The relationship between diabetes, insulin and zinc (Zn) is complex wi
th no clear cause and effect relationships. In Type 1 diabetes there i
s a lack of insulin production, in Type 2 diabetes resistance to the e
ffects of insulin are predominant. Both Type 1 and Type 2 have the sam
e long-term complications. Diabetes effects zinc homeostasis in many w
ays, although it is most probably the hyperglycemia, rather than any p
rimary lesion related to diabetes, which is responsible for the increa
sed urinary loss and decreases in total body zinc. The role of Zn defi
ciency, which could, at least potentially, exacerbate the cytokine-ind
uced damage in the autoimmune attack which destroys the islet cell in
Type 1 diabetes, is unclear. Since Zn plays a clear role in the synthe
sis, storage and secretion of insulin as well as conformational integr
ity of insulin in the hexameric form, the decreased Zn, which affects
the ability of the islet cell to produce and secrete insulin, might th
en compound the problem, particularly in Type 2 diabetes. Several of t
he complications of diabetes may be related to increased intracellular
oxidants and free radicals associated with decreases in intracellular
Zn and in Zn dependent antioxidant enzymes. There appears to be a com
plex interrelationship between Zn and both Type 1 and Type 2 diabetes.
The role of Zn in the clinical management of diabetes, its complicati
ons, or in its prevention is, at best, unclear.