on February 19, 2004
Arteriosclerosis, Thrombosis, and Vascular Biology. 2004
Published online before print February 19, 2004, doi: 10.1161/01.ATV.0000122852.22604.78
Published online before print February 19, 2004, doi: 10.1161/01.ATV.0000122852.22604.78
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Submitted on December 17, 2003
Accepted on February 5, 2004
Is Oxidative Stress the Pathogenic Mechanism Underlying Insulin Resistance, Diabetes, and Cardiovascular Disease? The Common Soil Hypothesis Revisited
Antonio Ceriello * and Enrico Motz
From Department of Pathology and Medicine, Experimental and Clinical, University of Udine, Italy.
* To whom correspondence should be addressed. E-mail: ceriello{at}uniud.it.
Abstract--Type 2 diabetes is a worldwide increasing disease resulting from the interaction between a subject’s genetic makeup and lifestyle. In genetically predisposed subjects, the combination of excess caloric intake and reduced physical activity induces a state of insulin resistance. When beta cells are no longer able to compensate for insulin resistance by adequately increasing insulin production, impaired glucose tolerance appears, characterized by excessive postprandial hyperglycemia. Impaired glucose tolerance may evolve into overt diabetes. These 3 conditions, ie, insulin resistance, impaired glucose tolerance, and overt diabetes, are associated with an increased risk of cardiovascular disease. Because all these conditions are also accompanied by the presence of an oxidative stress, this article proposes oxidative stress as the pathogenic mechanism linking insulin resistance with dysfunction of both beta cells and endothelium, eventually leading to overt diabetes and cardiovascular disease. This hypothesis, moreover, may also contribute to explaining why treating cardiovascular risk with drugs, such as calcium channel blockers, ACE inhibitors, AT-1 receptor antagonists, and statins, all compounds showing intracellular preventive antioxidant activity, results in the onset of new cases of diabetes possibly being reduced.
Key words: oxidative stress • insulin resistance • impaired glucose tolerance • diabetes • cardiovascular disease • statins • ACE inhibitors • AT-1 blockers • glitazones • calcium channel blockers
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