![]() The decrease in cellular ATP might partially explain the decrease in cellular Mg. The relationship between intracellular Mg and ATP concentration is rather complex. 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. Intracellular free Mg levels are consistently reduced in subjects with DM2, when compared with nondiabetic subjects. ![]() 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. We have recently confirmed that diabetic older patients are more prone to hypomagnesemia this condition being closely related to metabolic control as measured by glycated hemoglobin even after adjustment for relevant confounders. 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. A depletion in intracellular and/or ionized plasma Mg can be found in individuals with normal total serum Mg. However, hypomagnesemia, when present, is usually indicative of an important systemic Mg deficit. Mg deficiency can be present without hypomagnesemia. Mg concentrations ≤ 0.75 mmol/L or 1.8 mg/dL may be considered as preclinical hypomagnesemia. Patients are considered frankly hypomagnesemic with serum Mg concentrations ≤ 0.61 mmol/L or 1.5 mg/dL. Laboratory tests with a high sensitivity and specificity and easy to perform to allow an accurate clinical assessment of Mg status are missing. ![]() An increased prevalence of Mg deficits have 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. Type 2 diabetes mellitus (DM2) is often accompanied by alteration of Mg status. 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. ![]() The aim of this review is to revise current evidence on the mechanisms of Mg deficiency in diabetes and on the possible role of Mg supplementation in the prevention and management of the disease. Benefits of Mg supplementation on metabolic profiles in diabetic patients have been found in most, but not all clinical studies and larger prospective studies are needed to support the potential role of dietary Mg supplementation as a possible public health strategy in diabetes risk. Low dietary Mg intake has been related to the development of type 2 diabetes and metabolic syndrome. A low Mg intake and an increased Mg urinary loss appear the most important mechanisms that may favor Mg depletion in patients with type 2 diabetes. Reduced intracellular Mg concentrations result in a defective tyrosine-kinase activity, postreceptorial impairment in insulin action and worsening of insulin resistance in diabetic patients. Intracellular Mg plays a key role in regulating insulin action, insulin-mediated-glucose-uptake and vascular tone. Insulin and glucose are important regulators of Mg metabolism. A chronic latent Mg deficit or an overt clinical hypomagnesemia is common in patients with type 2 diabetes, especially in those with poorly controlled glycemic profiles. Type 2 diabetes is frequently associated with both extracellular and intracellular magnesium (Mg) deficits.
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