Person: ÇELİKEL, ÇİĞDEM
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ÇELİKEL
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ÇİĞDEM
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Publication Metadata only Increased serum FGF21 levels in patients with nonalcoholic fatty liver disease(WILEY-BLACKWELL, 2010) ÇELİKEL, ÇİĞDEM; Yilmaz, Yusuf; Eren, Fatih; Yonal, Oya; Kurt, Ramazan; Aktas, Bilge; Celikel, Cigdem Ataizi; Ozdogan, Osman; Imeryuz, Nese; Kalayci, Cem; Avsar, ErolP>Background The fibroblast growth factor 21 (FGF21) hormonal pathway is a metabolic signalling cascade and has been recently identified as the master hormonal regulator of glucose, lipids and overall energy balance. In this observational, case-control study, we assayed serum levels of FGF21 in patients with nonalcoholic fatty liver disease (NAFLD), a hepatic manifestation of the metabolic syndrome, and examined their association with clinical, biochemical and histological phenotypes. Materials and methods Serum levels of FGF21 were assayed by ELISA in 82 patients with biopsy-proven NAFLD and 77 controls. We analysed associations between FGF21 and the characteristics of patients with NAFLD by multiple linear regression analysis. Results Levels of FGF21 were significantly higher in patients with NAFLD (median 200 pg mL-1; interquartile range: 87-410 pg mL-1) than in healthy controls (median 93 pg mL-1; interquartile range: 70-180 pg mL-1, Mann-Whitney U-test, P < 0 center dot 001). There was a stepwise increase in serum FGF21 levels according to the liver steatosis score (median level in subjects with score 1: 170 pg mL-1; score 2: 220 pg mL-1; score 3: 280 pg mL-1, P for trend < 0 center dot 01). After stepwise linear regression analysis, serum FGF21 levels were the only independent predictor of hepatic steatosis scores in patients with NAFLD (beta = 0 center dot 26; t = 2 center dot 659, P < 0 center dot 01). Conclusions Serum FGF21 levels are increased in patients with NAFLD regardless of potential confounders and represent an independent predictor of liver steatosis. These findings support further investigation of this molecule in metabolic liver diseases.Publication Metadata only A comparison of FibroMeter (TM) NAFLD Score, NAFLD fibrosis score, and transient elastography as noninvasive diagnostic tools for hepatic fibrosis in patients with biopsy-proven non-alcoholic fatty liver disease(INFORMA HEALTHCARE, 2014) ÇELİKEL, ÇİĞDEM; Aykut, Umut Emre; Akyuz, Umit; Yesil, Atakan; Eren, Fatih; Gerin, Fatma; Ergelen, Rabia; Celikel, Cigdem Ataizi; Yilmaz, YusufBackground: Noninvasive markers that purport to distinguish patients with non-alcoholic fatty liver disease (NAFLD) with fibrosis from those without must be evaluated rigorously for their classification accuracy. Herein, we seek to compare the diagnostic performances of three different noninvasive methods (FibroMeter (TM) NAFLD score, NAFLD Fibrosis score (NFSA), and Transient Elastrography [TE]) for the detection of liver fibrosis in NAFLD patients. Methods: A total of 88 patients with biopsy-proven NAFLD were included. The Kleiner system was used for grading fibrosis in liver biopsies. The FibroMeter (TM) NAFLD score was determined using a proprietary algorithm (regression score). The NFSA score was calculated based on age, hyperglycemia, body mass index, platelets, albumin and serum aminotransferase levels. TE was performed using the Fibroscan apparatus. Results: The sensitivities/specificities for the FibroMeter (TM) NAFLD score, NFSA, and TE for the diagnosis of significant fibrosis (F2 + F3 + F4 fibrosis) were 38.6%/86.4%, 52.3%/88.6%, and 75.0%/93.2%, respectively. The areas under the receiver operating characteristic curves of TE were significantly higher than those of both the FibroMeter (TM) NAFLD score and NFSA. No significant differences were found between the FibroMeter (TM) NAFLD score and NFSA for the detection of significant and severe fibrosis, although the diagnostic performance of the FibroMeter (TM) NAFLD score was higher than that of the NFSA score for cirrhosis. Conclusions: In summary, TE showed the best diagnostic performance for the noninvasive assessment of liver fibrosis in NAFLD patients. The diagnostic performances of the FibroMeter (TM) NAFLD score and NFSA did not differ significantly for the detection of both significant and severe fibrosis.Publication Metadata only Effects of a long-acting somatostatin analogue, lanreotide, on bile duct ligation-induced liver fibrosis in rats(AVES, 2010) ÇELİKEL, ÇİĞDEM; Tahan, Gulgun; Eren, Fatih; Tarcin, Orhan; Akin, Hakan; Tahan, Veysel; Sahin, Hulya; Ozdogan, Osman; Imeryuz, Nese; Celikel, Cigdem; Avsar, Erol; Tozun, NurdanBackground/aims: Somatostatin receptors have been shown on hepatic stellate cells, and somatostatin infusion has been shown to inhibit hepatic stellate cells activation. We aimed to test the effects of a long-acting somatostatin analogue, lanreotide, on bile duct ligation- induced liver fibrosis in rats. Methods: Thirty-seven Wistar rats were divided into 5 groups as follows: Group 1, bile duct ligation+lanreotide; Group 2, bile duct ligation; Group 3, sham+lanreotide; Group 4, sham; and Group 5, control group. Lanreotide-autogel (20 mg/kg/month) or saline in intraperitoneal doses was administered. Serum biochemical parameters, liver collagen level, and oxidative stress and histological parameters were determined after 28 days. Results: The tissue collagen level, biochemical parameters (AST, ALT, bilirubins, alkaline phosphatase, gamma-glutamyl transpeptidase) and oxidative stress parameters (malondialdehyde, luminal, lucigenin) in the bile duct ligation groups were higher than in the sham-operated and control groups (p<0.001 for all). Lanreotide improved malondialdehyde and glutathione levels in the bile duct ligation+lanreotide group. In histopathological examination, bile duct ligation groups showed stage-3 liver fibrosis, while all the controls were normal. Lanreotide did not improve the liver fibrosis histologically or biochemically. Conclusions: A monthly active somatostatin analogue, lanreotide, improved malondialdehyde and glutathione; however, it was not able to improve bile duct ligation-induced liver fibrosis in rats. Although lanreotide is a long-acting medication, it did not show anti-fibrotic effects in the model.Publication Metadata only Hepatic expression and serum levels of syndecan 1 (CD 138) in patients with nonalcoholic fatty liver disease(INFORMA HEALTHCARE, 2012) ÇELİKEL, ÇİĞDEM; Yilmaz, Yusuf; Eren, Fatih; Colak, Yasar; Senates, Ebubekir; Celikel, Cigdem Ataizi; Imeryuz, NeseBackground and aims. Syndecan-1 (CD 138) is a transmembrane heparan sulfate proteoglycan expressed in the liver which may exert metabolic effects by mediating the hepatic clearance of triglyceride-rich lipoproteins. In the present study, we assayed serum levels and the hepatic expression of syndecan-1 and examined their association with clinical, biochemical, and histologic phenotypes in patients with histology-proven nonalcoholic fatty liver disease (NAFLD). Methods. A total of 59 patients with biopsy-proven NAFLD and 54 matched controls were enrolled. The analysis of syndecan-1 expression in liver biopsies was performed by immunohistochemistry on formalin-fixed, paraffin-embedded samples. Serum syndecan-1 levels were measured by ELISA. Results. NAFLD patients had significantly higher serum syndecan-1 levels [median: 61 ng/mL (interquartile range: 36-97 ng/mL)] than controls [median: 37 ng/mL (interquartile range: 25-59 ng/mL, Mann Whitney U test, p < 0.001]. However, we did not find any significant association between serum syndecan-1 and the mean syndecan-1 immunohistochemical score (n = 59, r = 0.064, p = 0.63). Interestingly, the syndecan-1 immunohistochemical score was an independent predictor of HDL cholesterol in NAFLD patients (beta = 0.27; t = 1.99, p < 0.05). Conclusions. Our data suggest that serum syndecan-1 levels are raised in patients with NAFLD. Moreover, the syndecan-1 immunohistochemical score in the liver is independently associated with HDL cholesterol in this group of patients. These pilot results support further investigation of this molecule in metabolic liver diseases.Publication Metadata only Serum Levels of Adipokines in Patients with Chronic HCV Infection: Relationship with Steatosis and Fibrosis(ELSEVIER SCIENCE INC, 2009) ÇELİKEL, ÇİĞDEM; Tiftikci, Arzu; Atug, Ozlen; Yilmaz, Yusuf; Eren, Fatih; Ozdemir, Filiz Ture; Yapali, Suna; Ozdogan, Osman; Celikel, Cigdem Ataizi; Imeryuz, Nese; Tozun, NurdanBackground and Aims. Hepatic steatosis and fibrosis are common histological findings in patients with chronic hepatitis C virus (HCV) infection. In this study we sought to determine whether serum levels of three adipokines (leptin, adiponectin and resistin) show any biochemical correlation with hepatic steatosis and fibrosis in patients with chronic HCV infection. Methods. We examined a total of 51 patients with chronic HCV infection (22 males and 29 females, mean BMI: 27.4 +/- 5 kg/m(2)) and 24 healthy control subjects (10 males and 14 females, mean BMI: 23.2 +/- 3 kg/m(2)). Liver steatosis and fibrosis were scored on biopsies. Serum levels of leptin, adiponectin and resistin were determined by ELISA. Results. HCV genotypes were 1b in 41 patients (80.4%), 3a in three patients (5.9%), 2a in two patients (3.9%), 1 a in two patients (3.9%), 1 c in one patient (2%), and 2b in one patient (2%). Serum levels of leptin, resistin, and the leptin-to-adiponectin ratio were significantly higher in patients with chronic HCV infection than in controls. Steatosis and fibrosis were detected in 33.3% and 70.5% of chronic HCV patients, respectively. No significant association with serum adipokine levels and degree of steatosis was evident. Low serum levels of resistin were associated with the presence of fibrosis independently of potential confounders. Conclusions. Patients with chronic HCV infection display elevated levels of adipokines in their sera. Reduced concentrations of resistin may be a biochemical marker of fibrosis in this patient group. (C) 2009 IMSS. Published by Elsevier Inc.Publication Metadata only Rosiglitazone attenuates liver inflammation in a rat model of nonalcoholic steatohepatitis(SPRINGER, 2007) ÇELİKEL, ÇİĞDEM; Tahan, Veysel; Eren, Fatih; Avsar, Erol; Yavuz, Dilek; Yuksel, Meral; Emekli, Ebru; Imeryuz, Nese; Celikel, Cigdem; Uzun, Hafize; Haklar, Goncagul; Tozun, NurdanRosiglitazone is an insulin-sensitizing agent. We aimed to assess the effects of rosiglitazone on a methionine- and choline-deficient diet (MCDD) model of nonalcoholic steatohepatitis (NASH) in rats. Wistar rats were fed either MCDD or a control diet in the 4-week induction study; they were given saline or 4 mg/kg/day rosiglitazone. After the induction study period, the rats were divided into four groups and fed MCDD or given a control diet for an additional 8 weeks and received saline or rosiglitazone. Serum and tissue samples were obtained. Rosiglitazone improved inflammation in NASH and improved ALT, alkaline phosphatase, and interleukin-6 levels in the induction study and interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha levels in the treatment study. Our preliminary study is the first to show the anti-inflammatory effects of rosiglitazone in NASH. Rosiglitazone's effect on cytokines may be a key mechanism of its anti-inflammatory effect in NASH.Publication Metadata only Role of ursodeoxycholic acid in prevention of methotrexate-induced liver toxicity(SPRINGER, 2008) ÇELİKEL, ÇİĞDEM; Uraz, Suleyman; Tahan, Veysel; Aygun, Cem; Eren, Fatih; Unluguzel, Goksenin; Yuksel, Meral; Senturk, Omer; Avsar, Erol; Haklar, Goncagul; Celikel, Cigdem; Hulagu, Sadettin; Tozun, NurdanAim Methotrexate (MTX)-induced hepatotoxicity restricts the clinical use of this immunosuppressive drug. In this study, our aim was to research the role of oxidative stress in the hepatic toxicity of MTX and the protective effect of ursodeoxycholic acid (UDCA) in this setting. Methods Wistar type rats (n = 32) were divided into four groups; group-1 as the MTX + UDCA, group-2 as the MTX, group-3 as the UDCA, group-4 as the saline-receiving groups. The MTX + UDCA and MTX groups of rats received 50 mg/kg of UDCA administered orally; whilst physiological saline was administered orally to the MTX and saline groups and continued for the next 6 days. On the second day of the study, the MTX + UDCA and MTX groups had a single intraperitoneal dose of MTX of 20 mg/kg. The UDCA and saline groups also received similar volumes of physiological saline intraperitoneally. On the sixth day, serum samples were collected and analyzed for ALT, alkaline phosphatase (ALP) and gamma glutamyl transpeptidase (GGT) and homogenated liver tissues were examined for reactive oxygen metabolites (ROM); luminol, lucigenin, lipid peroxygenation product malondialdehyde (MDA) and glutathione (GSH) levels. Results In the MTX group, serum ALT, ALP, GGT and tissue ROM levels were higher and GSH level was lower. On the histopathological examination, hepatocellular necrosis was clearly more evident in the MTX group than the MTX + UDCA group. Conclusions UDCA treatment protects against MTX-induced liver toxicity. Histopathologically hepatocyte necrosis can be prevented by UDCA treatment, indicating clearly the hepatoprotective effect of this agent on MTX-induced liver injury.Publication Metadata only Serum levels of osteoprotegerin in the spectrum of nonalcoholic fatty liver disease(TAYLOR & FRANCIS LTD, 2010) ÇELİKEL, ÇİĞDEM; Yilmaz, Yusuf; Yonal, Oya; Kurt, Ramazan; Oral, Arzu Y.; Eren, Fatih; Ozdogan, Osman; Ari, Ferda; Celikel, Cigdem A.; Korkmaz, Seniz; Ulukaya, Engin; Imeryuz, Nese; Kalayci, Cem; Avsar, ErolObjective. Osteoprotegerin (OPG) is a member of the tumor necrosis factor superfamily with pleiotropic effects on inflammation, endocrine function and the immune system. Reduced OPG levels are related to insulin resistance. We tested the hypothesis that serum levels of OPG may be associated with nonalcoholic fatty liver disease (NAFLD). Material and methods. Four groups of patients were enrolled in the present study: subjects with definite nonalcoholic steatohepatitis (NASH, n = 56), borderline NASH (n = 26), simple fatty liver (n = 17) and healthy controls without evidence of liver disease (n = 58). Serum levels of OPG were measured by ELISA. Results. Concentrations of OPG were significantly lower in patients with definite NASH (median: 45 pg/mL, p < 0.001) and borderline NASH (57 pg/mL, p < 0.001) than in controls (92 pg/mL). The area under the ROC curve for distinguishing between steatohepatitis (definite NASH plus borderline NASH) and healthy controls using OPG was 0.82. The use of a cut-off level < 74 pg/mL for serum OPG levels yielded sensitivity and specificity values of 75.6% and 75.9%, respectively. Conclusions. Serum osteoprotegerin concentrations are reduced in patients with the more severe forms of NAFLD and may serve as a noninvasive biomarker to identify patients with NASH.Publication Metadata only R72P Polymorphism of TP53 in Ulcerative Colitis Patients is Associated with the Incidence of Colectomy, Use of Steroids and the Presence of a Positive Family History(SPRINGER, 2010) ÇELİKEL, ÇİĞDEM; Eren, Fatih; Akkiprik, Mustafa; Atug, Ozlen; Sonmez, Ozgur; Tahan, Gulgun; Ozdemir, Filiz; Hamzaoglu, Hulya Over; Celikel, Cigdem Ataizi; Imeryuz, Nese; Avsar, Erol; Ozer, AyseP53 tumor suppressor protein is one of the pivotal regulators for genome integrity, cell cycle and apoptosis. The most commonly and extensively studied single nucleotide polymorphism (SNP) of p53 is Arg>Pro substitution on codon 72 (R72P). Although we know that the SNP has unique functional effects on the protein, its clinical significance is not clearly identified yet. Aim of the study was to access the relationship between R72P genotype distribution and clinical variables in patients with ulcerative colitis (UC) and colorectal cancer (CRC). Genomic DNA samples were extracted from 95 UC, 50 CRC, and 219 healthy controls. R72P genotype analysis was carried out with polymerase chain reaction following by restriction enzyme digestion. We observed that Pro allele carriage is a strong risk factor for CRC (OR=3.03; 95%CI=1.91-2.40; p=0.003), but only modest association with UC (OR=1.61; 95%CI=0.98-2.65; p =0.059) (Pro/Pro and Pro/Arg genotypes vs. Arg/Arg genotype). We did not find any correlation between genotype distribution of the polymorphism and clinical parameters of CRC, but in UC, Pro/Pro genotype was significantly related to an inflammatory bowel disease family history (OR=8.0; 95%CI=1.68-38.08, p=0.015), and Arg/Pro genotype was significantly associated with the history of disease-related colectomy (OR=17.77; 95%CI=0.98-323.34, p=0.012) and steroid use (OR=10.14; 95%CI=2.63-39.12, p=0.0002). Our data suggest that R72P variant seems to be associated with high risk for development of CRC but carries low risk for development of UC. R72P genotypes might be a useful predictive marker for surgical and medical treatment of UC.Publication Metadata only Serum levels of vaspin, obestatin, and apelin-36 in patients with nonalcoholic fatty liver disease(W B SAUNDERS CO-ELSEVIER INC, 2011) ÇELİKEL, ÇİĞDEM; Aktas, Bilge; Yilmaz, Yusuf; Eren, Fatih; Yonal, Oya; Kurt, Ramazan; Alandab, Yesim Ozen; Celikel, Cigdem Ataizi; Ozdogan, Osman; Imeryuz, Nese; Kalayci, Cem; Avsar, ErolThe novel adipokines vaspin, obestatin, and apelin-36 are associated with insulin resistance and the components of the metabolic syndrome. We assayed circulating levels of these molecules and examined their association with clinical, biochemical, and histologic phenotypes in patients with nonalcoholic fatty liver disease (NAFLD). Serum levels of vaspin, obestatin, and apelin-36 were assayed by enzyme-linked immunosorbent assay in 91 patients with biopsy-proven NAFLD and 81 controls. We analyzed associations between adipokines and the characteristics of patients with NAFLD using multivariable linear regression models. Univariable analysis showed that concentrations of vaspin and apelin-36 were significantly higher in patients with NAFLD than in controls, whereas no differences in obestatin levels were found. Serum vaspin levels showed a statistically significant association with C-reactive protein (r = 0.378, P < .001) and liver fibrosis scores (r = 0.401, P < .001), whereas apelin-36 levels showed a modest association with homeostasis model assessment of insulin resistance (r = 0.204, P < .01). After stepwise linear regression analysis, serum vaspin levels were the only independent predictor of liver fibrosis scores in patients with NAFLD (beta = 0.37, t = 3.99, P < .01). Serum vaspin levels are raised in patients with NAFLD regardless of potential confounders and represent an independent predictor of liver fibrosis scores. These findings support further investigation of this novel adipokine in metabolic liver diseases. (C) 2011 Elsevier Inc. All rights reserved.