Abstract
Magnesium (Mg2+) is an essential mineral for human health and plays an important role in the regulation of glucose homeostasis and insulin actions. Despite the widespread clinical evidences for the association of Mg2+ deficiency (MgD) and type 2 diabetes mellitus (T2D), molecular mechanisms by which Mg2+ contributes to insulin resistance (IR) are still under discussion. Mg2+ regulates electrical activity and insulin secretion in pancreatic beta-cells. Intracellular Mg2+ concentrations are critical for the phosphorylation of the insulin receptor and other downstream signal kinases of the target cells. Low Mg2+ levels result in a defective tyrosine kinase activity, post-receptor impairment in insulin action, altered cellular glucose transport, and decreased cellular glucose utilization, which promotes peripheral IR in T2D. MgD triggers chronic systemic inflammation that also potentiates IR. People with T2D may end up in a vicious circle in which MgD increases IR and IR causes MgD, that requires periodic monitoring of serum Mg2+ levels.
Highlights
Insulin resistance (IR) is associated with an impaired biological response to insulin stimulation of key target tissues, liver, muscle, and adipose tissue
Oral supplementation with MgCl2 solution restores serum Mg2+ levels, improving insulin sensitivity and metabolic control in type 2 diabetes mellitus (T2D) patients with decreased serum Mg2+ levels
Mg2+ supplementation resulted in a significant improvement in fasting plasma glucose and insulin sensitivity in normomagnesemic, overweight non-diabetic subjects
Summary
Insulin resistance (IR) is associated with an impaired biological response to insulin stimulation of key target tissues, liver, muscle, and adipose tissue. Magnesium deficiency (MgD) is a condition where the serum concentration of Mg2+ in the body is ≤0.75 mmol/L (1.8 mg/dL) [6]. A number of factors can negatively affect Mg2+ balance in the body and, in the long-term, may result in MgD Such factors may be a decreased intake of Mg2+ from the food or drinking water [8], an increased Mg2+ loss through the kidneys [9,10], an impaired intestinal absorption of Mg2+ [11], and prolonged use of some medications causing hypomagnesemia [12,13,14]. Metabolism: Pancreatic beta-cell dysfunction, IR, decreased glucose tolerance, increased risk of MetS and T2D, dyslipoproteinemia, disorders of vitamin D metabolism, resistance to PTH, and osteoporosis.
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