<<snip>>
this association is not restricted to insulin resistance in type 2
diabetes, but is also evident in obese, nondiabetic individuals, and in
those patients with the metabolic syndrome
<<snip>>
The molecular basis for oxidative stress-induced insulin resistances.
Evans JL, Maddux BA, Goldfine ID
Antioxid Redox Signal. 2005 Jul-Aug ; 7(7-8): 1040-52
Reactive oxygen and nitrogen molecules have been typically viewed as
the toxic by-products of metabolism. However, accumulating evidence has
revealed that reactive species, including hydrogen peroxide, serve as
signaling molecules that are involved in the regulation of cellular
function. The chronic and/or increased production of these reactive
molecules or a reduced capacity for their elimination, termed oxidative
stress, can lead to abnormal changes in intracellular signaling and
result in chronic inflammation and insulin resistance. Inflammation and
oxidative stress have been linked to insulin resistance in vivo. Recent
studies have found that this association is not restricted to insulin
resistance in type 2 diabetes, but is also evident in obese,
nondiabetic individuals, and in those patients with the metabolic
syndrome. An increased concentration of reactive molecules triggers the
activation of serine/threonine kinase cascades such as c-Jun N-terminal
kinase, nuclear factor-kappaB, and others that in turn phosphorylate
multiple targets, including the insulin receptor and the insulin
receptor substrate (IRS) proteins. Increased serine phosphorylation of
IRS reduces its ability to undergo tyrosine phosphorylation and may
accelerate the degradation of IRS-1, offering an attractive explanation
for the molecular basis of oxidative stress-induced insulin resistance.
Consistent with this idea, studies with antioxidants such as vitamin E,
alpha-lipoic acid, and N-acetylcysteine indicate a beneficial impact on
insulin sensitivity, and offer the possibility for new treatment
approaches for insulin resistance.
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