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Intracellular free magnesium deficiency plays a key role in increased platelet reactivity in type II diabetes
J L Nadler1, S Malayan, H Luong
1Department of Diabetes, Endocrinology and Metabolism, City of Hope National Medical Center, Duarte, California 91010.
Objective:
Mg deficiency may be an important factor leading to cardiovascular disease. Diabetic subjects show an increase in platelet reactivity that can enhance the risks of vascular disease. In addition, diabetic patients have been reported to be at risk of developing extracellular Mg deficiency. However, the intracellular free Mg concentration and its role in the enhanced platelet reactivity in diabetes is not known.
Research Design And Methods:
We evaluated the intracellular erythrocyte (RBC) Mg2+ concentration in 20 non-insulin-dependent (type II) diabetics. In addition, the effects of intravenous 3-h drip or 8 wk of oral Mg supplementation on intracellular RBC Mg2+ levels and platelet reactivity was studied. To more clearly evaluate the direct role of Mg in these effects, we induced isolated Mg deficiency in 16 nondiabetic control subjects with an Mg-free liquid diet for 3 wk.
Results:
The intracellular RBC Mg2+ concentration of diabetic patients was significantly reduced compared with values in nondiabetic control subjects (166 +/- 7 vs. 204 +/- 7 microM, P less than 0.01). Serum Mg levels were also reduced in the diabetic patients compared with the control subjects (1.59 +/- 0.04 vs. 1.9 +/- 0.1 mEq/L, P less than 0.05). Oral Mg supplementation for 8 wk (400 mg/day) restored RBC Mg2+ concentration to normal without significantly changing serum Mg concentration. Both intravenous and oral Mg supplementation markedly reduced platelet reactivity in response to the thromboxane A2 analog, U46619. The Mg-free diet resulted in a significant reduction in RBC Mg2+ concentration and markedly enhanced the sensitivity of platelet aggregation to U46619 and ADP.
Conclusions:
These results suggest that type II diabetic patients have intracellular Mg2+ deficiency and that Mg deficiency may be a key factor in leading to enhanced platelet reactivity in type II diabetes. Therefore, Mg supplementation may provide a new therapeutic approach to reducing vascular disease in patients with diabetes.
Insights
Type II diabetes is linked to lower intracellular magnesium (Mg) levels, increasing platelet reactivity and vascular disease risk. Mg supplementation can reduce this reactivity, offering a potential therapeutic strategy.
Area of Science:
- Cardiovascular Research
- Endocrinology
- Metabolic Disorders
Background:
- Magnesium (Mg) deficiency is implicated in cardiovascular disease.
- Diabetic patients exhibit increased platelet reactivity, elevating vascular disease risks.
- Diabetics are prone to extracellular Mg deficiency, but intracellular Mg levels and their role in platelet reactivity remain unclear.
Purpose of the Study:
- To evaluate intracellular erythrocyte (RBC) Mg2+ concentration in type II diabetics.
- To investigate the effects of Mg supplementation on RBC Mg2+ levels and platelet reactivity.
- To assess the direct role of Mg in platelet function by inducing Mg deficiency.
Main Methods:
- Intracellular RBC Mg2+ levels were measured in 20 type II diabetics and compared to controls.
- Mg supplementation (intravenous or oral) effects on RBC Mg2+ and platelet reactivity were studied.
- Controlled Mg deficiency was induced in 16 non-diabetic subjects using an Mg-free diet.
Main Results:
- Diabetic patients showed significantly lower intracellular RBC Mg2+ (166 +/- 7 microM) versus controls (204 +/- 7 microM).
- Oral Mg supplementation normalized RBC Mg2+ levels and reduced platelet reactivity.
- Induced Mg deficiency reduced RBC Mg2+ and enhanced platelet aggregation sensitivity.
Conclusions:
- Type II diabetic patients exhibit intracellular Mg2+ deficiency.
- Mg deficiency is a potential key factor in the enhanced platelet reactivity observed in type II diabetes.
- Mg supplementation may represent a novel therapeutic approach for reducing vascular disease in diabetic patients.