Hypomagnesemia and coagulation disorders are prevalent among diabetic patients, particularly in individuals with type 2 diabetes, and magnesium deficiency elevates thrombotic risk.
Magnesium is an essential human nutrient. Serving as a cofactor for approximately 600 enzymes and an activator for 200 enzymes, it plays critical roles in maintaining sodium, potassium, and calcium homeostasis, as well as in the formation, transfer, and utilization of adenosine triphosphate (ATP). Additionally, magnesium modulates the coagulation cascade by competing with calcium ions. In vitro experiments demonstrate its anticoagulant properties, and magnesium sulfate is routinely used as an anticoagulant in blood collection procedures.
Furthermore, magnesium homeostasis is closely linked to insulin metabolism. Insulin promotes magnesium reabsorption by regulating the activity of TRPM6 channels in the distal convoluted tubule, while magnesium participates in insulin secretion and signal transduction. Previous studies confirm that plasma magnesium levels in patients with type 1 diabetes mellitus (T1DM) are significantly lower than healthy controls and inversely correlated with glycemic control.
Regarding vascular complications, hypomagnesemia exacerbates diabetes-associated vasculopathy by disrupting inositol transport, elevating inflammatory cytokine levels, and accelerating advanced glycation end product (AGE) formation. Plasminogen activator inhibitor-1 (PAI-1), a key antifibrinolytic factor, is strongly associated with increased thrombotic risk when elevated.