Serum and intracellular magnesium deficiency in patients with metabolic syndrome—Evidences for its relation to insulin resistance Maria de Lourdes Lima a,b, *, Thomaz Cruz a , Luiz Erlon Rodrigues b , Olı ´via Bomfim b , Juliana Melo b , Raquel Correia b , Mirna Porto b , Alexandre Cedro b , Elie ´zer Vicente c a Department of Medicine, and Post Graduate Program in Medicine and Health, Faculty of Medicine, Federal University of Bahia, Brazil b Bahiana School of Medicine and Public Health, FBDC, Salvador, Bahia, Brazil c Endocrinology and Genetics Center (ENDOGENE), Salvador, Bahia, Brazil 1. Introduction Magnesium (Mg) is primarily found within the cell, where it is a metallic cofactor for over 300 enzymatic reactions involved in protein and nucleic acid synthesis and in energy metabolism [1]. It is necessary for glucose transportation between membranes, glucose oxidation, all reactions invol- ving phosphorylation and energy exchange, and it is essential for insulin action, since it is a cofactor of tyrosine kinase activity [2]. Less than 1% of the total body Mg is present in blood, 1/3 binding with protein, and 2/3 in ionized form; thus serum Mg (SMg) does not provide reliable information about total or intracellular magnesium concentration [3]. One of the reasons for magnesium metabolism not becoming routinely investigated is the fact that there is no diabetes research and clinical practice 83 (2009) 257–262 article info Article history: Received 15 May 2008 Received in revised form 9 November 2008 Accepted 13 November 2008 Published on line 4 January 2009 Keywords: Metabolic Syndrome Magnesium Insulin Resistance abstract This cross sectional study evaluated serum (SMg) and intramononuclear (MMg) magnesium in patients with metabolic syndrome without diabetes and correlated them with cardio- vascular risk factors. 72 patients and 57 controls (blood donors) were studied. Hypomagne- semia (SMg < 1.7 mg/dL) was seen in 23.2% and intracellular depletion in 36.1% of the patients. SMg and MMg means were significantly lower in patients than in controls: 1.80  0.18 mg/dL vs. 2.43  0.43 mg/dL and 0.98  0.55 mg/mg vs. 1.67  0.64 mg/mg of pro- tein (P < 0.001). Inverse correlation was observed between, SMg and MMg with BMI; SMg with systolic blood pressure and waist circumference in women. Patients with acanthosis nigricans had lower SMg (1.75  0.18 mg/dL vs. 1.85 0.18 mg/dL, P < 0.05). Non-white people had lower SMg (1.78  0.16 mg/dL vs. 1.92  0.24 mg/dL, P = 0.007) and MMg (0.95  0.59 mg/mg vs. 1.13  0.42 mg/mg, P = 0.03). Patients with IR showed lower MgM means (0.84  0.33 mg/mg vs. 1.14  0.69 mg/mg, P < 0.05). The same occurred in patients with low HDL-c levels (0.92  0.46 mg/mg vs. 1.20  0.70 mg/mg, P = 0.03), and those with moderate and severe hepatic steatosis (0.77  0.29 mg/mg vs. 1.21  0.80 mg/mg, P < 0.05). In conclusion, magnesium depletion in serum and mononuclear cells is common in obese people with metabolic syndrome, and it is more evident in non-white people with insulin resistance. This depletion may contribute to a post-receptor insulin resistance. # 2008 Elsevier Ireland Ltd. All rights reserved. * Corresponding author at: Rua Coronel Athur Gomes de Carvalho, 537/402-Pituba, Salvador, Bahia 41.810-640, Brazil. Tel.: +55 71 3359 0760; fax: +55 71 3355 0171. E-mail address: mlourdeslima@hotmail.com (M.d.L. Lima). Contents lists available at ScienceDirect Diabetes Research and Clinical Practice journal homepage: www.elsevier.com/locate/diabres 0168-8227/$ – see front matter # 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.diabres.2008.11.019