Telomere dysfunction-related serological markers are associated with type 2 diabetes

Area of Science:

• Biochemistry
• Genetics
• Endocrinology

Background:

• Telomere dysfunction and DNA damage are linked to serological markers.
• The role of these markers in type 2 diabetes (T2D) is not well understood.

Purpose of the Study:

• To investigate the association between serological markers (elongation factor 1α [EF-1α], stathmin, N-acetyl-glucosaminidase), leukocyte telomere length, and type 2 diabetes susceptibility.
• To examine the relationship with a functional variant of uncoupling protein-2 (UCP2).

Main Methods:

• Quantitative real-time PCR for telomere length.
• ELISAs for EF-1α, stathmin, and C-reactive protein.
• Enzyme activity assay for N-acetyl-glucosaminidase.
• PCR and restriction enzyme digestion for UCP2 variant (-886G>A).
• Study included 930 patients with T2D and 867 controls.

Main Results:

• Type 2 diabetes patients had significantly shorter leukocyte telomere length.
• Serological N-acetyl-glucosaminidase was higher in patients and correlated with age and telomere length.
• EF-1α and stathmin showed no significant differences.
• The UCP2-886G>A variant correlated with T2D status but not telomere length or serological markers.
• Multivariate analysis identified higher N-acetyl-glucosaminidase, shorter telomeres, and the UCP2-886G>A variant as independent T2D risk factors.

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 the UCP2-886G>A variant.