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

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

Front Nutr

Department of Medical Education, School of Medicine, University of Texas (UTRGV), Edinburg, TX, United States.

Published: September 2024

AI Article Synopsis

  • Magnesium is crucial for glucose utilization and insulin signaling; low levels can lead to issues such as insulin resistance and β-cell dysfunction, particularly in diabetics.
  • Research shows that magnesium deficiency leads to reduced pancreatic β-cell activity and worsens insulin resistance in type 2 diabetes patients.
  • Maintaining sufficient magnesium levels is important for overall health and can help prevent metabolic disorders like type 2 diabetes by supporting insulin secretion and other cellular functions.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11463151PMC
http://dx.doi.org/10.3389/fnut.2024.1458700DOI Listing

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