Magnesium and Type 2 Diabetes: A Vicious Circle

doi: 10.2337/db15-1028
Diabetes January 2016 vol. 65 no. 1 3-13

Hypomagnesemia in Type 2 Diabetes: A Vicious Circle?

Lisanne M.M. Gommers1, Joost G.J. Hoenderop1, René J.M. Bindels1 and Jeroen H.F. de Baaij1,2⇑

Author Affiliations

1Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands

2Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, U.K.

Corresponding author: Jeroen H.F. de Baaij, jeroen.debaaij@radboudumc.nl.

Abstract

Over the past decades, hypomagnesemia (serum Mg2+ <0.7 mmol/L) has been strongly associated with type 2 diabetes mellitus (T2DM).

Patients with hypomagnesemia show a more rapid disease progression and have an increased risk for diabetes complications.

Clinical studies demonstrate that T2DM patients with hypomagnesemia have reduced pancreatic β-cell activity and are more insulin resistant.

Moreover, dietary Mg2+ supplementation for patients with T2DM improves glucose metabolism and insulin sensitivity.

Intracellular Mg2+ regulates glucokinase, KATP channels, and L-type Ca2+ channels in pancreatic β-cells, preceding insulin secretion.

Moreover, insulin receptor autophosphorylation is dependent on intracellular Mg2+ concentrations, making Mg2+ a direct factor in the development of insulin resistance.

Conversely, insulin is an important regulator of Mg2+ homeostasis.

In the kidney, insulin activates the renal Mg2+ channel transient receptor potential melastatin type 6 that determines the final urinary Mg2+ excretion.

Consequently, patients with T2DM and hypomagnesemia enter a vicious circle in which hypomagnesemia causes insulin resistance and insulin resistance reduces serum Mg2+ concentrations.

This Perspective provides a systematic overview of the molecular mechanisms underlying the effects of Mg2+ on insulin secretion and insulin signaling.

In addition to providing a review of current knowledge, we provide novel directions for future research and identify previously neglected contributors to hypomagnesemia in T2DM.

  • Received July 24, 2015.
  • Accepted September 10, 2015.

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