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Magnesium increases insulin-dependent glucose uptake in adipocytes
Lynette J Oost1, Steef Kurstjens1,2, Chao Ma1,3
1Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, Netherlands.
Frontiers in Endocrinology
|September 12, 2022
Summary
Magnesium (Mg2+) deficiency is linked to insulin resistance in type 2 diabetes. Low Mg2+ impairs glucose uptake in fat cells by reducing Akt activation and GLUT4 transporter movement.
Area of Science:
- Biochemistry
- Cell Biology
- Endocrinology
Background:
- Type 2 diabetes (T2D) is marked by reduced insulin sensitivity.
- Magnesium (Mg2+) deficiency is prevalent in T2D patients.
- The molecular impact of low Mg2+ on adipocyte insulin sensitivity and glucose metabolism remains unclear.
Purpose of the Study:
- To investigate the association between plasma Mg2+ levels and insulin resistance markers in T2D.
- To elucidate the molecular role of Mg2+ in insulin-dependent glucose uptake in adipocytes.
Main Methods:
- Assessed plasma Mg2+ in 395 T2D patients.
- Utilized 3T3-L1 adipocytes treated with varying Mg2+ concentrations.
- Employed radioactive-glucose labeling, enzymatic assays, immunocytochemistry, live microscopy, and Seahorse analysis.
Main Results:
- Lower plasma Mg2+ correlated with increased insulin resistance in T2D.
- Mg2+-deficient adipocytes showed a ~50% reduction in insulin-dependent glucose uptake.
- Reduced Akt activation (via FoxO1 translocation) and diminished GLUT4 transporter translocation were observed in Mg2+-deficient cells.
- Glycolysis was decreased in Mg2+-deficient adipocytes upon insulin stimulation.
Conclusions:
- Mg2+ enhances insulin-dependent glucose uptake in adipocytes.
- Mg2+ deficiency may be a contributing factor to insulin resistance in type 2 diabetes.
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