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Review
. 2024 Sep 25:11:1458700.
doi: 10.3389/fnut.2024.1458700. eCollection 2024.

The role of magnesium in pancreatic beta-cell function and homeostasis

Nuraly S Akimbekov  1   2 , Seval Ozkan Coban  3 , Azeddine Atfi  4 , Mohammed S Razzaque  3
Affiliations
Review

The role of magnesium in pancreatic beta-cell function and homeostasis

Nuraly S Akimbekov et al. Front Nutr. .

Abstract

Magnesium plays an essential role in glucose utilization and insulin signaling. Recent advances have revealed a greater prevalence of hypomagnesemia in general, and low intracellular magnesium levels in individuals with diabetes contribute to β-cell dysfunction and insulin resistance. This article describes the documented effects of magnesium on various aspects of β-cells and glucose homeostasis. Studies have demonstrated that magnesium deficiency is associated with reduced pancreatic β-cell activity and increased insulin resistance in patients with type 2 diabetes. Additionally, magnesium is involved in many cellular events, including energy homeostasis, protein synthesis, and DNA stability. Furthermore, magnesium is critical for proper glucose utilization and insulin signaling, and magnesium deficiency can lead to the dysregulation of ATP-sensitive potassium (KATP) channels in pancreatic β-cells, impairing insulin secretion. Therefore, maintaining adequate magnesium levels is crucial for maintaining overall health and preventing of metabolic disorders such as type 2 diabetes.

Keywords: diabetes; glucose; insulin; magnesium; β-cells.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Figures

Figure 1
Figure 1
Simplified outlines of the complex dual role of magnesium in insulin secretion from pancreatic β-cells. Intracellular Mg2+ enhances the activity of key enzymes [glucokinase (GCK), phosphofructokinase, pyruvate kinase, and Krebs cycle enzymes], and elevated enzyme activity increases ATP levels; increased ATP inhibits ATP-dependent potassium (KATP) channels. This leads to cell membrane depolarization and Ca2+ influx through L-type channels. In addition, Mg2+ competitively inhibits L-type Ca2+ channels, potentially reducing insulin release. Mg2+ may also alter the expression of GLUT2 and L-type Ca2+ channel genes (7, 34).
Figure 2
Figure 2
Magnesium acts as a cofactor for the functionality of rate-limiting enzymes, including phosphoenolpyruvate carboxykinase (PEPCK), fructose-1,6-bisphosphatase (FBP1) and pyruvate carboxylase (PC), during gluconeogenesis. Magnesium is also an important regulator of enzymes involved in the glycolysis pathway, including hexokinase, phosphofructokinase (PFK1), and pyruvate kinase (PK). Magnesium inadequacy can impair the enzymatic activities to affect glucose homeostasis (–48).
Figure 3
Figure 3
Partial list of the wide range of health-promoting functions of magnesium.
See this image and copyright information in PMC

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