Arachidonate‐mediated bronchoconstriction and platelet activation are inhibited by microgram doses of compound L8027 which are not selective for thromboxane synthetase.
Shortly thereafter, we reported that infusing magnesium into healthy subjects reduced urinary thromboxane concentration and angiotensin II-induced plasma aldosterone levels; conversely, dietary induced magnesium deficiency led to increased thromboxane and aldosterone synthesis and decreased insulin sensitivity. Just this year, Rosolová and colleagues confirmed that magnesium deficiency decreases insulin-mediated glucose disposal in non-diabetic subjects, which is consistent with insulin resistance. There is, however, no consistent evidence supporting a direct effect of magnesium intake on glycemic control.
Magnesium deficiency is associated with insulin resistance and increased platelet reactivity, but studies of oral magnesium supplementation and changes in glycemic status or lipid levels in diabetes have not been conclusive. When my colleagues and I gave oral magnesium to 20 patients with type 2 diabetes, intracellular free magnesium concentration in erythrocytes normalized and the increase in platelet reactivity in response to thromboxanes decreased significantly. The oral dosage was 400 mg / d of elemental magnesium.