Abstract
Magnesium (Mg2+), 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 Mg2+([Mg2+]i) of platelets in diabetic and obese children. Under the basal condition, the platelet [Mg2+]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 μmol/L, 312 ± 72 μmol/L, 373 ± 35 μmol/L v 594 ± 62 μmol/L, respectively, P <.05). [Mg2+]i was increased after the stimulation with 100 μU/mL of insulin. After 60 seconds of insulin stimulation, the value of [Mg2+]i was lower in the type 1 DM group compared with the control group (729 ± 85 μmol/L v 1,078 ± 67 μmol/L, P <.005). The increase in percentage over the resting [Mg2+]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 [Mg2+]i did not reach the level of the control group. The diabetic patients and obese subjects have [Mg2+]i deficiency. In the type 2 DM and obese groups, platelets responded well to insulin. In children under insulin-resistant states, [Mg2+]i decreases before the poor reactivity to insulin occurs in platelets. Decreased [Mg2+]i might underlie the initial pathophysiologic events leading to insulin resistance and abnormality of platelet coagulation. Copyright 2003 Elsevier, Inc. All rights reserved.
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