Intracellular magnesium of platelets in children with diabetes and obesity.

Magnesium (Mg(2+)), the second most abundant intracellular cation, is a critical cofactor in numerous enzymatic reactions. By using a fluorescent probe, mag-fura-2, we examined the basal levels and changes in intracellular Mg(2+)([Mg(2+)](i)) of platelets in diabetic and obese children. Under the basal condition, the platelet [Mg(2+)](i) of both type 1 and type 2 diabetes mellitus (DM) and the obesity groups was significantly lower than the values in the nondiabetic control group (377 +/- 62 micromol/L, 312 +/- 72 micromol/L, 373 +/- 35 micromol/L v 594 +/- 62 micromol/L, respectively, P <.05). [Mg(2+)](i) was increased after the stimulation with 100 microU/mL of insulin. After 60 seconds of insulin stimulation, the value of [Mg(2+)](i) was lower in the type 1 DM group compared with the control group (729 +/- 85 micromol/L v 1,078 +/- 67 micromol/L, P <.005). The increase in percentage over the resting [Mg(2+)](i) was higher in the type 2 DM group than in the stimulated control group (222% +/- 51% v 98% +/- 18 %, P <.05), although the stimulated [Mg(2+)](i) did not reach the level of the control group. The diabetic patients and obese subjects have [Mg(2+)](i) deficiency. In the type 2 DM and obese groups, platelets responded well to insulin. In children under insulin-resistant states, [Mg(2+)](i) decreases before the poor reactivity to insulin occurs in platelets. Decreased [Mg(2+)](i) might underlie the initial pathophysiologic events leading to insulin resistance and abnormality of platelet coagulation.