes in gene expression and proteomic profiling consistent with favorable effects on several metabolic pathways. This trial was registered at clinicaltrials.gov as NCT00737815.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Magnesium supplementation, metabolic and inflammatory markers, and global genomic and proteomic profiling: a randomized, double-blind, controlled, crossover trial in overweight individuals

Chacko

Sul²,

Song³

et al. 2011

The American Journal of Clinical Nutrition

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“…18,19 The low serum magnesium levels are associated with coronary heart disease, 20,21 atherosclerosis, 22 dyslipidemia. 23,24 and high blood pressure. 22 These findings suggest that hypomagnesemia could be involved in the pathogenesis of cardiovascular disease, 22 insulin resistance, 25 -27 and type 2 diabetes.…”

Section: Introductionmentioning

confidence: 99%

Relationship between serum magnesium levels and C-reactive protein concentration, in non-diabetic, non-hypertensive obese subjects

Guerrero‐Romero

Rodrı́guez-Morán

2002

Int J Obes

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OBJECTIVE:To examine the association between serum magnesium levels and C-reactive protein (CRP) in non-diabetic, nonhypertensive obese subjects. DESIGN: Cross-sectional study. SUBJECTS: A total of 371 subjects, 101 men and 270 women. Of them 138 lean (37.2%), 133 (35.9%) overweight, and 100 (26.9%) were obese, matched by age. MEASUREMENTS: Fasting and 2 h serum glucose following a 75 g oral glucose load. Fasting serum total cholesterol, HDL-and LDL-cholesterol, triglycerides, C-reactive protein (CRP), albumin; and magnesium levels; urinary protein excretion; body mass index (BMI), waist-to-hip ratio (WHR), and blood pressure. RESULTS: The presence of CRP was documented in four (2.9%) lean, 13 (9.8%) overweight, and 20 (20.0%) obese subjects, and decreased magnesium levels (equal or less than 1.8 mg=dl), in 2 (1.45%) lean, 7 (5.2%) overweight, and 19 (19%) obese subjects. The lowest serum magnesium levels and the highest CRP concentrations were documented in the obese subjects. Twenty-three (82.1%) of the subjects with low serum magnesium (five overweight and 18 obese) showed CRP concentration equal or more than 10 mg=l. There was a graded significant decrease between CRP concentration and serum magnesium levels (r ¼ 70.39, P ¼ 0.002). The odds ratio (CI 95% ) between magnesium and CRP adjusted by age, sex, BMI and glucose tolerance status for the subjects within the low quartile of magnesium distribution was 2.11 (1.23 -3.84). CONCLUSION:The results of this study show that low serum magnesium levels are independently related to elevated CRP concentration, in non-diabetic, non-hypertensive obese subjects.

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“…In vitro studies have shown that increasing Mg concentration in the bathing solution attenuates HMGCoA reductase activity [54], and rats fed a Mg-deficient diet show increased serum triglycerides and reduced highdensity lipoprotein cholesterol, together with reduced serum activity of lipoprotein lipase [55]. Several other studies have examined the effect of Mg supplementation on lipid levels and have shown a reduction in serum triglyceride levels [56][57][58] or no effect on the lipids examined [59]. Visceral adiposity is another major component of the CMetS associated with a state of IR and impaired glucose tolerance [5, 6•, 7, 52].…”

Section: Magnesium Glucose Intolerance Insulin Resistance and Diabmentioning

confidence: 99%

Magnesium and the Cardiometabolic Syndrome

Barbagallo¹,

Domínguez²

2012

Curr Nutr Rep

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Effects of magnesium oxide on the lipid profile of healthy volunteers

Cited by 30 publications

References 24 publications

Magnesium supplementation, metabolic and inflammatory markers, and global genomic and proteomic profiling: a randomized, double-blind, controlled, crossover trial in overweight individuals

Magnesium supplementation, metabolic and inflammatory markers, and global genomic and proteomic profiling: a randomized, double-blind, controlled, crossover trial in overweight individuals

Relationship between serum magnesium levels and C-reactive protein concentration, in non-diabetic, non-hypertensive obese subjects

Magnesium and the Cardiometabolic Syndrome

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