1Institute for Veterinary Physiology,Freie Universität Berlin,Berlin,Germany.
2Department of Physiology,University of Veterinary Medicine,Foundation,Hannover,Germany.
Nutr Res Rev. 2018 Jun;31(1):114-130. doi: 10.1017/S0954422417000257. Epub 2018 Jan 10.
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.
镁（Mg2+）是一种必需的矿物质，没有已知的特定调节机制。在反刍动物中，血浆 Mg2+浓度主要取决于 Mg2+吸收和 Mg2+排泄之间的平衡。Mg2+吸收的主要部位是瘤胃，Mg2+通过电位依赖和非电位依赖的摄取机制在顶端被吸收，分别反映了离子通道和电中性转运体的参与。转运通过基底外侧 Na+/Mg2+交换器以继发性主动方式进行能量供应。瘤胃中 Mg2+的转运受到多种因素的显著影响，如高 K+浓度、氨、pH 值和 SCFA 浓度的突然增加。在肠道中，即使小或大肠中的转运增加，也不能补偿瘤胃中 Mg2+吸收受损。虽然肾脏排泄可以通过精确调节来补偿任何多余的 Mg2+摄取，但饮食中 Mg2+的不足既不能通过骨骼动员 Mg2+来补偿，也不能通过上调瘤胃吸收来补偿。在这种情况下，低镁血症会导致脑脊液中 Mg2+减少，并出现抽搐的临床症状。对调节 Mg2+稳态的因素有更好的了解，将有助于对充足的 Mg2+摄入和避免可能的紊乱做出可靠的建议。未来的研究应阐明建议的 Mg2+转运蛋白的分子特性和控制肾脏 Mg 排泄的调节机制，因为这些都是影响 Mg2+稳态的参数。
