Browsing by Author "Agirbasli, Deniz"

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Coronary artery disease from a perspective of genomic risk score, ethical approaches and suggestions
(AVES YAYINCILIK, 2012-01-01) Agirbasli, Deniz; Ulman, Yesim Isil
As a leading cause of mortality, coronary artery disease is on the focus of genetic research as a complex trait. Although predictive genetic testing for cardiovascular diseases is on the counter, it is still hard to aggregate information from multiple genetic variants, environmental factors and family history into a single score. Every susceptibility allele provides small contribution to disease formation. Biomarkers play a role in various metabolic pathways. Genetic information and data depend heavily on probabilities. This should be clearly explained by genetic counselor to the patient and relatives who are looking for certain answers. Presence of susceptibility alleles can be a source of anxiety and it may result as a reduced self-confidence in ability to change health behavior. Complex diseases set a new stage to study novel techniques that can elucidate interactions among genetic, environmental and ethnic factors. The cookbook approach to treat a complex disease can often be misleading. Future studies may provide personalized information, which can improve the outcome of standardized treatments. As knowing one's own genetic risk is becoming a task for the responsible individual it surely will add new challenges to ethical framework. Publicly marketing genetic tests for complex diseases raises ethical concerns. To avoid discriminatory use of genetic information
Leukocyte telomere length as a compensatory mechanism in vitamin D metabolism
(PUBLIC LIBRARY SCIENCE, 2022-01-01) Agirbasli, Deniz; Kalyoncu, Minenur; Muftuoglu, Meltem; Aksungar, Fehime Benli; Agirbasli, Mehmet
Vitamin D deficiency is common among postmenopausal women. Telomere length can be a potential protective mechanism for age-related diseases. The objective of our study is to examine the association of vitamin D supplementation on leukocyte telomere length (LTL) in healthy postmenopausal women with vitamin D deficiency. The study was designed as a placebo-controlled study to investigate the short-term effects of vitamin D supplementation and seasonal changes on vitamin D related parameters, including 25(OH)D, 1,25(OH)(2)D parathormone (PTH), Vitamin D binding protein (VDBP), vitamin D receptor (VDR), and telomere length in a cohort of postmenopausal women (n = 102). The group was divided as supplementation (n = 52) and placebo groups (n = 50). All parameters were measured before and after treatment. Serum VDBP levels were measured by ELISA method and VDR, GC (VDBP) gene expressions and relative telomere lengths were measured in peripheral blood mononuclear cells (PBMC) using a quantitative real-time PCR method. The results demonstrate that baseline levels were similar between the groups. After vitamin D supplementation 25(OH)D, 1,25(OH)(2)D, PTH and VDBP levels were changed significantly compared to the placebo group. At the end of the study period, LTL levels were significantly increased in both groups and this change was more prominent in placebo group. The change in GC expression was significant between treatment and placebo groups but VDR expression remained unchanged. Even though the study was designed to solely assess the effects of vitamin D supplementation, LTL was significantly increased in the whole study group in summer months suggesting that LTL levels are affected by sun exposure and seasonal changes rather than supplementation. The study displayed the short-term effect of Vitamin D supplementation on vitamin D, PTH levels, LTL and vitamin D associated gene expressions. The relation between Vitamin D and LTL is not linear and could be confounded by several factors such as the population differences, regional and seasonal changes in sun exposure.
Multi-Locus Candidate Gene Analyses of Lipid Levels in a Pediatric Turkish Cohort: Lessons Learned on LPL, CETP, LIPC, ABCA1, and SHBG
(MARY ANN LIEBERT, INC, 2013-01-01) Agirbasli, Mehmet; Eren, Fatih; Agirbasli, Deniz; White, Marquitta J.; Williams, Scott M.
Cardiovascular risk factors and atherosclerosis precursors were examined in 365 Turkish children and adolescents. Study participants were recruited at five different state schools. We tested single and multi-locus effects of six polymorphisms from five candidate genes, chosen based on prior known association with lipid levels in adults, for association with low (10(th) percentile) high density lipoprotein cholesterol (HDL-C) and high (90(th) percentile) triglycerides (TG), and the related continuous outcomes. We observed an association between CETP variant rs708272 and low HDL-C (allelic p=0.020, genotypic p=0.046), which was supported by an independent analysis, PRAT (PRAT control p=0.027). Sex-stratified logistic regression analysis showed that the B2 allele of rs708272 decreased odds of being in the lower tenth percentile of HDL-C measurements (OR=0.36, p=0.02) in girls
SHBG Gene Polymorphism (rs1799941) Associates with Metabolic Syndrome in Children and Adolescents
(PUBLIC LIBRARY SCIENCE, 2015-01-01) White, Marquitta J.; Eren, Fatih; Agirbasli, Deniz; Williams, Scott M.; Agirbasli, Mehmet
Background Metabolic syndrome (MetS) is a complex disorder characterized by coexistence of several cardiometabolic (CM) factors, i.e. hyperlipidemia, obesity, high blood pressure and insulin resistance. The presence of MetS is strongly associated with increased risk of cardiovascular disease (CVD). The syndrome was originally defined as an adult disorder, but MetS has become increasingly recognized in children and adolescents. Methods Genetic variants influence biological components common to the CM factors that comprise MetS. We investigated single locus associations between six single nucleotide polymorphisms (SNPs), previously shown to modulate lipid or sex hormone binding globulin (SHBG) levels, with MetS in a Turkish pediatric cohort (37 cases, 323 controls). Results Logistic regression analysis revealed a significant association between rs1799941, located in SHBG, and MetS (OR = 3.09, p-value = 0.006). The association with MetS remained after sequential adjustment for each CM factor included in the syndrome definition, indicating that the identified association is not being driven by any single trait. A relationship between rs1799941 and SHBG levels, was also discovered, but it was dependent on MetS status. In control subjects, the A allele of rs1799941 associated with a significant increase in SHBG levels (p = 0.012), while in cases there was no association between rs1799941 and SHBG levels (p = 0.963). Conclusions The significant association between rs1799941 and MetS in children is not contingent on any single CM trait. Additionally, the presence of MetS may abrogate effect of rs1799941 polymorphism on SHBG levels in children.