Abstract
 juvenile diabetes mellitus
There is accumulating evidence that the metabolism of several trace
elements is altered in insulin-dependent diabetes mellitus and that these
nutrients might have specific roles in the pathogenesis and progress of this
disease. Magnesium deficiency is the most evident disturbance of metal
metabolism in diabetes mellitus. Hypomagnesemia might increase the risk of ischemic
heart disease and severe retinopathy. Increased urinary loss of zinc is a
commonly encountered feature of diabetes. High-dose oral zinc might enhance
wound healing, although data regarding diabetes are lacking. Chromium increases
tissue sensitivity to insulin and tends to raise high-density lipoprotein (HDL)
cholesterol and the HDL:low-density lipoprotein ratio. Selenium is involved in
processes which protect the cell against oxidative damage by peroxides produced
from lipid metabolism. There is one report of elevated serum selenium in
diabetic children although the clinical significance of this finding is still
unclear. An insulin-like effect has recently been attributed to vanadium in
experimental animals, a finding of potential interest to man. Current knowledge
does not implicate iron, iodine, manganese, cobalt, nickel, silicone, fluoride,
molybdenum or tin in the pathophysiology of diabetes. Appropriate trace element
supplementation might prove beneficial in ameliorating some physiological
deficiencies associated with diabetes and prevent or retard secondary
complications. However, properly designed and well-documented trials,
especially on magnesium supplementation, need to be performed before rationales
for such supplementation are developed. The potential roles of vanadium,
chromium and selenium in diabetes constitute challenging areas for further
experimental and clinical research.
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