ABSTRACT
Nickel is generally considered to be an essential trace element. It is subject to homeostatic regulation and mobilization in response to disease and physiological stress, and its absence or lack in the mammalian organism produces well-defined deficiency symptoms (1). A number of critical physiological functions are clearly dependent on the metal-notably the metabolism of carbohydrates, as nickel titers were seen to rise in parallel with insulin following glucose intake in humans. Conversely, the liver could not build glycogen stores in a state of nickel deficiency (2,3).
