This observation in type diabetes would support the argument that increased oxidative stress is the dominant contributor to telomere attrition in diabetes. Telomere length was inversely related to measures of lipid peroxidation in this study, but DNA damage was not assessed and the relative contributions of sex, smoking, and antihypertensives or other medication to telomerel ength intypedi abetesnotexamined.Most type diabetic patients in this study were taking a statin, but this would not account for our observations, as the available data suggest a neutral or protective effect of statins on telomere length or damage in vitro. There was no signicant difference in telomere length between diabetic subjects treated or not treated with a statin, and it would have been unethical to withdraw statin therapy for research purposes in this study.There was no relationship between hsCRP and telomere length in the diabetic group, but there was a signicant inverse relationship between hsCRP and telomere length in control subjects.It is possible that this disparity between groups could reect the antiinammatory actions of statins, used in the diabetic group, blunting such a relationship in diabetic patients.Similarly, the control subjects did not demonstrate the signicant inverserelation sh ipbe tweente lomerelength and oxidative DNA damage seen in the diabetic group.This might reect increased levels of oxidative stress in the type patients, driving a trend toward both the increased DNA damage seen in this study and in our other studies and telomere shortening and producing a relationship absent in control subjects with lower levels of oxidative stress.It should be stressed that telomeres are particularly prone to damage at the GGG sequence compared with the rest of chromosomal DNA and that relatively modest degrees of oxidative DNA damage could be expressed as substantial telomere attrition, as in the present study.Similarly, we cannot exclude the possibility that the type diabetic population is preprogrammed toward both shorter telomere length and type diabetes, although this is highly unlikely and has not been examined in this study. The monocyte abnormalities in the present study cannot be extended to other cell types.However, endothelial cell precursors in the marrow are susceptible to oxidative damage, vascular endothelium is constantly repopulated by endothelial progenitor cells in adult life, and senescent endothelial cells appear to be a feature of type diabetes and atherosclerosis. In summary, we have shown that peripheral blood monocytes from type diabeticpati ents are ch aracteriz edby signicant telomere shortening.This implies that the peripheral venous monocyte population adhering to the vascular endothelium in type diabetes, entering the vascular wall, and undergoing macrophage transformation are a population at increased risk of replicative senescence and apoptosis within plaques.This suggestion is valid regardless of the mechanisms underlying this observation, which is likely to be due to oxidative DNA damage to monocyte precursors during replication.Hum Biol, DIABETES CARE, VOLUME, NUMBER, {|Targetmol’s {Endurobol|Amiodarone FEBRUARY The same agent has been used for other diverse investigations, ranging from subclassification of of lymphocyte hypoxic populations within. The spontaneous mutation frequency was xi.Panel a indicates time course of dye uptake, where the relative intensity of G peak plotted as a function of time and concentration.

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