title: Telomere dysfunction-related serological markers are associated with type 2 diabetes.
abstract: OBJECTIVE
  Recent studies have identified a set of serological markers for telomere dysfunction and DNA damage. The relevance of these serological markers in type 2 diabetes remains elusive. We investigated the association of serological markers (elongation factor 1α [EF-1α], stathmin, and N-acetyl-glucosaminidase) with leukocyte telomere length, a functional variant of uncoupling protein-2 (UCP2), and susceptibility of type 2 diabetes.
  
  
  METHODS
  A total of 930 patients and 867 control subjects were recruited to examine the association between leukocyte telomere length, UCP2 variant (-886G>A), recently identified serological markers, and type 2 diabetes. Telomere length was determined by a quantitative real-time PCR-based assay. EF-1α, stathmin, and C-reactive proteins were measured by enzyme-linked immunosorbent assays. N-acetyl-glucosaminidase was measured by an enzyme activity assay. The UCP2 variant was determined by PCR and restriction enzyme digestion.
  
  
  RESULTS
  The average telomere length of type 2 diabetic patients was significantly shorter than that of control subjects. Serological N-acetyl-glucosaminidase correlates with both age and telomere length and was significantly higher in patients than in control subjects. Neither EF-1α nor stathmin showed significant difference between patients and control subjects. The UCP2-886G>A variant correlated with type 2 diabetes status but did not correlate with telomere length or the serological markers. Multivariate analysis showed that higher serological N-acetyl-glucosaminidase, shorter telomeres, and the UCP2-886G>A variant are independent risk factors for type 2 diabetes.
  
  
  CONCLUSIONS
  Serological N-acetyl-glucosaminidase, telomere length, and the UCP2-886G>A variant are independent risk factors for type 2 diabetes. Serological N-acetyl-glucosaminidase correlates with telomere length but not with the UCP2-886G>A variant.
authors.affiliation: Capital Institute of Pediatrics, Beijing, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Xiao
authors.forename: Xiaoguo
authors.initials: X
authors.lastname: Zheng
authors.forename: Mingming
authors.initials: M
authors.lastname: Cui
authors.forename: Guiying
authors.initials: G
authors.lastname: Shi
authors.forename: Xianda
authors.initials: X
authors.lastname: Chen
authors.forename: Ruili
authors.initials: R
authors.lastname: Li
authors.forename: Zhangfa
authors.initials: Z
authors.lastname: Song
authors.forename: Karl Lenhard
authors.initials: KL
authors.lastname: Rudolph
authors.forename: Bowen
authors.initials: B
authors.lastname: Chen
authors.forename: Zhenyu
authors.initials: Z
authors.lastname: Ju
mesh_terms: D000118:Acetylglucosaminidase / Q000097:blood; D000367:Age Factors; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000235:genetics* / Q000473:pathology; D006801:Humans; D007473:Ion Channels / Q000235:genetics; D024101:Mitochondrial Proteins / Q000235:genetics; D020648:Peptide Elongation Factor 1 / Q000097:blood; D060888:Real-Time Polymerase Chain Reaction; D050777:Stathmin / Q000097:blood; D016615:Telomere / Q000235:genetics* / Q000473:pathology*; D000071246:Uncoupling Protein 2
chemical_list: D007473:Ion Channels; D024101:Mitochondrial Proteins; D020648:Peptide Elongation Factor 1; D050777:Stathmin; C000604389:UCP2 protein, human; D000071246:Uncoupling Protein 2; D000118:Acetylglucosaminidase