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Magnesium (Mg) is an electrolyte of chief physiological importance in the body, being the most abundant divalent intracellular cation in the cells, the second most abundant cellular ion next to potassium and the fourth cation in general in the human body. Type 2 diabetes mellitus (DM2) is often accompanied by alteration of Mg status. An increased prevalence of Mg deficits has been identified in DM2 patients, especially in those with poorly controlled glycemic profiles, with longer duration of the disease and with the presence of micro- and macrovascular chronic complications[2-6]. Laboratory tests with high sensitivity and specificity and easy to perform to allow an accurate clinical assessment of Mg status are missing. Patients are considered frankly hypomagnesemic with serum Mg concentrations ≤ 0.61 mmol/L or 1.5 mg/dL[7-9]. Mg concentrations ≤ 0.75 mmol/L or 1.8 mg/dL may be considered as preclinical hypomagnesemia[10,11]. Mg deficiency can be present without hypomagnesemia. However, hypomagnesemia, when present, is usually indicative of an important systemic Mg deficit. A depletion in intracellular and/or ionized plasma Mg can be found in individuals with normal total serum Mg. However, most of the studies in the literature have measured total serum Mg instead of the free, ionized (bioactive) or the intracellular Mg concentrations, which make it a challenge to correlate Mg deficits to diseases. We have recently confirmed that diabetic older patients are more prone to hypomagnesemia; this condition is closely related to metabolic control as measured by glycated hemoglobin even after adjustment for relevant confounders. Ionized Mg may help to identify diabetic older adults with low concentrations of blood Mg that are not evident with the only measurement of total Mg. Intracellular free Mg levels are consistently reduced in subjects with DM2 when compared with nondiabetic subjects[1,13,14]. Although the mechanism has not been fully elucidated, an alteration in the mechanism(s) of the Mg uptake in the cells, and/or a deficit of ATP, may help to understand the cellular Mg deficit observed in DM2.