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Insulin increases intracellular magnesium transport in human platelets
D L Hwang1, C F Yen, J L Nadler
1Department of Diabetes, Endocrinology and Metabolism, City of Hope National Medical Center, Duarte, California 91010.
The Journal of Clinical Endocrinology and Metabolism
|March 1, 1993
Summary
Insulin increases intracellular magnesium in human platelets via a receptor-mediated process, reducing platelet aggregation and thromboxane B2 production. This highlights insulin
Area of Science:
- Biochemistry
- Physiology
Background:
- Magnesium (Mg) deficiency is linked to cardiovascular disease and increased platelet aggregation.
- The regulation of intracellular-free Mg concentration ([Mg2+]i) in platelets remains unclear.
Purpose of the Study:
- To investigate the effect of insulin on intracellular-free Mg concentration ([Mg2+]i) in human platelets.
- To determine if insulin influences platelet aggregation and thromboxane B2 production.
Main Methods:
- Human platelets were incubated with varying concentrations of insulin.
- [Mg2+]i was measured using Mag-fura-2 and a fluorescence spectrophotometer.
- Platelet aggregation and thromboxane B2 production were assessed in response to insulin and thrombin.
Main Results:
- Insulin significantly increased [Mg2+]i in a dose- and time-dependent manner.
- The effect of insulin on [Mg2+]i was abolished by an anti-insulin receptor antibody, indicating receptor mediation.
- Insulin reduced thrombin-induced platelet aggregation and thromboxane B2 production.
Conclusions:
- Insulin plays a key role in regulating Mg transport in human platelets through its receptors.
- Insulin's ability to increase platelet Mg may contribute to its protective effects against cardiovascular events.
- Insulin modulates platelet function, potentially impacting thrombotic risk.