Browsing by Author "Verdi, Hasibe"

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Aspirin Resistance in Cerebrovascular Disease and the Role of Glycoprotein IIIa Polymorphism in Turkish Stroke Patients
(2016) Derle, Eda; Ocal, Ruhsen; Kibaroglu, Seda; Celikkol, Ceyda; Bayraktar, Nilufer; Verdi, Hasibe; Atac, Belgin F.; Can, Ufuk; https://orcid.org/0000-0002-3964-268X; https://orcid.org/0000-0002-7886-3688; https://orcid.org/0000-0003-0591-009X; https://orcid.org/0000-0001-6868-2165; https://orcid.org/0000-0001-8689-417X; 26809135; V-3553-2017; AAJ-2956-2021; Y-8758-2018; V-5499-2017; ABG-9966-2020; AAJ-2999-2021
Aspirin resistance occurs in 5-45% of high-risk patients, with various mechanisms proposed for its development. This study aimed to determine the relationships among aspirin resistance, aspirin dosage, type of aspirin and glycoprotein IIIa P1A1/A2 polymorphism in patients with vascular risk factors. Two hundred and eight (75 symptomatic, 133 asymptomatic) patients with vascular risk factors who were using aspirin for primary or secondary prevention were prospectively included. The symptomatic group was further classified into two groups according to aspirin use at the time of stroke. Aspirin resistance was measured by the PFA-100 system (collagen/epinephrine cartridge) and glycoprotein IIIa P1A1/A2 polymorphism was determined by PCR. The overall prevalence of aspirin resistance was 32.2%. The mean age of patients with aspirin resistance was significantly higher than that in those who did not have resistance (P=0.009). The prevalence of aspirin resistance was similar for the symptomatic and asymptomatic under aspirin therapy groups. The resistance rate was found to be highest with 100mg enteric-coated preparation use (39.3%). Increasing the aspirin dosage and/or shifting to uncoated preparations caused a change in aspirin sensitivity of 36-60%. Repeated measurements showed development of aspirin resistance in 14% of patients who were sensitive to aspirin in previous measurements. Glycoprotein IIIaP1A1/A2 polymorphism, aspirin resistance and development of atherothrombotic stroke were not significantly related. The effect of aspirin can change by time, dosage and type of preparation used. There are no relationships among glycoprotein IIIa P1A1/A2 polymorphism, aspirin resistance and development of atherothrombotic stroke. Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved.
beta-3AR W64R Polymorphism and 30-Minute Post-Challenge Plasma Glucose Levels in Obese Children
(2015) Verdi, Hasibe; Kinik, Sibel Tulgar; Yalcin, Yaprak Yilmaz; Sahin, Nursel Muratoglu; Yazici, Ayse Canan; Atac, F.Belgin; 25800470
Objective: In this study, we aimed to investigate the association of W64R polymorphism of the beta 3-adrenergic receptor gene (beta-3AR) with childhood obesity and related pathologies. Methods: beta-3AR gene W64R genotyping was carried out in 251 children aged 6-18 years. Of these subjects, 130 were obese (62 boys) and 121 were normal-weight (53 boys). In the obese group, fasting lipids, glucose and insulin levels were measured. Oral glucose tolerance test (OGTT) was performed in 75 of the obese patients. Results: The frequency of W64R genotype was similar in obese and nonobese children. In obese children, relative body mass index, waist-to-hip ratio, serum lipid, glucose and insulin levels, as well as homeostasis model assessment of insulin resistance (HOMA-IR) scores were not different between Arg allele carriers (W64R and R64R) and noncarriers (W64W). In 75 obese children, OGTT results showed that Arg allele carriers had significantly higher 30-minute glucose levels (p=0.027). Conclusion: W64R polymorphism of the beta-3AR gene is not associated with obesity and waist-to-hip ratio in Turkish children. Although there were no relationships between the genotypes and lipid, glucose/insulin levels or HOMA-IR, the presence of W64R variant seemed to have an unfavorable influence on early glucose excursion after glucose loading.
Beta-Cell Golgi Stress Response to Lipotoxicity and Glucolipotoxicity: A Preliminary Study of a Potential Mechanism of Beta-Cell Failure in Posttransplant Diabetes and Intraportal Islet Transplant
(2022) Tutuncu, Neslihan Bascil; Verdi, Hasibe; Yalcin, Yaprak; Cebi, Pinar Baysan; Kinik, Sibel; Tutuncu, Tanju; Atac, Fatma Belgin; 0000-0002-1816-3903; 0000-0002-9337-9106; 0000-0002-9141-9987; 35791832; ABG-5027-2020; ABB-4078-2020
Objectives: Lipotoxicity and glucolipotoxicity are among the most important triggers of beta-cell failure in patients with type 2 and posttransplant diabetes. Because the Golgi apparatus is a vital organelle in secretory cells like beta cells, its behavior under stress conditions determines the cell's functional capacity.Materials and Methods: To mimic lipotoxicity and glucolipotoxicity as metabolic stresses for beta-cell failure, rat insulinoma INS-1E cells were treated with palmitic acid, glucose, or both. Cells were cultured in the presence of 5.0, 16.7, or 33 mM glucose with or without 0.5 mM palmitic acid for 8, 16, 24, and 48 hours. Incubation in the presence of any of the 3 concentrations of glucose with 0.5 mM palmitic acid provided glucolipotoxicity. In addition to the endop-lasmic reticulum stress marker (Hspa5), we evaluated changes in Golgi function under experimental metabolic stresses. In doing this, we measured expression levels of the genes coding Golgi structural proteins (Acbd3, Golga2, and Arf1), Golgi glycosylation enzymes sialyltransferaz10 and sialyltransferase 1 (St3gal1), and Golgi stress mediators (Creb3 and Arf4).Results: Golgi responded to lipotoxicity and glucolipotoxicity by increasing the expression of St3gal1 (P = .05 in both conditions) and Creb3 (P = .022 and P = .01, respectively). The Arf4 gene transcript also increased in glucolipotoxic media (P = .03). Glucotoxicity alone did not induce a change in the transcript levels of Creb3 and Arf4. Lipotoxicity and glucolipotoxicity induced Creb3 and Arf4 expression, which are important Golgi stress response mediators leading to apoptosis.Conclusions: This preliminary study showed that the Golgi stress response is important in lipotoxic and glucolipotoxic conditions in terms of beta-cell failure. Solving the mystery of intracellular molecular mechanisms leading to beta-cell dysfunction is crucial to understanding the pathophysiology of posttrans-plant diabetes and most probably the failure of intraportal islet transplants in the long term.
Effect of Maternal and Neonatal Interleukin-6-174 G/C Polymorphism on Preterm Birth and Neonatal Morbidity
(2018) Karakas, N. Mutlu; Ecevit, Ayse N.; Yalcin, Yaprak; Ozdemir, Beril; Verdi, Hasibe; Tekindal, M. Agah; Ozbek, Namik Y.; Tarcan, Aylin; Atac, Fatma B.; Haberal, Ali; 0000-0002-9337-9106; 0000-0003-4286-7086; 0000-0001-6857-0681; 0000-0002-4060-7048; 0000-0002-2232-8117; 0000-0003-0591-009X; 0000-0002-1486-7209; 0000-0001-6868-2165; 28279124; ABB-4078-2020; AAX-3831-2020; HPC-6496-2023; U-9270-2018; AAJ-4616-2021; ABG-9940-2020; AAI-9331-2021; ABG-9966-2020
Objective: The aim of this study was to analyze maternal and neonatal interleukin 6 (IL-6) (-174 G/C) polymorphism and to determine effect on preterm birth and neonatal morbidity. Study Design: One hundred and sixty-four mothers (100 term births, 64 preterm births) and 183 newborn infants who were 100 healthy term and 83 preterm babies followed in newborn intensive care units were evaluated. PCR-RFLP was performed for IL-6 (-174 G/C) genotyping. Results: The rate of GG genotype in mothers of term and preterm infants were 54% (n = 54/100), 75% (n = 48/64), respectively (p>.05) and the rate of GC+CC genotype was 46% (n = 46/100) and 25% (n = 16/64) in mothers giving term and preterm birth (PTB), respectively (p<.05). Additionally, the rate of GG genotype was 65% (n = 65/100) and 81.9% (n = 68/83) in term infants and preterm infants, respectively. GC+CC genotype was 35% (n = 35/100) in term infants and 18.1% (n = 15/83) in preterm infants (p<.05). The effect of IL-6 (-174) GC+CC genotype on PTB was statistically significant. Conclusion: The IL-6 174 G/C gene polymorphism was significantly different between mothers who were giving to term and preterm birth. The presence of polymorphism is protective against preterm birth and was not associated with neonatal outcome.
Endoplasmic Reticulum Stress Response in Non-Alcholic Fatty Liver Disease: Sophisticated Pathways
(2023) Etik, Digdem Ozer; Verdi, Hasibe; Atac, Fatma Belgin; https://orcid.org/0000-0001-6868-2165; V-5499-2017; ABG-9966-2020
Non-alcoholic fatty liver disease comprises a broad spectrum of fat-associated liver conditions that can result in end-stage liver disease and the need for liver transplantation. The multiparallel hypothesis suggests that steatohepatitis is the result of numerous conditions acting in parallel, including form genetic susceptibility, lipotoxicity, disturbed gut microbiata to mitochondrial dysfunction, and endoplasmic reticulum(ER) stress. The unfolded protein response as the ER stress response is coordinated primarily by ER transmembrane stress transducers which is a defensive response initially activates the cell to recover from stress or adapt to stress. It reduces the secretory protein load, enhances protein folding and increases clearance capacity by promoting autophagy and ER-associated degradation. However, if these attempts fail or the ER stress gets prolonged, it will induce cell death programs to eliminate the stressed cells. In recent years, ER stress response has been identified as a crucial mechanism in steatohepatitis by leading improper lipid biosynthesis, inflammation, and autophagy or apoptosis.
Endothelial nitric oxide synthase gene polymorphisms in patients with slow coronary flow
(2017) Tekin, Abdullah; Sezgin, Nurzen; Atac, Fatma Belgin; Verdi, Hasibe; Sezgin, Alpay Turan; 0000-0002-5658-870X; 0000-0001-6868-2165; 0000-0003-0591-009X; 29201435; ABG-9940-2020; ABD-7304-2021; ABG-9966-2020
Background and aims: The aim of this study was to explore potential associations of the intron 4 variable number of tandem repeats (VNTR) and E298A polymorphisms of the endothelial nitric oxide synthase (eNOS) gene with slow coronary flow (SCF). The association between plasma nitrate and nitrite (NOx) concentrations and eNOS gene polymorphisms was also assessed. Materials and methods: The intron 4 VNTR and E298A polymorphisms of the eNOS gene were evaluated in the isolated DNA blood samples obtained from the SCF patient group (n = 30) and healthy group consisted of age- and sex-matched controls (n = 61). Results: Plasma NOx level was significantly lower in patients with SCF than in controls. In addition, patients with SCF have significantly lower nitric oxide levels than control subjects within each genotype variants. The allele and genotyped frequencies of the eNOS intron 4 VNTR and E298A polymorphisms were similar between patients with SCF and the controls. Plasma NOx concentrations with respect to the relevant genotypes were found insignificant. Discussion and conclusion: Plasma NOx is lower in patients with SCF than in healthy subjects. Our findings may suggest the lack of association between intron 4 VNTR and E298A polymorphisms of the eNOS gene and SCF.
Karaciğer iskemi reperfüzyon modelinde karaciğer ve uzak organ hasarında endoplazmik retikulum stresinin rolü
(Başkent Üniversitesi Sağlık Bilimler Enstitüsü, 2016) Ermiş, Erkan; Verdi, Hasibe
Amaç: Karaciğer iskemi/reperfüzyon hasarı, pringle manevrası gerektiren karaciğer cerrahisinde ve karaciğer transpantasyonunda geçici iskemi ve sonrasında dolaşımın tekrar sağlanmasıyla oluşmaktadır. Reperfüzyon sırasında açığa çıkan serbest oksijen radikalleri iskemi/reperfüzyon hasarında önemli rol oynamaktadır. Ortaya çıkan bu serbest radikallerin de etkisiyle endoplazmik retikulumda biriken katlanmamış ya da hatalı katlanmış proteinler sonucu endoplazmik retikulum stresi tetiklenmektedir. Bu tez kapsamında karaciğerde oluşan hasarla birlikte hem karaciğerde hem de akciğer, böbrek, beyin gibi uzak organlardaki endoplazmik retikulum stresinin varlığının ve hücre ölümü üzerindeki rolünün araştırılması amaçlanmaktadır. Gereç ve yöntem: Çalışmamızda ağırlıkları 180-300 gr arasında değişen 15 adet Wistar Albino cinsi erişkin erkek sıçan kullanıldı. Sıçanlar rastlantısal olarak 3 gruba ayrıldı. Grup 1: İskemi/reperfüzyon: Sıçanlar, orta hat insizyonu ile açılarak karaciğere giden hepatik portal ven ve hepatik arter bulldog klemp ile kapatıldı. 60 dk iskemi süresi sonunda, 60 dk reperfüzyona bırakılmışdı. 60 dk’nın sonunda ise sıçanlar sakrifiye edilip karaciğer, akciğer, böbrek ve beyin dokuları alındı. Dokuların bir kısmı patoloji için %10’luk formaldehitde saklanıp diğer kısımları ise RNA izolosyonu için, RNAlater’da saklanıp -80 ºC ye kaldırıldı. Grup 2: Sham: sıçanlar yine orta hat insizyonu ile açılarak 120 dk bekletilip, yine patoloji ve RNA izolasyonu için karaciğer, akciğer, beyin ve böbrekleri alındı. Grup 3: Kontrol: Bu gruptaki sıçanlara hiçbir işlem uygulanmayıp, yine karaciğer, akciğer, beyin ve böbrek dokuları patoloji ve RNA izolasyonu için alındı. Toplanan tüm dokulardan, bir kısmı histopatolojik incelemeler için %10’luk formaline alındı. Bir kısmı ise RNA izolasyonu için kullanıldı. Elde edilen RNA’lar cDNA’ya çevrilip, light cycler 480 cihazında ER stres genleri olan GRP78, PERK, ATF6 ve CHOP ifadelenmelerine bakıldı. Sonuçlar istatiksel olarak student- t testi ile değerledirildi. p≤ 0.05 anlamlı olarak kabul edildi. Bulgular: Karaciğer, akciğer, böbrek ve beyinde ER stres gen ifadelerinde sham grubuna göre belli oranda bir artış gözlenirken istatiksel olarak anlamlı bulunamadı. Karaciğerde ATF6, PERK ve CHOP genlerinde, aynı zamanda akciğer, böbrek ve beyinde CHOP ifadelenmelerinde istatiksel olarak anlamlı bir artış görüldü. Ayrıca histopatolojik incelemeler sonucunda İskemi/reperfüzyon grubunda, hepatosit kordonlarında daralma ve hepatoselüler kayıp ile karakterize parankim hücre zedelenmesi ve nötrofil lökosit infiltrasyonu görüldü. Sonuç: Karaciğer I/R hasarı sonrası karaciğer yanı sıra akciğer, böbrek ve beyin gibi uzak organlarda ER stresinin etkisi gözlendi. Bunun sonucu olarak ER stresinin I/R hem lokal hem de uzak organlarda etkili bir rol oynadığı ve bu stresi azaltmak adına yapılacak olan çalışmalara ışık tutacaktır. Aim: Liver ischemia / reperfusion injury, occurs in pringle maneuver requiring liver surgery and liver transplantation by transient ischemia, and after that re-establishment of circulation. Free oxygen radicals, which emerge during reperfusion, play an important role in ischemia / reperfusion injury. With the effects of these free radicals, unfolded or missfolded proteins in endoplasmic reticulum can trigger endoplasmic reticulum stress. Them aim of this study to understand role of endoplasmic reticulum stress in cell death and the presence of this stress in both liver and in distant organs such as lung, kidney, brain. Material and Method: Total 15 adult male Wistar Albino rats, weight between 180-300 gr, was used. Rats were randomized into 3 groups. Group 1: Ischemia / reperfusion: Rats were opened with midline incision and hepatic portal vein and the hepatic artery were closed with a bulldog clamp. At the end of 60 minutes ischemia period, 60 minutes of reperfusion was applied. At the end of reperfusion; rats were sacrified and their liver, lung, kidney and brain tissues were collected. Some of these tissues were stored for pathology in 10% formaldehyde and the remaining tissues were stored at -80 ºC in RNA later for RNA isolation. Group 2: Sham: rats were opened with midline incision and after waiting for 120 minutes they were sacrified and their liver, lung, kidney and brain tissues were collected for pathology and RNA isolation. Group 3: Control: No procedures were applied to this group, and again their liver, lung, kidney and brain tissues were collected for pathology and RNA isolation. Some of these collected tissues were taken into 10% formaldehyde for histopathological studies and the remaining parts were used for RNA isolation. RNAs were converted to cDNA and the expression levels of ER stress genes, GRP78, PERK, ATF6 and CHOP, were examined with lightcycler 480 device. Results were evaluated with student-t test p≤ 0.05 was accepted as statistically significant. Results: There was a slight increase in the expression levels of ER stress genes in liver, lung, kidney and brain when copared with sham group but this difference was not statistically significant. There was a statistically significant increase for the expression levels of ATF6, PERK and CHOP genes in liver and the expression level of CHOP gene in lung, kidney and brain. Moreover as a result of histopathological studies; there was parenchymal cell injury and neutrophil leukocytes infiltration which was characterized with narrowing of hepatocytes cords and hepatocellular loss in ischemia reperfusion group. Conclusion: After liver I/R injury; effect of ER stress was observed in distant organs such as lung, kidney and brain in addition to liver. As a result of this we understand that ER stress after I/R can effect both local and distant organs and this study will set light to further studies for reducing this stress.
Lack of association between MMP13 (rs3819089), ADAM12 (rs3740199-rs1871054) and ADAMTS14 (rs4747096) genotypes and advanced-stage knee osteoarthritis
(2021) Haberal, Bahtiyar; Simsek, Ekin Kaya; Cebi, Hatice Pinar Baysan; Tuc, Ozer; Verdi, Hasibe; Atac, Fatma Belgin; 0000-0002-1668-6997; 0000-0002-9141-9987; 0000-0002-2228-6893; 0000-0003-0591-009X; 34145804; W-9080-2019
Objectives: The aim of this study was to investigate the relationship between MMP13 rs3819089, ADAM12 rs3740199 and rs1871054, and ADAMTS14 rs4747096 genotypes in patients with radiologically diagnosed knee osteoarthritis (OA). Patients and methods: A total of 300 patients (68 males, 232 females; mean age: 61.6 years; range, 25 to 89 years) who were admitted to the orthopedics and traumatology clinic and diagnosed with knee OA according to the 2000 American College of Rheumatology (ACR) criteria between October 2018 and March 2019 were prospectively analyzed. Patients with Grades III-IV OA according to the KellgrenLawrence (K-L) grading system were included in the patient group (n=150) and those without radiological features of knee OA (K-L Grades I-II) were included in the control group (n=150) voluntarily. The presence of single nucleotide polymorphisms (SNPs) in the targeted genes in both groups was assessed by real-time polymerase chain reaction in the peripheral blood sample. Results: The most common nucleotides in both the control and patient groups were CG for rs3740199 and CT for rs1871054 in the ADAM12 gene, and the most common nucleotides in alleles were GG for MMP13 rs3819089 and AA for ADAMTS14 rs4747096. No statistically significant relationship was detected between the gene polymorphisms and advanced OA. Conclusion: The study results suggest that ADAM12 rs3740199 and rs1871054, MMP13 rs3819089, and ADAMTS14 rs4747096 polymorphisms have no relationship with knee OA susceptibility in the Turkish population. However, as this is the first study to investigate the relationship between the SNPs of ADAM12, ADAMTS14, and MMP13 genes and the development of OA in the Turkish population, it would contribute to our understanding of the molecular bases of OA.
Multidrug Resistance 1 (MDR1) 3435C/T Genotyping in Childhood Drug-Resistant Epilepsy
(2014) Saygi, Semra; Alehan, Fusun; Atac, Fatma Belgin; Erol, Ilknur; Verdi, Hasibe; Erdem, Remzi; https://orcid.org/0000-0002-8522-5078; https://orcid.org/0000-0001-6868-2165; https://orcid.org/0000-0002-3530-0463; https://orcid.org/0000-0003-0591-009X; https://orcid.org/0000-0002-7537-2170; 23465586; AAB-1203-2021; ABG-9966-2020; AAK-4825-2021; ABG-9940-2020
Introduction: A mutation at nucleotide position 3435 in exon 26 of the multidrug resistance 1 (MDR1) gene is the most frequently studied polymorphism in relation to multidrug resistance. However, there are conflicting data as to whether the CC or TT genotype of the 3435C>T polymorphism is associated with drug resistance. Methods and results: We investigated the association between this polymorphism in drug-resistant childhood epilepsy by comparison with drug-responsive patients. In total, 59 patients with drug-resistant epilepsy, defined as having four or more seizures within a 12-month period while using three or more AEDs, 60 children with drug-responsive epilepsy who had remained seizure-free for 12 months on their current AED regimen and 76 healthy children were involved in this study. Genotype frequencies in drug-resistant patients were as follows: 32.2% CC, 44.1% CT, 23.7% TT; in the drug-responsive group: 20.0% CC, 50.0% CT, 30.0% TT; in the control group: 24.3% CC, 50.0% CT, 25.7% TT. Comparison of drug-resistant and drug-responsive patients revealed no significant difference in genotype frequency. The findings of the epilepsy patients were not significantly different from those of the healthy control subjects. Conclusions: Our study does not support any significant association between the MDR1 polymorphism and drug-resistant childhood epilepsy. (C) 2013 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
The Role of miRNA in Endometriosis
(2021) Bilgili, Gamze; Verdi, Hasibe; Zeyneloglu, B. Hulusi; Tohma, Y. Aytac; Atac, F. Belgin
Endometriosis is characterized by the presence of endometrial gland and stroma outside of the endometrial cavity. Not only the complex nature of disease limits the identification of the pathogenic mechanisms of endometriosis but the lack of simple diagnostic procedure is the major limitation. So identification of a simple clinical tool for the diagnosis of endometriosis has become a high priority research objective. MicroRNAs (miRNAs), a class of small noncoding RNA molecules, have been recognized as key post- transcriptional regulators those may associate with endometriosis. In the present paper, we aimed to review the studies which focused on the prognosis and diagnosis of the endometriosis and miRNAs. As studies on the role of miRNAs in the pathogenesis of endometriosis increase in the literature, new ideas can be put forward for early diagnosis, prevention and treatment of the endometriosis.
The Role of Parkin in Rat Pancreatic Beta Cells Fate
(2023) Verdi, Hasibe; Cebi, Hatice Pinar Baysan; Yalcin, Yaprak Yilmaz; Ozkan, Tulin; Mehtap, Akcil; Sunguroglu, Asuman; Atac, Fatma Belgin; 0000-0002-9337-9106; 0000-0001-7693-0958; 37715413; ABB-4078-2020; AAQ-4882-2020
Parkin is a member of the mitochondrial quality control system that plays a major role in mitophagy. Although the loss of function mutations in the Parkin gene has been associated with the Familial Parkinson's pheno-type, research in recent years points out that Parkin's function is not limited to neurodegenerative diseases. Parkin's function impressing key cellular quality control mechanisms, including the ubiquitin-proteasome and autophagy-lysosome systems, makes it an important player in the maintenance of cellular homeostasis. In this study, we investigated whether Parkin affects cell viability and ER stress responses under lipotoxic conditions in INS-1E cells. Our results may suggest that silencing Parkin may affect autophagy in addition to apoptosis. We also showed that Parkin may have a protective effect against lipo-toxic effects in INS-1E cells. Consistent with previous studies, we observed that stress responses were different for high and low palmitic acid doses. The Parkin being inhibited under high-dose PA treatment and active under low-dose PA treatment indicate that regulation of stress responses is controlled by environmental conditions. Our preliminary findings may suggest that in low lipotoxic conditions, Parkin affects the ER stress response by modulating Chop activity and Ca2+ release from the ER to the cytoplasm.
Uncoupling protein gene UCP1-3826A/G, UCP2 Ins/Del and UCP3-55C/T polymorphisms in obese Turkish children
(2020) Verdi, Hasibe; Kinik, Sibel Tulgar; Cebi, H. Pinar Baysan; Yalcin, Yaprak Yilmaz; Guvercin, Ayse Canan Yazici; Aydin, Beril; Tutunc, Neslihan Bascil; Atac, F. Belgin; 0000-0002-9141-9987; 0000-0002-9337-9106; 0000-0002-1816-3903; 33372430; AAH-2620-2021; ABB-4078-2020; ABG-5027-2020
Background. Mitochondrial uncoupling proteins (UCP) 1, 2 and 3 are members of the anion carrier protein family located in the inner mitochondrial membrane. There are various controversial reports on UCP genotypes and obesity in adults and children. This study aims to investigate the link between mostly studied UCP polymorphisms (UCP1-3826A/G, UCP2 Insertion/Deletion ans/Del) polymorphism of exon 8, and UCP3-55C/T Polymorphisms) and obesity in Turkish children. Furthermore, the relationships of UCP polymorphisms are also analyzed within the scope of metabolic parameters of obese children. Methods. Molecular screening of the UCP2, UCP2, and UCP3 gene polymorphisms was carried out in 189 children aged 6 to 18 years, 102 of who had exogenous obesity (54 girls) and 87 of whom were healthy controls (48 girls). In the obese group, fasting lipids, glucose and insulin levels were measured. In 60 obese children, an oral glucose tolerance test (OGTT) was performed with 0, 30, 60, 90 and 120 minutes of sampling for plasma glucose and insulin levels. Results. The frequency of UCP polymorphisms was similar in obese and non-obese children. In obese children, fasting lipids, glucose and insulin levels were not different among the UCP1, 2 and 3 genotypes. While no relationship was found between the UCP1 and 3 genotypes and glucose/insulin levels during OGTT, carriers of the Insertion allele with UCP2 Ins/Del polymorphism had significantly higher 30-minute insulin levels (p=0.018). Conclusions. Polymorphisms of the UCP1-3826A/G, UCP2 Ins/Del, and UCP3-55C/T are not associated with obesity and related pathologies in Turkish children. However, the presence of the Ins allele of the UCP2 gene has been found to have an unfavorable influence on early insulin excursion after glucose loading.