Magnesium is an essential (macro) mineral in vertebrates with many biochemical and physiological functions including activation of enzymes, involvement into metabolic pathways, regulation of membrane channels and muscle contraction. Despite these important functions, Mg++ homeostasis is not regulated by hormones, but depends on absorption from the gastrointestinal tract, requirement of the body, and excretion via the kidneys. The present review summarizes data on epithelial Mg++ transport in the gut via paracellular and cellular pathways. Paracellular movement of Mg++ is only important in leaky epithelia as in the small intestine. The transcellular transport of Mg++, luminal uptake and basolateral extrusion, require membrane proteins which increase the low permeability of the membranes and facilitate the movement of Mg++ through these lipid bilayers. Proposals have been made how these proteins could mediate Mg++ transport. There is now a growing body of evidence for a PD-dependent luminal Mg++ uptake via a carrier or channel. Furthermore, PD-independent uptake mechanisms have been demonstrated which may be represented by Mg++/2cation+ exchange or co-transport of Mg++ with anions. The mechanism of a basolateral extrusion is not clear. A Na+/Mg++ exchange, well characterized in non-polar cells, has been suggested which leads to the proposal that there is a secondary active transport system for Mg++. It can readily be learned from this fragmentary knowledge of transepithelial Mg++ transport that future research must be directed to a study of the relevant membrane proteins (carriers or channel for Mg++) in order to close the gap between the incompletely described epithelial Mg++ transport mechanisms and the well established transport systems, e.g. , sodium or glucose.