Magnesium absorption mechanisms
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Magnesium Absorption Mechanisms: Intestinal and Renal Pathways
Intestinal Magnesium Absorption Mechanisms
Magnesium (Mg) absorption in the intestine occurs through two main pathways: passive paracellular transport and active transcellular transport. The majority of Mg absorption—up to 90%—takes place via the paracellular route, where Mg moves between cells through tight junctions formed by claudin proteins, especially claudin-2 and claudin-12 in the small intestine. This process is largely unregulated and depends on the concentration gradient of Mg in the intestinal lumen, making it a form of passive diffusion or solvent drag 124710.
At lower dietary Mg intakes, a saturable, active transcellular mechanism becomes more important. This involves specific Mg channels, such as TRPM6 and TRPM7, which are especially active in the distal small intestine and colon. These channels allow Mg to move directly through the cells, and their activity can be regulated by hormones and other factors 2410.
Regulation and Influencing Factors in Intestinal Absorption
Several factors influence intestinal Mg absorption. Vitamin D can increase Mg absorption, particularly in cases of deficiency, but a significant portion of Mg absorption occurs independently of vitamin D. Interactions with other minerals, such as calcium and phosphate, can also affect Mg absorption, though the exact mechanisms are not fully understood. Additionally, factors like parathyroid hormone, fibroblast growth factor-23, intestinal pH, and the presence of certain medications (e.g., proton pump inhibitors) can modulate Mg uptake 14.
The efficiency of Mg absorption decreases as intake increases, indicating a combination of saturable (active) and non-saturable (passive) mechanisms. At high intakes, passive diffusion dominates, while at low intakes, the active, saturable process is more significant 12679.
Renal Magnesium Reabsorption Mechanisms
After absorption from the intestine, Mg is filtered by the kidneys, where its reabsorption is crucial for maintaining serum Mg levels. In the kidney, Mg reabsorption occurs mainly through paracellular pathways in the proximal tubule and thick ascending limb, mediated by claudin-16 and claudin-19. Fine-tuning of Mg reabsorption happens in the distal convoluted tubule (DCT), where transcellular uptake is facilitated by TRPM6/7 channels. The activity of these channels is regulated by hormones such as insulin and epidermal growth factor, as well as by the NaCl cotransporter 35810.
Basolateral extrusion of Mg from kidney cells into the blood is thought to depend on the sodium gradient, with proteins like CNNM2 and SLC41A3 acting as Na+-Mg2+ exchangers. Disruptions in these processes can lead to Mg loss and hypomagnesemia 35810.
Conclusion
Magnesium absorption is a complex process involving both passive and active mechanisms in the intestine, with regulation by dietary intake, hormones, and other minerals. The kidney further fine-tunes Mg balance through specialized transport pathways. Understanding these mechanisms is essential for managing conditions related to Mg deficiency and for developing targeted therapies.
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