Manganese forms the core of an antioxidant superoxide dismutase enzyme, this one located inside the mitochondria, the intracellular organs where the Krebs cycle operates. It is a cofactor for enzymes involved in proteoglycan synthesis so central to the formation of cartilage and the connective tissue skeleton of bone. It is a cofactor in gluconeogensis (the manufacture of glucose by the liver) and in the release of insulin by the pancreas. It is involved as a catalyst in the metabolism and transformation of fats and proteins, including the synthesis of cholesterol.
Manganese is a poorly understood mineral, both in horses and humans. Reports of deficiencies are extremely rare. No naturally occurring manganese deficiencies have been reported for horses – which isn’t too surprising considering that it is very rarely deficient at baseline levels in hays and grains. Young animals are the most susceptible and the main symptom in the young is deformed bones. Low cholesterol and altered glucose metabolism may be seen in adults. These are probably the functions that depend heavily on manganese. Otherwise, other divalent cations (two positive charges,++) may substitute for manganese.
The relationship between iron and manganese is interesting. Iron (Fe++) can substitute for manganese (Mn++) in the superoxide dismutase enzyme. Manganese and iron compete for some absorption pathways in other species, although at the commonly found levels of iron and manganese naturally occurring in the equine diet this does not seem to be an issue. As above, inside the body iron may substitute for manganese in some situations. Manganese also has a strong affinity for ferritin, the protein that normally keeps ionized iron out of the circulation. Ionized iron is a very strong oxidizing agent (think of the body rusting from the inside out!). Because of the strong affinity for ferritin, manganese actually may worsen iron’s toxic effects by reducing the number of available binding sites on ferritin.
Manganese excess also disrupts iron sensing in liver cells, leading to overabsorption of iron and a pattern of elevated serum iron, elevated iron binding capacity, elevated transferrin saturation but normal ferritin (see blog on iron). I have seen this pattern in insulin resistant horses on high manganese diets.
In many areas of the country, no manganese supplementation is needed. The only way to confirm this is by diet analysis. If unsure of your status, at least make sure your supplement contains more zinc than manganese.
Eleanor M Kellon,VMD