Endocrine Abstracts

Both type 1 and type 2 diabetes are associated with accelerated atherosclerosis. Multiple mechanisms contribute to the atherosclerotic process; however, inflammation and oxidative stress are underlying common factors. In genetically-prone atherosclerotic mouse models, inhibition of macrophage inflammatory capacity and oxidative stress substantially attenuate atherosclerosis extent and complexity. These approaches also attenuate the adipocyte response to high fat diet and adoipokine production, as well as development of the metabolic syndrome. Activation of nuclear receptors, such as PPAR gamma PPAR delta and their combination, through antiinflammatory and antioxidant activities may be useful in the fight against the metabolic syndrome and atherosclerosis. An early effect on both pathologies may involve improvement in endothelial function.