There is ample evidence that oxidized lipoproteines exist in vivo, not only in atherosclerotic lesions, but also associated with some experimental models of diabetes. Whether the lipoprotein oxidation is an eplphenomenon of other atherogenic or diabetogenic agents or processes or whether it is causally related to lesion formation in atherosclerosis or other forms of tissue damage in people with diabetes is unresolved. Intense Interest in testing these ideas derives from in vitro observations of the ways in which oxidized lipoproteines interact with cells that are unlike the Interactions with native lipoproteins. Many of these altered Interactions suggest known features of atherosclerotic lesions, and recent data show that antioxidant treatment reduces the progression of vascular lesions. There are reasons to believe that hyperglycemia may worsen lipid and lipoprotein oxidation. If this observation is the case in vivo, and If it is ultimately proved that lipoprotein oxidation facilltates lesion development, these events may help explain the accelerated atherosclerosis suffered by diabetic patients. The multiple pathways for which there is evidence that hyperglycemia may contribute to oxldative events—for example, by enhancing free radical production in stimulated inflammatory cells or by forming glycation products that can propagate free radical events—suggest avenues for further research and may ultimately indicate points for intervention in the various manifestations of the disease.

This content is only available via PDF.