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ERENBERK, UFUK

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Author: Erenberk, UFUK × Author: Uysal, Omer ×

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    SIRT1 gene variants are related to risk of childhood obesity
    (2015-04-01) Kilic, Ulkan; GOK, Ozlem; ELIBOL-CAN, BİRSEN; Ozgen, Ilker Tolga; Erenberk, UFUK; Uysal, Omer; DUNDAROZ, Mehmet Rusen; ELİBOL, BİRSEN; ÖZGEN, İLKER TOLGA; ERENBERK, UFUK; UYSAL, ÖMER
    Obesity is a multifactorial disorder resulting from the interaction between genetic, psychological, physical, environmental, and socioeconomic factors. SIRT1 gene has important effects on the regulation of adiponectin, caloric restriction, insulin sensitivity, coronary atherosclerosis, and cardiovascular diseases. The aim of this study was to investigate the association between childhood obesity and SIRT1 gene polymorphisms regarding rs7895833 A > G in the promoter region, rs7069102 C > G in intron 4, and rs2273773 C > T in exon 5 using PCR-CTPP method in 120 obese and 120 normal weight children. In this study, BMI, systolic and diastolic blood pressure, LDL cholesterol, triglyceride, and insulin levels were significantly higher and HDL-cholesterol levels were significantly lower in obese children compared to normal weight children. For rs7895833 A > G, the rate of having AG genotype and G allele was significantly higher in obese children compared to non-obese group (p T. There was no significant difference for rs7069102 C > G gene polymorphism between groups.
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    A Remarkable Age-Related Increase in SIRT1 Protein Expression against Oxidative Stress in Elderly: SIRT1 Gene Variants and Longevity in Human
    (2015-03-18) Elibol-Can, BİRSEN; Kilic, Ulkan; Gok, Ozlem; DUNDAR, TOLGA TURAN; DUNDAROZ, Mehmet Rusen; Torun, EMEL; Erenberk, UFUK; Uysal, Omer; ERENBERK, UFUK; TORUN, EMEL; ELİBOL, BİRSEN; UYSAL, ÖMER; DÜNDAR, TOLGA TURAN
    Aging is defined as the accumulation of progressive organ dysfunction. Controlling the rate of aging by clarifying the complex pathways has a significant clinical importance. Nowadays, sirtuins have become famous molecules for slowing aging and decreasing age-related disorders. In the present study, we analyzed the SIRT1 gene polymorphisms (rs7895833 A>G, rs7069102 C>G and rs2273773 C>T) and its relation with levels of SIRT1, eNOS, PON-1, cholesterol, TAS, TOS, and OSI to demonstrate the association between genetic variation in SIRT1 and phenotype at different ages in humans. We observed a significant increase in the SIRT1 level in older people and found a significant positive correlation between SIRT1 level and age in the overall studied population. The oldest people carrying AG genotypes for rs7895833 have the highest SIRT1 level suggesting an association between rs7895833 SNP and lifespan longevity. Older people have lower PON-1 levels than those of adults and children which may explain the high levels of SIRT1 protein as a compensatory mechanism for oxidative stress in the elderly. The eNOS protein level was significantly decreased in older people as compared to adults. There was no significant difference in the eNOS level between older people and children. The current study is the first to demonstrate age-related changes in SIRT1 levels in humans and it is important for a much better molecular understanding of the role of the longevity gene SIRT1 and its protein product in aging. It is also the first study presenting the association between SIRT1 expression in older people and rs7895833 in SIRT1 gene.
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    Melatonin attenuates phenytoin sodium-induced DNA damage
    (2014-04-01) Erenberk, UFUK; DUNDAROZ, Rusen; GOK, Ozlem; Uysal, Omer; AGUS, Sami; Yuksel, Adnan; Yilmaz, Bayram; KILIC, Ulkan; ERENBERK, UFUK; UYSAL, ÖMER
    Phenytoin sodium (PHT Na+) is a potent antiepileptic drug against epileptic seizures and is used as a prophylactic treatment in traumatic brain injury. PHT Na+ leads to the formation of reactive oxygen species (ROS), and DNA is a crucial molecular target of ROS-initiated toxicity. Melatonin and its metabolites possess free-radical-scavenging activity. We therefore designed this study to investigate the potential protective effect of melatonin against PHT Na+-induced DNA damage by using the comet assay in a rat model in vivo. Thirty-three 3-month-old male Wistar rats were divided into five groups of control treated with isotonic sodium chloride (a single injection of isotonic sodium chloride and 100 mL in drinking water for 10 days), ethanol treated (in drinking water for 10 days containing 100 mL of ethanol in each 300-mL drinking bottle), melatonin treated (4 mg/kg body weight [b.w.] intraperitoneally [i.p.] at the start, in drinking water for 10 days), PHT Na+ treated (a single i.p. injection of 50 mg/kg) and PHT Na+ (50 mg/kg b.w., single i.p.) and melatonin (4 mg/kg b.w. i.p. at the start and 4 mg/kg in drinking water for 10 days) cotreated. To determine the protective effects of melatonin, the comet assay was performed using lymphocytes isolated in different time intervals (0, 15, 30, 45 and 60 minutes) from each group of animals. On days 1, 3, 7 and 10, blood samples were taken and the comet assay technique was performed. Our present data suggest that melatonin reversed PHT Na+-induced DNA damage.