ECE2020 Audio ePoster Presentations Hot topics (including COVID-19) (110 abstracts)
Association between variants in clock genes and type 2 diabetes in an elderly greek population
Xanthippi Tsekmekidou 1 , Fotis Tsetsos 2 , Theocharis Koufakis 1 , Maria Grammatiki 1 , Marianthi Georgitsi 3 , Athanasios Roumeliotis 4 , Stylianos Panagoutsos 4 , Elias Thodis 4 , Marios Theodoridis 4 , Nikolaos Papanas 5 , Dimitrios Papazoglou 5 , Ploumis Pasadakis 4 , Peristera Paschou 2 , Pantelis Zebekakis 1 & Kalliopi Kotsa 1
1Division of Endocrinology and Metabolism and Diabetes Center, First Department of Internal Medicine, Medical School, Aristotle University of Thessaloniki, AHEPA University Hospital, Thessaloniki, Greece; 2Department of Molecular Biology and Genetics, Democritus University of Thrace, Alexandroupolis, Greece; 3; 4Department of Nephrology, Democritus University of Thrace, Alexandroupolis, Greece; 5Diabetes Centre, Second Department of Internal Medicine, Democritus University of Thrace, Alexandroupolis, Greece
Background: Recent data suggest that disturbances in circadian clock functioning are implicated in the pathogenesis of type 2 diabetes (T2D), through alterations in plasma glucose levels, insulin secretion and sensitivity, energy intake, and genomic expression in liver and pancreas. This study aimed to assess a potential association between variants in clock genes and T2D risk in a population of Greek elderly people.
Methods: In a case-control design, 1258 participants aged 65 and above, were categorized either as T2D patients (Group A, n = 716) according to diabetes history, HbA1c ≥ 6.5% and fasting plasma glucose (FPG) ≥ 126 mg/dl, or non-diabetic controls (Group B, n = 569). Informed consent was obtained from participants and whole blood was collected for DNA extraction. Samples were analyzed on Illumina Infinium PsychArray. After individual and SNP quality control, polymorphisms in PPARA, PPARD, PKDREJ, UTS2, CLOCK/TMEM165, VAMP2, HES6 and PER2 genes were selected and allele frequencies between groups were compared (primary analysis). For the purpose of the compound analysis, the PLINK software suite (v1.9) was used. Permutation test analysis was implemented to determine statistical significance (P < 0.05). In order to eliminate the impact of prediabetes on the results, participants from Group B with HbA1c levels < 5.7% and FPG < 100 mg/dl were selected to form a control subgroup (Group n = 393) and a secondary analysis was undertaken.
Results: In the primary analysis, a protective effect of 14 PPARAvariants against T2D was established. A similar trend was evident for rs7291444_G/T (Pemp = 0.031, OR = 0.7843), rs36125344_C/G (Pemp = 0.043, OR = 0.758) and rs6008384_C/T (Pemp = 0.036, OR = 0.798) in PKDREJ, in both primary and secondary analyses. Interestingly, rs6744132_A/G, located downstream HES6 and PER2 genes was positively associated with T2D (Pemp = 0.044, OR = 1.183). rs2859389 in UTS2 gene was found to be protective against T2D (Pemp = 0.046, OR = 0.8454). Only in the secondary analysis, rs2278637_G/T (Pemp = 0.015, OR = 0.784) in VAMP2 and rs11943456 (Pemp = 0.018, OR = 0.787) in TMEM165 exhibited a protective role against T2D.
Conclusion: Our data indicate a potential role of variation in clock genes in T2D genetic susceptibility in an elderly Greek population. Further studies are required to replicate our findings and clarify the complex underlying interactions between genetic, environmental and life-style components that result in the development of the disorder.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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