Magnesium is an essential (macro) mineral in vertebrates with many biochemi
cal and physiological functions including activation of enzymes, involvemen
t into metabolic pathways, regulation of membrane channels and muscle contr
action. Despite these important functions, Mg++ homeostasis is not regulate
d by hormones, but depends on absorption from the gastrointestinal tract, r
equirement of the body, and excretion via the kidneys. The present review s
ummarizes data on epithelial Mg++ transport in the gut via paracellular and
cellular pathways. Paracellular movement of Mg++ is only important in leak
y 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 pr
oteins could mediate Mg++ transport. There is now a growing body of evidenc
e for a PD-dependent luminal Mg++ uptake via a carrier or channel. Furtherm
ore, PD-independent uptake mechanisms have been demonstrated which may be r
epresented 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 nonpolar cells, has been suggested which leads to t
he proposal that there is a secondary active transport system for Mg++. It
can readily be learned from this fragmentary knowledge of transepithelial M
g++ transport that future research must be directed to a study of the relev
ant 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.