Clinical Research

Effects of telomere length and plasma AGEs on bone mineral density in type 2 diabetic patients

  • Menglu ZHU ,
  • Fengjiao ZHANG ,
  • Zhiqiang KANG
Expand
  • Zhengzhou Central Hospital Affiliated to Xinxiang Medicial University,Zhengzhou 450000,He′nan,China

Received date: 2024-06-28

  Online published: 2024-11-05

Abstract

Objective To investigate the correlation between telomere length of peripheral white blood cells and the levels of advanced glycosylation end products, as well as bone mineral density in patients with type 2 diabetes mellitus, and to assess the impact of advanced glycosylation end product levels on telomere length. Methods From May 1, 2023, to May 1, 2024, 174 patients with T2DM who underwent dual-energy X-ray BMD examination at the Department of Endocrinology, Zhengzhou Central Hospital, were selected. T2DM patients were divided into osteoporosis group, osteopenia group, and normal bone mass group based on the T-value in BMD. qPCR method was used to measure telomere length in peripheral blood leukocytes, and ELISA method was used to determine AGEs levels. General patient data were collected along with measurements for blood glucose, blood lipid levels, 25-hydroxy-vitamin D, and other indicators. Bone mineral density was evaluated using dual-energy X-ray imaging while plasma CTX and PINP levels were measured via ELISA. SPSS 26.0 statistical software was utilized to analyze differences and correlations among all indicators. Results (1)The telomere length of OP group, osteopenia group and normal bone mass group was different, and the telomere length of the three groups increased successively. (2) In individuals with type 2 diabetes mellitus, telomere length exhibited a positive correlation with BMD and a negative correlation with CTX and PINP. Plasma AGEs level showed a negative correlation with BMD and a positive correlation with CTX and PINP, while telomere length demonstrated a negative correlation with AGEs level.(3) Telomere length was an independent factor of BMD, and AGEs level was an independent factor of BMD (P < 0.05). Conclusion The reduction of telomere length and the increase of AGEs in patients with type 2 diabetes are related to the decrease of bone mineral density, and the reduction of telomere length is related to the increase of AGEs. Telomere length of peripheral leucocytes and plasma AGEs level can jointly evaluate the bone metabolism status of T2DM patients.

Cite this article

Menglu ZHU , Fengjiao ZHANG , Zhiqiang KANG . Effects of telomere length and plasma AGEs on bone mineral density in type 2 diabetic patients[J]. The Journal of Practical Medicine, 2024 , 40(20) : 2860 -2866 . DOI: 10.3969/j.issn.1006-5725.2024.20.008

References

1 杨亚军,崔燎. FoxO/Wnt通路在氧化应激介导的骨质疏松中的调控机制[J]. 中国药理学通报,2013,29(1):27-30.
2 WANG L, YU W, YIN X, et al. Prevalence of Osteoporosis and Fracture in China: The China Osteoporosis Prevalence Study[J]. JAMA Netw Open, 2021, 4(8):e2121106. doi:10.1001/jamanetworkopen.2021.21106
3 中华医学会骨质疏松和骨矿盐疾病分会,章振林. 原发性骨质疏松症诊疗指南(2022)[J]. 中国全科医学,2023,26(14):1671-1691.
4 SI Y, WANG C, GUO Y, et al. Prevalence of Osteoporosis in Patients with Type 2 Diabetes Mellitus in the Chinese Mainland: A Systematic Review and Meta-Analysis[J]. Iran J Public Health, 2019, 48(7): 1203-1214.
5 TURNER K J, VASU V, GRIFFIN D K. Telomere Biology and Human Phenotype [J]. Cells, 2019, 8(1):73. doi:10.3390/cells8010073
6 HERRMANN M, PUSCEDDU I, MARZ W, et al. Telomere biology and age-related diseases [J]. Clin Chem Lab Med, 2018, 56(8): 1210-1222. doi:10.1515/cclm-2017-0870
7 CHENG F, CARROLL L, JOGLEKAR M V, et al. Diabetes, metabolic disease, and telomere length [J]. Lancet Diabetes Endocrinol, 2021, 9(2): 117-126. doi:10.1016/s2213-8587(20)30365-x
8 SNELSON M, LUCUT E, COUGHLAN M T. The Role of AGE-RAGE Signalling as a Modulator of Gut Permeability in Diabetes [J]. Int J Mol Sci, 2022, 23(3):1766. doi:10.3390/ijms23031766
9 DEO P, MCCULLOUGH C L, ALMOND T, et al. Dietary sugars and related endogenous advanced glycation end-products increase chromosomal DNA damage in WIL2-NS cells, measured using cytokinesis-block micronucleus cytome assay [J]. Mutagenesis, 2020, 35(2): 169-177. doi:10.1093/mutage/geaa002
10 陈晨,李莉. 晚期糖基化终产物及其受体在新疆维吾尔族2型糖尿病性骨质疏松症中的作用研究[J]. 中国社区医师,2020,36(32):22-23.
11 CAWTHON R M. Telomere measurement by quantitative PCR [J]. Nucleic Acids Res, 2002, 30(10): e47. doi:10.1093/nar/30.10.e47
12 RHARASS T, LUCAS S. High Glucose Level Impairs Human Mature Bone Marrow Adipocyte Function Through Increased ROS Production [J]. Front Endocrinol (Lausanne), 2019, 10: 607. doi:10.3389/fendo.2019.00607
13 BERGAMINI C M, GAMBETTI S, DONDI A D, et al. Oxygen, reactive oxygen species and tissue damage [J]. Curr Pharm Des, 2004, 10(14): 1611-1626. doi:10.2174/1381612043384664
14 ZHAO F, GUO L, WANG X, et al. Correlation of oxidative stress-related biomarkers with postmenopausal osteoporosis: a systematic review and meta-analysis [J]. Arch Osteoporos, 2021, 16(1): 4. doi:10.1007/s11657-020-00854-w
15 PERRONE A, GIOVINO A, BENNY J, et al. Advanced Glycation End Products (AGEs): Biochemistry, Signaling, Analytical Methods, and Epigenetic Effects [J]. Oxid Med Cell Longev, 2020, 2020: 3818196. doi:10.1155/2020/3818196
16 FISHMAN S L, SONMEZ H, BASMAN C, et al. The role of advanced glycation end-products in the development of coronary artery disease in patients with and without diabetes mellitus: a review [J]. Mol Med, 2018, 24(1): 59. doi:10.1186/s10020-018-0060-3
17 SUZUKI A, YABU A, NAKAMURA H. Advanced glycation end products in musculoskeletal system and disorders [J]. Methods, 2022, 203: 179-186. doi:10.1016/j.ymeth.2020.09.012
18 SAKAMOTO E, KIDO J I, TAKAGI R, et al. Advanced glycation end-product 2 and Porphyromonas gingivalis lipopolysaccharide increase sclerostin expression in mouse osteocyte-like cells [J]. Bone, 2019, 122: 22-30. doi:10.1016/j.bone.2019.02.001
19 LLABRE J E, SROGA G E, TICE M J L, et al. Induction and rescue of skeletal fragility in a high-fat diet mouse model of type 2 diabetes: An in vivo and in vitro approach [J]. Bone, 2022, 156: 116302. doi:10.1016/j.bone.2021.116302
20 GE W, JIE J, YAO J, et al. Advanced glycation end products promote osteoporosis by inducing ferroptosis in osteoblasts [J]. Mol Med Rep, 2022, 25(4):140. doi:10.3892/mmr.2022.12656
21 HEIN G, WIEGAND R, LEHMANN G, et al. Advanced glycation end-products pentosidine and N epsilon-carboxymethyllysine are elevated in serum of patients with osteoporosis [J]. Rheumatology (Oxford), 2003, 42(10): 1242-1246. doi:10.1093/rheumatology/keg324
22 YAVUZ D G, APAYDIN T. Skin autofluorescence Is associated With low bone mineral density in type 2 diabetic patients [J]. J Clin Densitom, 2022, 25(3): 373-379. doi:10.1016/j.jocd.2021.11.010
23 AHMAD S, KHAN M S, AKHTER F, et al. Glycoxidation of biological macromolecules: a critical approach to halt the menace of glycation [J]. Glycobiology, 2014, 24(11): 979-990. doi:10.1093/glycob/cwu057
24 BARNES R P, FOUQUEREL E, OPRESKO P L. The impact of oxidative DNA damage and stress on telomere homeostasis [J]. Mech Ageing Dev, 2019, 177: 37-45. doi:10.1016/j.mad.2018.03.013
25 CHAKRAVARTI D, LABELLA K A, DEPINHO R A. Telomeres: history, health, and hallmarks of aging [J]. Cell, 2021, 184(2): 306-322. doi:10.1016/j.cell.2020.12.028
26 WANG J, DONG X, CAO L, et al. Association between telomere length and diabetes mellitus: A meta-analysis [J]. J Int Med Res, 2016, 44(6): 1156-1173. doi:10.1177/0300060516667132
27 TAMAYO M, MOSQUERA A, REGO J I, et al. Differing patterns of peripheral blood leukocyte telomere length in rheumatologic diseases [J]. Mutat Res, 2010, 683(1-2): 68-73. doi:10.1016/j.mrfmmm.2009.10.010
28 VALDES A M, RICHARDS J B, GARDNER J P, et al. Telomere length in leukocytes correlates with bone mineral density and is shorter in women with osteoporosis [J]. Osteoporos Int, 2007, 18(9): 1203-1210. doi:10.1007/s00198-007-0357-5
29 FRAGKIADAKI P, NIKITOVIC D, KALLIANTASI K, et al. Telomere length and telomerase activity in osteoporosis and osteoarthritis [J]. Exp Ther Med, 2020, 19(3): 1626-1632.
30 GRUBER H J, SEMERARO M D, RENNER W, et al. Telomeres and Age-Related Diseases [J]. Biomedicines, 2021, 9(10):1355. doi:10.3390/biomedicines9101335
31 PIGNOLO R J, LAW S F, CHANDRA A. Bone Aging, Cellular Senescence, and Osteoporosis [J]. JBMR Plus, 2021, 5(4): e10488. doi:10.1002/jbm4.10488
Outlines

/