Leukocyte telomere length is associated with complications of Type 2 diabetes mellitus

Diabet. Med. 28, 1388–1394 (2011) Objective  The key goal of diabetes management is to prevent complications. While the patho‐physiological mechanisms responsible for diabetes complications have been extensively studied, at present it is impossible to predict which patient with diabetes could develo...

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Published inDiabetic medicine Vol. 28; no. 11; pp. 1388 - 1394
Main Authors Testa, R., Olivieri, F., Sirolla, C., Spazzafumo, L., Rippo, M. R., Marra, M., Bonfigli, A. R., Ceriello, A., Antonicelli, R., Franceschi, C., Castellucci, C., Testa, I., Procopio, A. D.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.11.2011
Blackwell
Subjects
Online AccessGet full text
ISSN0742-3071
1464-5491
1464-5491
DOI10.1111/j.1464-5491.2011.03370.x

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Abstract Diabet. Med. 28, 1388–1394 (2011) Objective  The key goal of diabetes management is to prevent complications. While the patho‐physiological mechanisms responsible for diabetes complications have been extensively studied, at present it is impossible to predict which patient with diabetes could develop complications. In recent years, the role of leukocyte telomere length in the pathogenesis of cardiovascular disease and Type 2 diabetes has been investigated. However, studies aiming to investigate the role of telomeres in the development and progression of Type 2 diabetes, as well as diabetic complications, are still lacking. As a consequence, this study aimed to verify whether leukocyte telomere length is associated with the presence and the number of diabetic complications in a sample of patients with Type 2 diabetes. Methods  This is a cross‐sectional study. Nine hundred and one subjects were enrolled, including 501 patients with Type 2 diabetes, of whom 284 had at least one complication and 217 were without complications, and 400 control subjects. Leukocyte telomere length was measured by quantitative real‐time PCR. Results  Patients with diabetes complications had significantly shorter leukocyte telomere length than both patients without diabetes complications and healthy control subjects. Moreover, among patients with diabetes complications, leukocyte telomere length became significantly and gradually shorter with the increasing number of diabetes complications. The magnitude of the effect of the decrease of the abundance of telomeric template vs. a single‐copy gene length (T/S ratio) on complications is described by the estimated odds ratio OR = 5.44 (95% CI 3.52–8.42). Conclusions  The results of the study support the hypothesis that telomere attrition may be a marker associated with the presence and the number of diabetic complications.
AbstractList The key goal of diabetes management is to prevent complications. While the patho-physiological mechanisms responsible for diabetes complications have been extensively studied, at present it is impossible to predict which patient with diabetes could develop complications. In recent years, the role of leukocyte telomere length in the pathogenesis of cardiovascular disease and Type 2 diabetes has been investigated. However, studies aiming to investigate the role of telomeres in the development and progression of Type 2 diabetes, as well as diabetic complications, are still lacking. As a consequence, this study aimed to verify whether leukocyte telomere length is associated with the presence and the number of diabetic complications in a sample of patients with Type 2 diabetes. This is a cross-sectional study. Nine hundred and one subjects were enrolled, including 501 patients with Type 2 diabetes, of whom 284 had at least one complication and 217 were without complications, and 400 control subjects. Leukocyte telomere length was measured by quantitative real-time PCR. Patients with diabetes complications had significantly shorter leukocyte telomere length than both patients without diabetes complications and healthy control subjects. Moreover, among patients with diabetes complications, leukocyte telomere length became significantly and gradually shorter with the increasing number of diabetes complications. The magnitude of the effect of the decrease of the abundance of telomeric template vs. a single-copy gene length (T/S ratio) on complications is described by the estimated odds ratio OR=5.44 (95%CI 3.52-8.42). The results of the study support the hypothesis that telomere attrition may be a marker associated with the presence and the number of diabetic complications.
Diabet. Med. 28, 1388–1394 (2011) Objective  The key goal of diabetes management is to prevent complications. While the patho‐physiological mechanisms responsible for diabetes complications have been extensively studied, at present it is impossible to predict which patient with diabetes could develop complications. In recent years, the role of leukocyte telomere length in the pathogenesis of cardiovascular disease and Type 2 diabetes has been investigated. However, studies aiming to investigate the role of telomeres in the development and progression of Type 2 diabetes, as well as diabetic complications, are still lacking. As a consequence, this study aimed to verify whether leukocyte telomere length is associated with the presence and the number of diabetic complications in a sample of patients with Type 2 diabetes. Methods  This is a cross‐sectional study. Nine hundred and one subjects were enrolled, including 501 patients with Type 2 diabetes, of whom 284 had at least one complication and 217 were without complications, and 400 control subjects. Leukocyte telomere length was measured by quantitative real‐time PCR. Results  Patients with diabetes complications had significantly shorter leukocyte telomere length than both patients without diabetes complications and healthy control subjects. Moreover, among patients with diabetes complications, leukocyte telomere length became significantly and gradually shorter with the increasing number of diabetes complications. The magnitude of the effect of the decrease of the abundance of telomeric template vs. a single‐copy gene length (T/S ratio) on complications is described by the estimated odds ratio OR = 5.44 (95% CI 3.52–8.42). Conclusions  The results of the study support the hypothesis that telomere attrition may be a marker associated with the presence and the number of diabetic complications.
The key goal of diabetes management is to prevent complications. While the patho-physiological mechanisms responsible for diabetes complications have been extensively studied, at present it is impossible to predict which patient with diabetes could develop complications. In recent years, the role of leukocyte telomere length in the pathogenesis of cardiovascular disease and Type 2 diabetes has been investigated. However, studies aiming to investigate the role of telomeres in the development and progression of Type 2 diabetes, as well as diabetic complications, are still lacking. As a consequence, this study aimed to verify whether leukocyte telomere length is associated with the presence and the number of diabetic complications in a sample of patients with Type 2 diabetes.OBJECTIVEThe key goal of diabetes management is to prevent complications. While the patho-physiological mechanisms responsible for diabetes complications have been extensively studied, at present it is impossible to predict which patient with diabetes could develop complications. In recent years, the role of leukocyte telomere length in the pathogenesis of cardiovascular disease and Type 2 diabetes has been investigated. However, studies aiming to investigate the role of telomeres in the development and progression of Type 2 diabetes, as well as diabetic complications, are still lacking. As a consequence, this study aimed to verify whether leukocyte telomere length is associated with the presence and the number of diabetic complications in a sample of patients with Type 2 diabetes.This is a cross-sectional study. Nine hundred and one subjects were enrolled, including 501 patients with Type 2 diabetes, of whom 284 had at least one complication and 217 were without complications, and 400 control subjects. Leukocyte telomere length was measured by quantitative real-time PCR.METHODSThis is a cross-sectional study. Nine hundred and one subjects were enrolled, including 501 patients with Type 2 diabetes, of whom 284 had at least one complication and 217 were without complications, and 400 control subjects. Leukocyte telomere length was measured by quantitative real-time PCR.Patients with diabetes complications had significantly shorter leukocyte telomere length than both patients without diabetes complications and healthy control subjects. Moreover, among patients with diabetes complications, leukocyte telomere length became significantly and gradually shorter with the increasing number of diabetes complications. The magnitude of the effect of the decrease of the abundance of telomeric template vs. a single-copy gene length (T/S ratio) on complications is described by the estimated odds ratio OR=5.44 (95%CI 3.52-8.42).RESULTSPatients with diabetes complications had significantly shorter leukocyte telomere length than both patients without diabetes complications and healthy control subjects. Moreover, among patients with diabetes complications, leukocyte telomere length became significantly and gradually shorter with the increasing number of diabetes complications. The magnitude of the effect of the decrease of the abundance of telomeric template vs. a single-copy gene length (T/S ratio) on complications is described by the estimated odds ratio OR=5.44 (95%CI 3.52-8.42).The results of the study support the hypothesis that telomere attrition may be a marker associated with the presence and the number of diabetic complications.CONCLUSIONSThe results of the study support the hypothesis that telomere attrition may be a marker associated with the presence and the number of diabetic complications.
Author Bonfigli, A. R.
Procopio, A. D.
Marra, M.
Rippo, M. R.
Testa, R.
Spazzafumo, L.
Olivieri, F.
Sirolla, C.
Ceriello, A.
Antonicelli, R.
Franceschi, C.
Castellucci, C.
Testa, I.
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  organization: Department of Molecular Pathology and Innovative Therapies, Università Politecnica delle Marche, Ancona
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  surname: Marra
  fullname: Marra, M.
  organization: Metabolic and Nutrition Research Centre on Diabetes, INRCA Ancona
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  organization: Metabolic and Nutrition Research Centre on Diabetes, INRCA Ancona
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  fullname: Ceriello, A.
  organization: Insititut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain
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  surname: Testa
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  organization: Department of Molecular Pathology and Innovative Therapies, Università Politecnica delle Marche, Ancona
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Issue 11
Keywords Endocrinopathy
Type 2 diabetes
Obesity
Nutrition
Leukocyte
Nutrition disorder
telomeres
Metabolic diseases
diabetes complications
Telomere
Association
Length
Complication
Endocrinology
Nutritional status
Language English
License CC BY 4.0
2011 The Authors. Diabetic Medicine © 2011 Diabetes UK.
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References Adaikalakoteswari A, Balasubramanyam M, Mohan V. Telomere shortening occurs in Asian Indian Type 2 diabetic patients. Diabet Med 2005; 22: 1151-1156.
Artandi SE, Attardi LD. Pathways connecting telomeres and p53 in senescence, apoptosis, and cancer. Biochem Biophys Res Commun 2005; 331: 881-890.
Atzmon G, Cho M, Cawthon RM, Budagov T, Katz M, Yang X et al. Evolution in health and medicine Sackler colloquium: genetic variation in human telomerase is associated with telomere length in Ashkenazi centenarians. Proc Natl Acad Sci U S A 2010; 107: 1710-1717.
Tentolouris N, Nzietchueng R, Cattan V, Poitevin G, Lacolley P, Papazafiropoulou A et al. White blood cells telomere length is shorter in males with type 2 diabetes and microalbuminuria. Diabetes Care 2007; 30: 2909-2915.
Aviv A. The epidemiology of human telomeres: faults and promises. J Gerontol A Biol Sci Med Sci 2008; 63: 979-983.
Oeseburg H, de Boer RA, van Gilst WH, van der Harst P. Telomere biology in healthy aging and disease. Pflugers Arch 2010; 459: 259-268.
Salpea KD, Talmud PJ, Cooper JA, Maubaret CG, Stephens JW, Abelak K et al. Association of telomere length with type 2 diabetes, oxidative stress and UCP2 gene variation. Atherosclerosis 2010; 209: 42-50.
Adaikalakoteswari A, Balasubramanyam M, Ravikumar R, Deepa R, Mohan V. Association of telomere shortening with impaired glucose tolerance and diabetic macroangiopathy. Atherosclerosis 2007; 195: 83-89.
Farzaneh-Far R, Lin J, Epel E, Lapham K, Blackburn E, Whooley MA. Telomere length trajectory and its determinants in persons with coronary artery disease: longitudinal findings from the heart and soul study. PLoS One 2010; 5: e8612.
Ceriello A, Testa R. Antioxidant anti-inflammatory treatment in type 2 diabetes. Diabetes Care 2009; 32: S232-236.
Olivieri F, Lorenzi M, Antonicelli R, Testa R, Sirolla C, Cardelli M et al. Leukocyte telomere shortening in elderly Type 2 DM patients with previous myocardial infarction. Atherosclerosis 2009; 206: 588-593.
DeFronzo RA. Lilly lecture 1987. The triumvirate: beta-cell, muscle, liver. A collusion responsible for NIDDM. Diabetes 1988; 37: 667-687.
Uziel O, Singer JA, Danicek V, Sahar G, Berkov E, Luchansky M et al. Telomere dynamics in arteries and mononuclear cells of diabetic patients: effect of diabetes and of glycemic control. Exp Gerontol 2007; 42: 971-978.
Sampson MJ, Hughes DA. Chromosomal telomere attrition as a mechanism for the increased risk of epithelial cancers and senescent phenotypes in type 2 diabetes. Diabetologia 2006; 49: 1726-1731.
Zee RY, Castonguay AJ, Barton NS, Germer S, Martin M. Mean leukocyte telomere length shortening and type 2 diabetes mellitus: a case-control study. Transl Res 2010; 155: 166-169.
American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care 2007; 30: S42-S47.
Testa R, Bonfigli AR, Salvioli S, Invidia L, Pierini M, Sirolla C et al. The Pro/Pro genotype of the p53 codon 72 polymorphism modulates PAI-1 plasma levels in ageing. Mech Ageing Dev 2009; 130: 497-500.
Gilley D, Herbert BS, Huda N, Tanaka H, Reed T. Factors impacting human telomere homeostasis and age-related disease. Mech Ageing Dev 2008; 129: 27-34.
Verzola D, Gandolfo MT, Gaetani G, Ferraris A, Mangerini R, Ferrario F et al. Accelerated senescence in the kidneys of patients with type 2 diabetic nephropathy. Am J Physiol Renal Physiol 2008; 295: F1563-F1573.
Cawthon RM. Telomere measurement by quantitative PCR. Nucleic Acids Res 2002; 30: e47.
Salpea KD, Humphries SE. Telomere length in atherosclerosis and diabetes. Atherosclerosis 2010; 209: 35-38.
Astrup AS, Tarnow L, Jorsal A, Lajer M, Nzietchueng R, Benetos A et al. Telomere length predicts all-cause mortality in patients with type 1 diabetes. Diabetologia 2010; 53: 45-48.
Turner RC, Millns H, Neil HA, Stratton IM, Manley SE, Matthews DR et al. Risk factors for coronary artery disease in non-insulin dependent diabetes mellitus: UK Prospective Diabetes Study (UKPDS 23). Br Med J 1998; 316: 823-828.
Riethman H. Human telomere structure and biology. Annu Rev Genomics Hum Gene 2008; 9: 1-19.
Ceriello A, Kumar S, Piconi L, Esposito K, Giugliano D. Simultaneous control of hyperglycemia and oxidative stress normalizes endothelial function in type 1 diabetes. Diabetes Care 2007; 30: 649-654.
2010; 53
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References_xml – reference: Tentolouris N, Nzietchueng R, Cattan V, Poitevin G, Lacolley P, Papazafiropoulou A et al. White blood cells telomere length is shorter in males with type 2 diabetes and microalbuminuria. Diabetes Care 2007; 30: 2909-2915.
– reference: Salpea KD, Talmud PJ, Cooper JA, Maubaret CG, Stephens JW, Abelak K et al. Association of telomere length with type 2 diabetes, oxidative stress and UCP2 gene variation. Atherosclerosis 2010; 209: 42-50.
– reference: Testa R, Bonfigli AR, Salvioli S, Invidia L, Pierini M, Sirolla C et al. The Pro/Pro genotype of the p53 codon 72 polymorphism modulates PAI-1 plasma levels in ageing. Mech Ageing Dev 2009; 130: 497-500.
– reference: American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care 2007; 30: S42-S47.
– reference: Astrup AS, Tarnow L, Jorsal A, Lajer M, Nzietchueng R, Benetos A et al. Telomere length predicts all-cause mortality in patients with type 1 diabetes. Diabetologia 2010; 53: 45-48.
– reference: Turner RC, Millns H, Neil HA, Stratton IM, Manley SE, Matthews DR et al. Risk factors for coronary artery disease in non-insulin dependent diabetes mellitus: UK Prospective Diabetes Study (UKPDS 23). Br Med J 1998; 316: 823-828.
– reference: Ceriello A, Testa R. Antioxidant anti-inflammatory treatment in type 2 diabetes. Diabetes Care 2009; 32: S232-236.
– reference: Zee RY, Castonguay AJ, Barton NS, Germer S, Martin M. Mean leukocyte telomere length shortening and type 2 diabetes mellitus: a case-control study. Transl Res 2010; 155: 166-169.
– reference: Adaikalakoteswari A, Balasubramanyam M, Ravikumar R, Deepa R, Mohan V. Association of telomere shortening with impaired glucose tolerance and diabetic macroangiopathy. Atherosclerosis 2007; 195: 83-89.
– reference: Sampson MJ, Hughes DA. Chromosomal telomere attrition as a mechanism for the increased risk of epithelial cancers and senescent phenotypes in type 2 diabetes. Diabetologia 2006; 49: 1726-1731.
– reference: Cawthon RM. Telomere measurement by quantitative PCR. Nucleic Acids Res 2002; 30: e47.
– reference: DeFronzo RA. Lilly lecture 1987. The triumvirate: beta-cell, muscle, liver. A collusion responsible for NIDDM. Diabetes 1988; 37: 667-687.
– reference: Ceriello A, Kumar S, Piconi L, Esposito K, Giugliano D. Simultaneous control of hyperglycemia and oxidative stress normalizes endothelial function in type 1 diabetes. Diabetes Care 2007; 30: 649-654.
– reference: Uziel O, Singer JA, Danicek V, Sahar G, Berkov E, Luchansky M et al. Telomere dynamics in arteries and mononuclear cells of diabetic patients: effect of diabetes and of glycemic control. Exp Gerontol 2007; 42: 971-978.
– reference: Farzaneh-Far R, Lin J, Epel E, Lapham K, Blackburn E, Whooley MA. Telomere length trajectory and its determinants in persons with coronary artery disease: longitudinal findings from the heart and soul study. PLoS One 2010; 5: e8612.
– reference: Riethman H. Human telomere structure and biology. Annu Rev Genomics Hum Gene 2008; 9: 1-19.
– reference: Oeseburg H, de Boer RA, van Gilst WH, van der Harst P. Telomere biology in healthy aging and disease. Pflugers Arch 2010; 459: 259-268.
– reference: Adaikalakoteswari A, Balasubramanyam M, Mohan V. Telomere shortening occurs in Asian Indian Type 2 diabetic patients. Diabet Med 2005; 22: 1151-1156.
– reference: Artandi SE, Attardi LD. Pathways connecting telomeres and p53 in senescence, apoptosis, and cancer. Biochem Biophys Res Commun 2005; 331: 881-890.
– reference: Atzmon G, Cho M, Cawthon RM, Budagov T, Katz M, Yang X et al. Evolution in health and medicine Sackler colloquium: genetic variation in human telomerase is associated with telomere length in Ashkenazi centenarians. Proc Natl Acad Sci U S A 2010; 107: 1710-1717.
– reference: Salpea KD, Humphries SE. Telomere length in atherosclerosis and diabetes. Atherosclerosis 2010; 209: 35-38.
– reference: Olivieri F, Lorenzi M, Antonicelli R, Testa R, Sirolla C, Cardelli M et al. Leukocyte telomere shortening in elderly Type 2 DM patients with previous myocardial infarction. Atherosclerosis 2009; 206: 588-593.
– reference: Aviv A. The epidemiology of human telomeres: faults and promises. J Gerontol A Biol Sci Med Sci 2008; 63: 979-983.
– reference: Verzola D, Gandolfo MT, Gaetani G, Ferraris A, Mangerini R, Ferrario F et al. Accelerated senescence in the kidneys of patients with type 2 diabetic nephropathy. Am J Physiol Renal Physiol 2008; 295: F1563-F1573.
– reference: Gilley D, Herbert BS, Huda N, Tanaka H, Reed T. Factors impacting human telomere homeostasis and age-related disease. Mech Ageing Dev 2008; 129: 27-34.
– volume: 129
  start-page: 27
  year: 2008
  end-page: 34
  article-title: Factors impacting human telomere homeostasis and age‐related disease
  publication-title: Mech Ageing Dev
– volume: 316
  start-page: 823
  year: 1998
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  article-title: Risk factors for coronary artery disease in non‐insulin dependent diabetes mellitus: UK Prospective Diabetes Study (UKPDS 23)
  publication-title: Br Med J
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  publication-title: Atherosclerosis
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  article-title: Lilly lecture 1987. The triumvirate: beta‐cell, muscle, liver. A collusion responsible for NIDDM
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Snippet Diabet. Med. 28, 1388–1394 (2011) Objective  The key goal of diabetes management is to prevent complications. While the patho‐physiological mechanisms...
The key goal of diabetes management is to prevent complications. While the patho-physiological mechanisms responsible for diabetes complications have been...
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SubjectTerms Adult
Aged
Aged, 80 and over
Analysis of Variance
Biological and medical sciences
Cross-Sectional Studies
diabetes complications
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - genetics
Diabetes Mellitus, Type 2 - physiopathology
Diabetes. Impaired glucose tolerance
Diabetic Angiopathies - etiology
Diabetic Angiopathies - genetics
Diabetic Angiopathies - physiopathology
Diabetic Nephropathies - genetics
Diabetic Nephropathies - physiopathology
Disease Progression
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Feeding. Feeding behavior
Female
Fundamental and applied biological sciences. Psychology
Humans
Leukocytes - pathology
Male
Medical sciences
Middle Aged
Predictive Value of Tests
Real-Time Polymerase Chain Reaction
Risk Factors
Telomere - genetics
Telomere - pathology
telomeres
Vertebrates: anatomy and physiology, studies on body, several organs or systems
Vertebrates: endocrinology
Title Leukocyte telomere length is associated with complications of Type 2 diabetes mellitus
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https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1464-5491.2011.03370.x
https://www.ncbi.nlm.nih.gov/pubmed/21692845
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Volume 28
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