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    Magnesium homeostasis in cattle:
    absorption and excretion (2018)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Martens, Holger (WE 2)
    Leonhard-Marek, Sabine
    Röntgen, Monika
    Stumpff, Friederike (WE 2)
    Quelle
    Nutrition research reviews : NRR
    Bandzählung: 31
    Heftzählung: 1
    Seiten: 114 – 130
    ISSN: 0954-4224
    Sprache
    Englisch
    Verweise
    DOI: 10.1017/S0954422417000257
    Pubmed: 29318981
    Kontakt
    Institut für Veterinär-Physiologie

    Oertzenweg 19 b
    14163 Berlin
    +49 30 838 62600
    physiologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Magnesium (Mg2+) is an essential mineral without known specific regulatory mechanisms. In ruminants, plasma Mg2+ concentration depends primarily on the balance between Mg2+ absorption and Mg2+ excretion. The primary site of Mg2+ absorption is the rumen, where Mg2+ is apically absorbed by both potential-dependent and potential-independent uptake mechanisms, reflecting involvement of ion channels and electroneutral transporters, respectively. Transport is energised in a secondary active manner by a basolateral Na+/Mg2+ exchanger. Ruminal transport of Mg2+ is significantly influenced by a variety of factors such as high K+ concentration, sudden increases of ammonia, pH, and the concentration of SCFA. Impaired Mg2+ absorption in the rumen is not compensated for by increased transport in the small or large intestine. While renal excretion can be adjusted to compensate precisely for any surplus in Mg2+ uptake, a shortage in dietary Mg2+ cannot be compensated for either via skeletal mobilisation of Mg2+ or via up-regulation of ruminal absorption. In such situations, hypomagnesaemia will lead to decrease of a Mg2+ in the cerebrospinal fluid and clinical manifestations of tetany. Improved knowledge concerning the factors governing Mg2+ homeostasis will allow reliable recommendations for an adequate Mg2+ intake and for the avoidance of possible disturbances. Future research should clarify the molecular identity of the suggested Mg2+ transport proteins and the regulatory mechanisms controlling renal Mg excretion as parameters influencing Mg2+ homeostasis.