Shortened telomere length in white blood cells of patients with IDDM.

Jeanclos, Elisabeth; Królewski, Andrzej S.; Skurnick, Joan; Kimura, Masayuki; Aviv, Hana; Warram, James H.; Aviv, Abraham

doi:10.2337/diabetes.47.3.482

Cited by 182 publications

(130 citation statements)

References 10 publications

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“…We note, however, that because telomere length at any age is the product of telomere length at birth and telomere attrition rate thereafter, cross-sectional analysis of telomere length, based on single measurements, requires large cohorts to capture links of biological variables with telomere attrition. This may be the reason that Jeanclos et al 32 did not observe significantly lower TRF length in patients with non-insulin-dependent diabetes mellitus than in their nondiabetic peers.…”

Section: Discussionmentioning

confidence: 68%

Rise in Insulin Resistance Is Associated With Escalated Telomere Attrition

et al. 2005

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Background-Insulin resistance predisposes to cardiovascular disease and shortens human lifespan. We therefore tested the hypothesis that a rise in insulin resistance in concert with gain in body mass is associated with accelerated white blood cell telomere attrition. Methods and Results-We measured white blood cell telomere dynamics and age-related changes in insulin resistance and body mass index in young adults of the Bogalusa Heart Study.

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Section: Discussionmentioning

confidence: 68%

Rise in Insulin Resistance Is Associated With Escalated Telomere Attrition

et al. 2005

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“…Once telomeres are shortened to a critical length, cells are triggered into replicative senescence, resulting in cell cycle arrest and phenotypic and functional alterations [11,12]. Previous studies have demonstrated telomere shortening in adults with type 1 diabetes [13,14] and we and others have shown that patients with type 2 diabetes have shorter telomeres than age-matched controls [15,16]. Rates of telomere shortening at cell division are highly dependent on oxidatively induced strand breaks in telomeric DNA and oxidative DNA damage [11,12,17,18].…”

Section: Introductionmentioning

confidence: 99%

Absence of telomere shortening and oxidative DNA damage in the young adult offspring of women with pre-gestational type 1 diabetes

et al. 2008

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Aims/hypothesis The offspring of mothers with pre-gestational type 1 diabetes (PGDM) may be at increased risk of glucose intolerance and cardiovascular disease in childhood. The underlying causes of these observations, and whether they persist into adulthood, are unknown. The aim of the present study was to test the hypothesis that fetal chromosomal telomere oxidative DNA damage resulting from maternal PGDM programmes the offspring towards a senescent phenotype that is detectable in young adulthood. Methods We studied 21 young adult offspring (age 16-23 years) with a maternal history of PGDM and 23 age-and weight-matched controls with no maternal history of diabetes. All participants underwent anthropometric assessments, a standard 75 g OGTT, measurement of peripheral blood mononuclear cell and skin fibroblast telomere length, fibroblast senescence, cell DNA damage (by determination of 8-oxoguanine levels using flow cytometry), plasma lipoprotein profiles (determined by nuclear magnetic resonance) and plasma levels of soluble adhesion molecules and inflammatory markers. ResultsThe groups did not differ significantly with respect to anthropometric measures, glucose tolerance, fasting and 2 h plasma insulin levels during OGTT, estimated peripheral insulin resistance, peripheral blood mononuclear cell or fibroblast telomere length, DNA damage or senescence in vitro, plasma NMR lipoprotein profiles or levels of highsensitivity C-reactive protein. Plasma concentrations of soluble intercellular adhesion molecule 1 (sICAM-1; p< 0.05) and IL-6 (p=0.08) were higher in the PGDM offspring. Conclusions/interpretation Young adult offspring of mothers with PGDM do not differ in terms of glucose tolerance, DNA damage or telomere length from controls of the same weight and BMI. This does not preclude such abnormalities at an earlier age, but there is no evidence of telomere damage as a pre-programming mechanism in the young adults enrolled in this study.

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“…35 The circulating white blood cells of insulin-dependent diabetics have shorter telomere lengths than those from normoglycemic controls or noninsulin-dependent diabetics. 36 Patients with atherosclerosis have increased thickness, 3,37 and stiffness 38 of their central arterial walls, greater central pressure augmentation, 39 and shorter telomere lengths on their circulating white blood cells. 40,41 They also exhibit endothelial dysfunction, 42 which has been implicated in the pathogenesis of atherosclerosis 43 and is one of its earliest pathologic manifestations.…”

Section: Arterial Aging In Cardiovascular Diseasesmentioning

confidence: 99%

Arterial Aging

2005

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Abstract-Age is the dominant risk factor for cardiovascular diseases. However, until recently, convincing mechanistic or molecular explanations for the increased cardiovascular risks conferred by aging have been elusive. Aging is associated with alterations in a number of structural and functional properties of large arteries, including diameter, wall thickness, wall stiffness, and endothelial function. Emerging evidence indicates that these age-associated changes are also accelerated in the presence of cardiovascular diseases, and that these changes are themselves risk factors for the appearance or progression of these diseases. In this review, the evidence demonstrating that arterial aging is accelerated in cardiovascular diseases and that accelerated arterial aging is a risk factor for adverse cardiovascular outcomes is briefly reviewed, and selected advances in vascular biology that provide insights into the mechanisms that may underlie the increased risks conferred by arterial aging are summarized. Remarkably, a host of biochemical, enzymatic, and cellular alterations that are operative in accelerated arterial aging have also been implicated in the pathogenesis and progression of arterial diseases. These vascular alterations are thus putative candidates that could be targeted by interventions aimed at attenuating arterial aging, similar to the lifestyle and pharmacological interventions that have already been proven effective. Therefore, the notion that aging is a chronological process and that its risky components cannot be modulated is no longer tenable. It is our hope that a greater appreciation of the links between arterial aging and cardiovascular diseases will stimulate further investigation into strategies aimed at preventing or retarding arterial aging.

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Shortened telomere length in white blood cells of patients with IDDM.

Cited by 182 publications

References 10 publications

Rise in Insulin Resistance Is Associated With Escalated Telomere Attrition

Rise in Insulin Resistance Is Associated With Escalated Telomere Attrition

Absence of telomere shortening and oxidative DNA damage in the young adult offspring of women with pre-gestational type 1 diabetes

Arterial Aging

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