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Magnesium is an essential mineral that is not regulated by hormones. The blood Mg concentration under steady state conditions depends on Mg influx (absorption) > Mg efflux (growth, milk secretion, endogenous secretion). A surplus of Mg (influx > efflux) is excreted by the kidneys and is related to the difference between influx minus requirement.
The main and essential site of absorption for Mg (influx) homeostasis is the rumen, where Mg is absorbed by an active transport mechanism including an apical PD-dependent and a PD-independent uptake mechanism. This transport mechanism represents Mg influx and is probably not regulated but is influenced by a variety of factors such as high K concentration, sudden increase of ammonia, pH (solubility of Mg), and SCFA. Possible impaired Mg absorption in the rumen is not compensated by increased transport in the small or large intestine.
The kidney has the capability for fine tuning the surplus of Mg by regulated excretion with the urine adjusted to requirement. However, a shortage of Mg can hardly be compensated because Mg cannot be mobilized from bone or by increased absorption from the rumen.
Hypomagnesemia (influx < efflux) is causing the clinical complex tetany. A growing body of evidence indicates that a subclinical deficiency of Mg is involved in the pathogenesis of milk fever.
Meta-analysis of Mg digestibility permits the calculation of Mg requirements, and the characteristics of Mg transport explain the variations in this calculation.
The recommendations for Mg intake with diet are suggested to be too low.
The framework including the functions of Mg, the principles of Mg homeostasis, and the meta-analysis of Mg digestibility allows sufficient understanding for the proposal of reliable recommendations for an adequate Mg intake in the diet according to actual requirements and for the avoidance of possible disturbances.