Is telemore shortening "pre-programmed" pathogenic factor for diabetes type 2 or diabetic Nephropathy?

Janice, thank you for sharing the article: “Monocytes Telomere Shortening and Oxidative DNA Damage in Type 2 Diabetes" and points out to the significant role that oxidative stress may play in the pathogenesis of diabetic microvascular and macrovascular disease. It is interesting that telomere shortening has been associated with aging and it is relevant to diabetes type 2, metabolic syndrome, heart failure, Parkinson’s disease, etc. There is one study "Accelerated senescence in the kidneys of patients with type 2 diabetic nephropathy" published in the Am J Physiol Renal Physiol 295: F1563-F1573, 2008, and another study entitled ”White Blood Cells Telomere Length Is Shorter in Males with Type 2 Diabetes and Micro- albuminuria” published in Diabetes Care 30:2909–2915, 2007. These articles report a telomere size difference among individuals with diabetes as compared to non-diabetics and between diabetics with microalbuminuria as opposed to diabetics without microalbuminuria. So the big question is whether the shortened telomere present in diabetics with complications is “programmed” or it is the result of oxidative stress imposed by a decompensated metabolic state. There is a study on "Multivitamin use and telomere length in women" by Xu et al. Am J Clin Nutr 89: 1857-1863, 2009 that shows a benefit from these supplements. On the other direction, Cross et. at. Published: "Absence of telomere shortening and oxidative DNA damage in the young adult offspring of women with pre-gestational type 1 diabetes", Diabetologia 52: 226-234, 2009. They conclude that there is no evidence of telomere damage as a pre-programming mechanism in the young adults enrolled in their study. My feeling is that a metabolic component "a syndrome" is the initial component that triggers maladaptive responses that result in oxidative stress adding injury to insult. It appears that hyperglycemia or a byproduct could be sensed by a metabolic receptor like "Succinate G protein-couple receptor GRP61" and this unleashes a myriad of pathogenic mechanism that result in diabetic nephropathy, retinopathy, cardiovascular disease, etc. Of course there are environmental and individuals’ genetic variations (polymorphism) that affect the response to metabolic injury and in some cases those genetic factors could be determinant, but in the majority of cases it appears that changes in life style or appropriate medication provided at early stages of disease could improve and ameliorate the effects of environmental and genetic factors.