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Oxidative stress is an acknowledged pathogenetic mechanism in diabetic complications.
Hyperglycemia is a widely known cause of enhanced free radical concentration, whereas
oxidative stress involvement in glycemic regulation is still debated. Glucose transport
is a cascade of events starting from the interaction of insulin with its own receptor
at the plasma membrane and ending with intracellular glucose metabolism. In this complex
series of events, each step plays an important role and can be inhibited by a negative
effect of oxidative stress. Several studies show that an acute increase in the blood
glucose level may impair the physiological homeostasis of many systems in living organisms.
The mechanisms through which acute hyperglycemia exerts these effects may be identified
in the production of free radicals. It has been suggested that insulin resistance
may be accompanied by intracellular production of free radicals. In adipocytes cultured
in vitro, insulin increases the production of hydrogen peroxide, which has been shown
to mimic the action of insulin. These data allow us to hypothesize that a vicious
circle between hyperinsulinemia and free radicals could be operating: insulin resistance
might cause elevated plasma free radical concentrations, which, in turn, might be
responsible for a deterioration of insulin action, with hyperglycemia being a contributory
factor. Data supporting this hypothesis are available. Vitamin E improves insulin
action in healthy, elderly, and non-insulin-dependent diabetic subjects. Similar results
can be obtained by vitamin C administration.
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© 2000 W.B. Saunders Company. All rights reserved. Published by Elsevier Inc.
