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 in | Diabetic medicine Vol. 28; no. 11; pp. 1388 - 1394 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.11.2011
Blackwell |
Subjects | |
Online Access | Get full text |
ISSN | 0742-3071 1464-5491 1464-5491 |
DOI | 10.1111/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. |
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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. |
Author_xml | – sequence: 1 givenname: R. surname: Testa fullname: Testa, R. organization: Metabolic and Nutrition Research Centre on Diabetes, INRCA Ancona – sequence: 2 givenname: F. surname: Olivieri fullname: Olivieri, F. organization: Department of Molecular Pathology and Innovative Therapies, Università Politecnica delle Marche, Ancona – sequence: 3 givenname: C. surname: Sirolla fullname: Sirolla, C. organization: Statistical Centre, INRCA Ancona, Italy – sequence: 4 givenname: L. surname: Spazzafumo fullname: Spazzafumo, L. organization: Statistical Centre, INRCA Ancona, Italy – sequence: 5 givenname: M. R. surname: Rippo fullname: Rippo, M. R. organization: Department of Molecular Pathology and Innovative Therapies, Università Politecnica delle Marche, Ancona – sequence: 6 givenname: M. surname: Marra fullname: Marra, M. organization: Metabolic and Nutrition Research Centre on Diabetes, INRCA Ancona – sequence: 7 givenname: A. R. surname: Bonfigli fullname: Bonfigli, A. R. organization: Metabolic and Nutrition Research Centre on Diabetes, INRCA Ancona – sequence: 8 givenname: A. surname: Ceriello 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 – sequence: 9 givenname: R. surname: Antonicelli fullname: Antonicelli, R. organization: Cardiologic Unit, INRCA Ancona – sequence: 10 givenname: C. surname: Franceschi fullname: Franceschi, C. organization: Department of Experimental Pathology, University of Bologna, Bologna, Italy – sequence: 11 givenname: C. surname: Castellucci fullname: Castellucci, C. organization: Department of Molecular Pathology and Innovative Therapies, Università Politecnica delle Marche, Ancona – sequence: 12 givenname: I. surname: Testa fullname: Testa, I. organization: Metabolic and Nutrition Research Centre on Diabetes, INRCA Ancona – sequence: 13 givenname: A. D. surname: Procopio fullname: Procopio, A. D. organization: Department of Molecular Pathology and Innovative Therapies, Università Politecnica delle Marche, Ancona |
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Keywords | Endocrinopathy Type 2 diabetes Obesity Nutrition Leukocyte Nutrition disorder telomeres Metabolic diseases diabetes complications Telomere Association Length Complication Endocrinology Nutritional status |
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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 2009; 32 2010; 209 2010; 459 2002; 30 2010; 107 2005; 331 2007; 195 2006; 49 1988; 37 2008; 9 1998; 316 2010; 155 2008; 129 2008; 63 2009; 130 2007; 30 2007; 42 2009; 206 2010; 5 2005; 22 2008; 295 e_1_2_7_5_2 e_1_2_7_4_2 e_1_2_7_3_2 e_1_2_7_2_2 e_1_2_7_9_2 e_1_2_7_8_2 e_1_2_7_7_2 e_1_2_7_6_2 e_1_2_7_19_2 e_1_2_7_18_2 e_1_2_7_17_2 e_1_2_7_16_2 e_1_2_7_15_2 e_1_2_7_14_2 e_1_2_7_13_2 e_1_2_7_12_2 e_1_2_7_11_2 e_1_2_7_10_2 e_1_2_7_26_2 e_1_2_7_25_2 e_1_2_7_24_2 e_1_2_7_23_2 e_1_2_7_22_2 e_1_2_7_21_2 e_1_2_7_20_2 |
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 end-page: 828 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 – volume: 459 start-page: 259 year: 2010 end-page: 268 article-title: Telomere biology in healthy aging and disease publication-title: Pflugers Arch – volume: 195 start-page: 83 year: 2007 end-page: 89 article-title: Association of telomere shortening with impaired glucose tolerance and diabetic macroangiopathy publication-title: Atherosclerosis – volume: 37 start-page: 667 year: 1988 end-page: 687 article-title: Lilly lecture 1987. The triumvirate: beta‐cell, muscle, liver. A collusion responsible for NIDDM publication-title: Diabetes – volume: 30 start-page: 2909 year: 2007 end-page: 2915 article-title: White blood cells telomere length is shorter in males with type 2 diabetes and microalbuminuria publication-title: Diabetes Care – volume: 49 start-page: 1726 year: 2006 end-page: 1731 article-title: Chromosomal telomere attrition as a mechanism for the increased risk of epithelial cancers and senescent phenotypes in type 2 diabetes publication-title: Diabetologia – volume: 209 start-page: 35 year: 2010 end-page: 38 article-title: Telomere length in atherosclerosis and diabetes publication-title: Atherosclerosis – volume: 9 start-page: 1 year: 2008 end-page: 19 article-title: Human telomere structure and biology publication-title: Annu Rev Genomics Hum Gene – volume: 30 start-page: 649 year: 2007 end-page: 654 article-title: Simultaneous control of hyperglycemia and oxidative stress normalizes endothelial function in type 1 diabetes publication-title: Diabetes Care – volume: 63 start-page: 979 year: 2008 end-page: 983 article-title: The epidemiology of human telomeres: faults and promises publication-title: J Gerontol A Biol Sci Med Sci – volume: 30 start-page: S42 year: 2007 end-page: S47 article-title: Diagnosis and classification of diabetes mellitus publication-title: Diabetes Care – volume: 206 start-page: 588 year: 2009 end-page: 593 article-title: Leukocyte telomere shortening in elderly Type 2 DM patients with previous myocardial infarction publication-title: Atherosclerosis – volume: 42 start-page: 971 year: 2007 end-page: 978 article-title: Telomere dynamics in arteries and mononuclear cells of diabetic patients: effect of diabetes and of glycemic control publication-title: Exp Gerontol – volume: 32 start-page: S232 year: 2009 end-page: 236 article-title: Antioxidant anti‐inflammatory treatment in type 2 diabetes publication-title: Diabetes Care – volume: 155 start-page: 166 year: 2010 end-page: 169 article-title: Mean leukocyte telomere length shortening and type 2 diabetes mellitus: a case–control study publication-title: Transl Res – volume: 331 start-page: 881 year: 2005 end-page: 890 article-title: Pathways connecting telomeres and p53 in senescence, apoptosis, and cancer publication-title: Biochem Biophys Res Commun – volume: 53 start-page: 45 year: 2010 end-page: 48 article-title: Telomere length predicts all‐cause mortality in patients with type 1 diabetes publication-title: Diabetologia – volume: 22 start-page: 1151 year: 2005 end-page: 1156 article-title: Telomere shortening occurs in Asian Indian Type 2 diabetic patients publication-title: Diabet Med – volume: 107 start-page: 1710 year: 2010 end-page: 1717 article-title: Evolution in health and medicine Sackler colloquium: genetic variation in human telomerase is associated with telomere length in Ashkenazi centenarians publication-title: Proc Natl Acad Sci U S A – volume: 209 start-page: 42 year: 2010 end-page: 50 article-title: Association of telomere length with type 2 diabetes, oxidative stress and UCP2 gene variation publication-title: Atherosclerosis – volume: 295 start-page: F1563 year: 2008 end-page: F1573 article-title: Accelerated senescence in the kidneys of patients with type 2 diabetic nephropathy publication-title: Am J Physiol Renal Physiol – volume: 5 year: 2010 article-title: Telomere length trajectory and its determinants in persons with coronary artery disease: longitudinal findings from the heart and soul study publication-title: PLoS One – volume: 30 year: 2002 article-title: Telomere measurement by quantitative PCR publication-title: Nucleic Acids Res – volume: 130 start-page: 497 year: 2009 end-page: 500 article-title: The Pro/Pro genotype of the p53 codon 72 polymorphism modulates PAI‐1 plasma levels in ageing publication-title: Mech Ageing Dev – ident: e_1_2_7_13_2 doi: 10.1016/j.exger.2007.07.005 – ident: e_1_2_7_10_2 doi: 10.1111/j.1464-5491.2005.01574.x – ident: e_1_2_7_8_2 doi: 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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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