1.
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.
Toprak, O, Kurt, H, Sarı, Y, Şarkış, C, Us, H, Kırık, A
Kidney & blood pressure research. 2017;(1):33-42
Abstract
BACKGROUND/AIMS: Magnesium is an essential mineral for many metabolic functions. There is very little information on the effect of magnesium supplementation on metabolic profiles of chronic kidney disease (CKD) patients. The aim of this study was to assess the influence of magnesium supplementation on metabolic profiles of pre-diabetic, obese and mild-to-moderate CKD patients with hypomagnesemia. METHODS A total of 128 hypomagnesemic, pre-diabetic and obese patients with an estimated glomerular filtration rate between 90 and 30 ml/min/1.73m2 were enrolled in a randomised, double-blind, placebo-controlled trial. Patients in the magnesium group received 365 mg of oral magnesium (n = 57) once daily for 3 months, while patients in the control group received a placebo (n = 61), also once daily for 3 months. Hypomagnesemia is defined by a serum magnesium level <1.8 mg/dl in males and <1.9 mg/dl in females; obesity is defined as a body mass index ≥30 kg/m2; and pre-diabetes is defined as fasting plasma glucose ≥100 but <126 mg/dl. The primary end point of the study was the change in insulin resistance measured by the homeostastic model assessment for insulin resistance (HOMA-IR). RESULTS At the end of follow-up, insulin resistance (-24.5 vs. -8.2%, P = 0.007), HOMA-IR index (-31.9 vs. -3.3%, P < 0.001), hemoglobin A1c (-6.6 vs. -0.16%, P < 0.001), insulin (-29.6 vs. -2.66%, P < 0.001), waist circumference (-4.8 vs. 0.55%, P < 0.001) and uric acid (-0.8 vs. 2.2%, P = 0.004) were significantly decreased in terms of mean changes; albumin (0.91 vs. -2.91%, P = 0.007) and magnesium (0.21 ± 0.18 vs. -0.04 ± 0.05 mg/dl, P < 0.001) were significantly increased in those taking magnesium compared with a placebo. The decrease in metabolic syndrome (-10.5 vs. -4.9%, P = 0.183), obesity (-15.7 vs. -8.2%, P = 0.131), pre-diabetes (-17.5 vs. -9.8%, P = 0.140), and systolic (-5.0 ± 14.8 vs. 0.22 ± 14.9 mm Hg, P = 0.053) and diastolic (-3.07 ± 9.7 vs. 0.07 ± 9.6 mm Hg, P = 0.071) blood pressure did not achieve to a significant level after study. CONCLUSION Our data support the argument that magnesium supplementation improves the metabolic status in hypomagnesemic CKD patients with pre-diabetes and obesity.
2.
Dietary magnesium intake improves insulin resistance among non-diabetic individuals with metabolic syndrome participating in a dietary trial.
Wang, J, Persuitte, G, Olendzki, BC, Wedick, NM, Zhang, Z, Merriam, PA, Fang, H, Carmody, J, Olendzki, GF, Ma, Y
Nutrients. 2013;(10):3910-9
Abstract
Many cross-sectional studies show an inverse association between dietary magnesium and insulin resistance, but few longitudinal studies examine the ability to meet the Recommended Dietary Allowance (RDA) for magnesium intake through food and its effect on insulin resistance among participants with metabolic syndrome (MetS). The dietary intervention study examined this question in 234 individuals with MetS. Magnesium intake was assessed using 24-h dietary recalls at baseline, 6, and 12 months. Fasting glucose and insulin levels were collected at each time point; and insulin resistance was estimated by the homeostasis model assessment (HOMA-IR). The relation between magnesium intake and HOMA-IR was assessed using linear mixed models adjusted for covariates. Baseline magnesium intake was 287 ± 93 mg/day (mean ± standard deviation), and HOMA-IR, fasting glucose and fasting insulin were 3.7 ± 3.5, 99 ± 13 mg/dL, and 15 ± 13 μU/mL, respectively. At baseline, 6-, and 12-months, 23.5%, 30.4%, and 27.7% met the RDA for magnesium. After multivariate adjustment, magnesium intake was inversely associated with metabolic biomarkers of insulin resistance (P < 0.01). Further, the likelihood of elevated HOMA-IR (>3.6) over time was 71% lower [odds ratio (OR): 0.29; 95% confidence interval (CI): 0.12, 0.72] in participants in the highest quartile of magnesium intake than those in the lowest quartile. For individuals meeting the RDA for magnesium, the multivariate-adjusted OR for high HOMA-IR over time was 0.37 (95% CI: 0.18, 0.77). These findings indicate that dietary magnesium intake is inadequate among non-diabetic individuals with MetS and suggest that increasing dietary magnesium to meet the RDA has a protective effect on insulin resistance.