Kardelen Büşra Ege Gündüz

Dr. Kardelen Büşra Ege Gündüz

orcid

Research Focus & Metrics

Academic Career Length

4Years (2023-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 February 2023 in Journal of Surgery and Medicine
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CAGLAR DOGUERCAGLAR DOGUER
CAGLAR DOGUER
NDNazan Tokatlı Demirok
Nazan Tokatlı Demirok
KGKardelen Büşra Ege Gündüz
Kardelen Büşra Ege Gündüz
Background/Aim: At present, a gluten-free diet is the only efficient way to treat celiac disease (CD). The development of novel approaches to lessen or counteract the pathogenic effects of gluten remains crucial for the treatment of CD. The aim in this investigation was to examine the restorative effects of Acetobacter ghanensis as a novel probiotic against gliadin-induced modulation in the barrier integrity of an intestinal epithelial cell (IEC) model (Caco-2). Methods: Fully differentiated Caco-2 cell monolayers were subjected to enzymatically digested gliadin with a pepsin and trypsin (PT) in the presence or absence of A. ghanensis for 90 min. The relative amounts of zonulin, zonula occludens-1 (ZO-1), claudin-1, and occludin mRNA expression were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Transepithelial electrical resistance (TEER) was evaluated to monitor the barrier integrity of cell monolayers. Statistical analyses were carried out using one- or two-way ANOVA followed by Tukey’s post-hoc analysis for multiple pairwise comparisons. Results: A significant upregulation (4.7-fold) of zonulin was noted in the PT-gliadin treated Caco-2 cells in comparison with the untreated controls (P<0.001). Conversely, gliadin-induced zonulin expression was markedly downregulated in the Caco-2 cells following exposure to A. ghanensis in the presence of PT-gliadin (P<0.001). Furthermore, prominent decreases in the mRNA expression levels of ZO-1 (45%) and occludin (40%) were seen in the PT-gliadin exposed Caco-2 cells compared to the untreated control cells (P<0.001). PT-gliadin in the Caco-2 cells did not significantly alter the mRNA levels of claudin-1 (P=0.172). Similarly to zonulin expression, the decreasing effect of PT-gliadin on ZO-1 was completely attenuated in the PT-gliadin-administrated Caco-2 cells following exposure to A. ghanensis (P<0.001). Conclusion: A. ghanensis restored the pathogenicity of PT-gliadin on intestinal barrier integrity. function ready(callback){ // in case the document is already rendered if (document.readyState!='loading') callback(); // modern browsers else if (document.addEventListener) document.addEventListener('DOMContentLoaded', callback); // IE <= 8 else document.attachEvent('onreadystatechange', function(){ if (document.readyState=='complete') callback(); }); } ready(function(){ var abstract = document.getElementById("abstract"); //declare your possible strings in vars let st = innerHTML; st = st.replace(//g,""); st = st.replace(/<\/p>/g,""); st = st.replace(//g,""); st = st.replace(/<\/strong>/g,""); st = st.replace(/ /g,""); let title = "Background/Aim:"; if(st.includes(title)){ st = st.replace(title, ""+title+" "); } else{ title = "Aim:"; st = st.replace(title, ""+title+""); } let titles = ["Methods:", "Conclusion:", "Results:"]; titles.forEach((title, ndx) => { //console.log(title); st = st.replace(title, " "+title+""); }); //console.log(st); innerHTML = ''+st+''; }); Downloads Download data is not yet available. 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Int Rev Cell Mol Biol. 2021;358:165-205. doi: 10.1016/bs.ircmb.2020.10.003. DOI: https://doi.org/10.1016/bs.ircmb.2020.10.003 Falcigno L, Calvanese L, Conte M, Nanayakkara M, Barone MV, D'Auria G. Structural Perspective of Gliadin Peptides Active in Celiac Disease. Int J Mol Sci. 2020;21(23). doi: 10.3390/ijms21239301. DOI: https://doi.org/10.3390/ijms21239301 Chelakkot C, Ghim J, Ryu SH. Mechanisms regulating intestinal barrier integrity and its pathological implications. Exp Mol Med. 2018;50(8):1-9. doi: 10.1038/s12276-018-0126-x. DOI: https://doi.org/10.1038/s12276-018-0126-x Lammers KM, Lu R, Brownley J, Lu B, Gerard C, Thomas K, et al. Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3. Gastroenterology. 2008;135(1):194-204.e3. doi: 10.1053/j.gastro.2008.03.023. DOI: https://doi.org/10.1053/j.gastro.2008.03.023 Drago S, El Asmar R, Di Pierro M, Grazia Clemente M, Tripathi A, Sapone A, et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol. 2006;41(4):408-19. doi: 10.1080/00365520500235334. DOI: https://doi.org/10.1080/00365520500235334 Fasano A. Zonulin, regulation of tight junctions, and autoimmune diseases. Ann N Y Acad Sci. 2012;1258:25-33. doi: 10.1111/j.1749-6632.2012.06538.x. DOI: https://doi.org/10.1111/j.1749-6632.2012.06538.x Håkansson Å, Andrén Aronsson C, Brundin C, Oscarsson E, Molin G, Agardh D. Effects of. Nutrients. 2019;11(8). doi: 10.3390/nu11081925. DOI: https://doi.org/10.3390/nu11081925 Marasco G, Cirota GG, Rossini B, Lungaro L, Di Biase AR, Colecchia A, et al. Probiotics, Prebiotics and Other Dietary Supplements for Gut Microbiota Modulation in Celiac Disease Patients. Nutrients. 2020;12(9). doi: 10.3390/nu12092674. DOI: https://doi.org/10.3390/nu12092674 Gujral N, Suh JW, Sunwoo HH. Effect of anti-gliadin IgY antibody on epithelial intestinal integrity and inflammatory response induced by gliadin. BMC Immunol. 2015;16:41. doi: 10.1186/s12865-015-0104-1. DOI: https://doi.org/10.1186/s12865-015-0104-1 Doguer C, Akalan H, Tokatlı Demirok N, Erdal B, Mete R, Bilgen T. Protective effects of Acetobacter ghanensis against gliadin toxicity in intestinal epithelial cells with immunoregulatory and gluten-digestive properties. Eur J Nutr. 2022. doi: 10.1007/s00394-022-03015-6. DOI: https://doi.org/10.1007/s00394-022-03015-6 Gulec S, Collins JF. Silencing the Menkes copper-transporting ATPase (Atp7a) gene in rat intestinal epithelial (IEC-6) cells increases iron flux via transcriptional induction of ferroportin 1 (Fpn1). J Nutr. 2014;144(1):12-9. doi: 10.3945/jn.113.183160. DOI: https://doi.org/10.3945/jn.113.183160 Gujral N, Freeman HJ, Thomson AB. Celiac disease: prevalence, diagnosis, pathogenesis and treatment. World J Gastroenterol. 2012;18(42):6036-59. doi: 10.3748/wjg.v18.i42.6036. DOI: https://doi.org/10.3748/wjg.v18.i42.6036 Ludvigsson JF, Murray JA. Epidemiology of Celiac Disease. Gastroenterol Clin North Am. 2019;48(1):1-18. doi: 10.1016/j.gtc.2018.09.004. DOI: https://doi.org/10.1016/j.gtc.2018.09.004 Makharia GK, Singh P, Catassi C, Sanders DS, Leffler D, Ali RAR, et al. The global burden of coeliac disease: opportunities and challenges. Nat Rev Gastroenterol Hepatol. 2022;19(5):313-27. doi: 10.1038/s41575-021-00552-z. DOI: https://doi.org/10.1038/s41575-021-00552-z Su GL, Ko CW, Bercik P, Falck-Ytter Y, Sultan S, Weizman AV, et al. AGA Clinical Practice Guidelines on the Role of Probiotics in the Management of Gastrointestinal Disorders. Gastroenterology. 2020;159(2):697-705. doi: 10.1053/j.gastro.2020.05.059. DOI: https://doi.org/10.1053/j.gastro.2020.05.059 Seiler CL, Kiflen M, Stefanolo JP, Bai JC, Bercik P, Kelly CP, et al. Probiotics for Celiac Disease: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Am J Gastroenterol. 2020;115(10):1584-95. doi: 10.14309/ajg.0000000000000749. DOI: https://doi.org/10.14309/ajg.0000000000000749 Cristofori F, Indrio F, Miniello VL, De Angelis M, Francavilla R. Probiotics in Celiac Disease. Nutrients. 2018;10(12). doi: 10.3390/nu10121824. DOI: https://doi.org/10.3390/nu10121824 Clemente MG, De Virgiliis S, Kang JS, Macatagney R, Musu MP, Di Pierro MR, et al. Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function. Gut. 2003;52(2):218-23. doi: 10.1136/gut.52.2.218. DOI: https://doi.org/10.1136/gut.52.2.218 Hollon J, Puppa EL, Greenwald B, Goldberg E, Guerrerio A, Fasano A. Effect of gliadin on permeability of intestinal biopsy explants from celiac disease patients and patients with non-celiac gluten sensitivity. Nutrients. 2015;7(3):1565-76. doi: 10.3390/nu7031565. DOI: https://doi.org/10.3390/nu7031565 Orlando A, Linsalata M, Notarnicola M, Tutino V, Russo F. Lactobacillus GG restoration of the gliadin induced epithelial barrier disruption: the role of cellular polyamines. BMC Microbiol. 2014;14:19. doi: 10.1186/1471-2180-14-19. DOI: https://doi.org/10.1186/1471-2180-14-19 Lindfors K, Blomqvist T, Juuti-Uusitalo K, Stenman S, Venäläinen J, Mäki M, et al. Live probiotic Bifidobacterium lactis bacteria inhibit the toxic effects induced by wheat gliadin in epithelial cell culture. Clin Exp Immunol. 2008;152(3):552-8. oi: 10.1111/j.1365-2249.2008.03635.x. DOI: https://doi.org/10.1111/j.1365-2249.2008.03635.x Silano M, Vincentini O, Luciani A, Felli C, Caserta S, Esposito S, et al. Early tissue transglutaminase-mediated response underlies K562(S)-cell gliadin-dependent agglutination. Pediatr Res. 2012;71(5):532-8. doi: 10.1038/pr.2012.4. DOI: https://doi.org/10.1038/pr.2012.4 Sander GR, Cummins AG, Henshall T, Powell BC. Rapid disruption of intestinal barrier function by gliadin involves altered expression of apical junctional proteins. FEBS Lett. 2005;579(21):4851-5. doi: 10.1016/j.febslet.2005.07.066. DOI: https://doi.org/10.1016/j.febslet.2005.07.066 Orlando A, Linsalata M, Bianco G, Notarnicola M, D'Attoma B, Scavo MP, et al. GG Protects the Epithelial Barrier of Wistar Rats from the Pepsin-Trypsin-Digested Gliadin (PTG)-Induced Enteropathy. Nutrients. 2018;10(11). doi: 10.3390/nu10111698. DOI: https://doi.org/10.3390/nu10111698 Bhat MI, Sowmya K, Kapila S, Kapila R. Potential Probiotic Lactobacillus rhamnosus (MTCC-5897) Inhibits Escherichia coli Impaired Intestinal Barrier Function by Modulating the Host Tight Junction Gene Response. Probiotics Antimicrob Proteins. 2020;12(3):1149-60. doi: 10.1007/s12602-019-09608-8. DOI: https://doi.org/10.1007/s12602-019-09608-8 Anderson RC, Cookson AL, McNabb WC, Park Z, McCann MJ, Kelly WJ, et al. Lactobacillus plantarum MB452 enhances the function of the intestinal barrier by increasing the expression levels of genes involved in tight junction formation. BMC Microbiol. 2010;10:316. doi: 10.1186/1471-2180-10-316. DOI: https://doi.org/10.1186/1471-2180-10-316 Herrán AR, Pérez-Andrés J, Caminero A, Nistal E, Vivas S, Ruiz de Morales JM, et al. Gluten-degrading bacteria are present in the human small intestine of healthy volunteers and celiac patients. Res Microbiol. 2017;168(7):673-84. doi: 10.1016/j.resmic.2017.04.008. DOI: https://doi.org/10.1016/j.resmic.2017.04.008 Greco L, Gobbetti M, Auricchio R, Di Mase R, Landolfo F, Paparo F, et al. Safety for patients with celiac disease of baked goods made of wheat flour hydrolyzed during food processing. Clin Gastroenterol Hepatol. 2011;9(1):24-9. doi: 10.1016/j.cgh.2010.09.025. DOI: https://doi.org/10.1016/j.cgh.2010.09.025 Francavilla R, De Angelis M, Rizzello CG, Cavallo N, Dal Bello F, Gobbetti M. Selected Probiotic Lactobacilli Have the Capacity to Hydrolyze Gluten Peptides during Simulated Gastrointestinal Digestion. Appl Environ Microbiol. 2017;83(14). doi: 10.1128/AEM.00376-17. DOI: https://doi.org/10.1128/AEM.00376-17 <!-- .main_entry --> Downloads PDF 162 241 Published 2023-02-03 Issue Vol. 7 No. 2 (2023): 133-137 Section Research Article How to Cite 1. Doguer C, Tokatlı Demirok N, Ege Gunduz KB. Restorative effects of Acetobacter ghanensis on the pathogenicity of gliadin-induced modulation of tight junction-associated gene expression in intestinal epithelial cells: Impacts of Acetobacter ghanensis on the intestinal epithelial barrier. J Surg Med [Internet]. 2023 Feb. 3 [cited 2023 Dec. 5];7(2):133-7. Available from: https://jsurgmed.com/article/view/7585 More Citation Formats ACM ACS APA ABNT Chicago Harvard IEEE MLA Turabian Vancouver Download Citation Endnote/Zotero/Mendeley (RIS) BibTeX License Copyright (c) 2023 Caglar Doguer, Nazan Tokatlı Demirok, Kardelen Busra Ege Gunduz This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. Citations <!-- AddThis Button BEGIN --> <!-- AddThis Button END --> #7585 <!-- .entry_details -->

19 April 2026 in Food Science & Nutrition
Verified
Journal Article
Open access
KGKardelen Büşra Ege Gündüz
Kardelen Büşra Ege Gündüz
SBSümeyye Bora
Sümeyye Bora
BBBerrak Baştürk
Berrak Baştürk
COCeyda Okudu
Ceyda Okudu
Non‐alcoholic fatty liver disease (NAFLD) is closely associated with obesity, insulin resistance, and increased cardiometabolic risk. Dietary fat quality has emerged as a modifiable factor in NAFLD management; however, the specific effects of canola oil on hepatic and metabolic markers remain unclear. This systematic review and meta‐analysis evaluated randomized controlled trials investigating the effects of canola oil consumption in adults with NAFLD. Searches were conducted in PubMed, Web of Science, Scopus, and Cochrane Library databases through December 2024 in accordance with PRISMA guidelines (PROSPERO: CRD42024593566). Random‐effects models were applied to estimate pooled effect sizes. Risk of bias was assessed using the Cochrane Risk of Bias 2 tool, and certainty of evidence was graded using the GRADE framework. Three randomized controlled trials (four intervention arms; n = 220 participants) were included. Canola oil consumption was associated with significant reductions in alanine aminotransferase (ALT) (effect size: −0.472, 95% CI: −0.711 to −0.233; p < 0.001) and aspartate aminotransferase (AST) (effect size: −0.505, 95% CI: −0.745 to −0.264; p < 0.001). Triglyceride levels were also significantly reduced (effect size: −0.593, 95% CI: −1.151 to −0.036; p = 0.037), although heterogeneity was substantial. No significant effects were observed for HDL (effect size: 0.154, 95% CI: −0.604 to 0.912; p = 0.69) or gamma‐glutamyl transferase (GGT) (effect size: 0.156, 95% CI: −0.173 to 0.486; p = 0.352). The certainty of evidence was moderate for ALT and low for AST, triglycerides, HDL, and GGT, primarily because of small sample sizes and clinical heterogeneity. Dietary canola oil may contribute to modest improvements in hepatic enzymes and triglyceride levels in adults with NAFLD. However, the limited number of trials, variability in intervention protocols, and absence of long‐term clinical outcomes warrant cautious interpretation. Larger, well‐designed studies are needed to clarify its role within cardiometabolic risk management strategies for NAFLD.

30 September 2025 in Haliç Üniversitesi Sağlık Bilimleri Dergisi
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DDDilara Doğanay
Dilara Doğanay
KGKardelen Büşra Ege Gündüz
Kardelen Büşra Ege Gündüz
Sustainable nutrition is an essential approach to ensuring global food security, environmental protection, and public health. It focuses on dietary patterns that have a low environmental impact while promoting optimal health and well-being for present and future generations. Key sustainable diet models such as the Mediterranean, Nordic, DASH, and vegetarian/vegan diets emphasize plant-based foods, seasonal and local produce, reduced meat consumption, and minimal processed foods. These models not only support human health but also significantly reduce greenhouse gas emissions, water usage, and land degradation. Alternative protein sources are increasingly vital in addressing sustainability concerns. Plant-based proteins (like legumes, soy, and nuts), single-cell proteins (derived from algae, fungi, and bacteria), and edible insects are emerging as efficient, eco-friendly substitutes to traditional animal proteins. They require fewer resources and generate less environmental harm. Despite the benefits, global adoption of sustainable diets faces several barriers. Limited awareness, economic constraints, accessibility issues, and cultural resistance to alternative foods hinder progress. Overcoming these challenges requires coordinated efforts in public education, policy-making, and innovation in food production. Promoting sustainable nutrition is not just a health strategy but a critical response to climate change and environmental degradation.

19 September 2026 in Nutrients
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KGKardelen Büşra Ege Gündüz
Kardelen Büşra Ege Gündüz
COCeyda Okudu
Ceyda Okudu
SGSongül Güder
Songül Güder
ISİsa Sevindir
İsa Sevindir
Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is related to insulin resistance, dyslipidemia, and oxidative stress. Vitamin E and low-density lipoprotein receptor-related protein 5 (LRP5) may be involved, but evidence remains limited. This study compared dietary vitamin E intake and LRP5 rs4988321 genotype distributions between adults with and without MASLD. Methods: This single-center case–control study included 59 adults with ultrasonographically confirmed MASLD and 47 controls. Vitamin E intake was assessed using two non-consecutive 24-h dietary recalls and a vitamin E-focused food frequency questionnaire. The rs4988321 variant was genotyped using a TaqMan assay. Group comparisons and multivariable models were used. Results: Vitamin E intake did not differ between groups using 24-h recalls (11.81 vs. 9.35 mg/day; p = 0.246) or the FFQ (16.47 vs. 17.58 mg/day; p = 0.834); only the recall-derived estimate was energy-adjusted and remained unassociated with MASLD. The rs4988321 genotype distributions were similar (p = 0.548). After adjustment for age, sex, genotype, and BMI, ALT, LDL cholesterol, and triglyceride levels were nominally higher in participants with MASLD. However, only ALT remained significant after false discovery rate correction (q = 0.021). In the BMI-adjusted logistic model, higher TyG index (OR = 2.360; 95% CI: 1.067–5.218; p = 0.034) and BMI (OR = 1.304; 95% CI: 1.108–1.535; p = 0.001) were associated with greater odds of MASLD. Conclusions: Dietary vitamin E intake and the rs4988321 genotype were not associated with MASLD status in this sample. ALT remained higher after multivariable adjustment, whereas the TyG and BMI associations were specific to the BMI-adjusted model.

26 June 2025 in The North African Journal of Food and Nutrition Research
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BBBerrak Basturk
Berrak Basturk
ZOZeynep Koc Ozerson
Zeynep Koc Ozerson
AKAysu Yıldız karaahmet
Aysu Yıldız karaahmet
KGKardelen Büşra Ege Gündüz
Kardelen Büşra Ege Gündüz
SBSumeyye Bora
Sumeyye Bora
Background: Aronia melanocarpa, commonly known as chokeberry, is a fruit experiencing increasing cultivation and recognition due to its health-promoting properties. Its primary bioactive components are (poly)phenols, which are recognized for their crucial role in modulating the intestinal microbiota and exerting beneficial effects on human health. Aims: This study aimed to systematically synthesize and critically evaluate the findings of randomized clinical trials investigating the impact of Aronia melanocarpa consumption on the modulation of gut microbiota composition and its metabolism-mediated physiological consequences in human subjects. Methods: Randomized controlled trials published in English were considered for inclusion. Comprehensive searches were conducted across the Cochrane Library, Scopus, PubMed/MEDLINE, and Web of Science databases up to October 20, 2024. A systematic evaluation of gut microbiota parameters was performed. For secondary metabolite levels, biochemical markers, and cardiovascular risk parameters, a meta-analysis utilizing a mean effect model was conducted. Results: Four articles, collectively involving 200 participants, met the inclusion criteria for this systematic review. Of these, three articles were subsequently incorporated into the meta-analysis. Consumption of Aronia melanocarpa intervention periods ranging from 4 to12 weeks did not yield significant differences in the α-diversity or β-diversity of the gut microbiota. However, increased levels of specific bacterial genera and species, including Intestinimonas butyriciproducens, Lawsonibacter asaccharolyticus, Bacteroides xylanisolvens, Bacteroides, Anaerostipes, Butyricimonas faecihominis, were observed in individuals consuming Aronia capsules for 12 weeks. Furthermore, Aronia melanocarpa consumption significantly increased non-flavonoid polyphenol stilbenes by a mean difference of 0.11 (95% CI: 0.03, 0.20, p = 0.010) compared to control groups. No significant differences were detected in vascular function or fasting plasma glucose levels. Conclusions: The included studies indicate that Aronia melanocarpa exerts positive effects on the gut microbiota. Notably, interventions involving Aronia melanocarpa consumption for 12 weeks and those with high polyphenol content appeared to be more effective in modulating the microbiota. However, no statistically significant beneficial impact on broader health parameters was identified in this meta-analysis. This outcome is likely attributable to variations in dosage, product type, intervention durations, participant characteristics, and the specific final measurements employed across the included studies. Keywords: Aronia melanocarpa; Gut function; Gut symptoms; Meta-analysis; Microbiota; Systematic review.