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BAŞARANOĞLU, METİN

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Sağlık Bilimleri Fakültesi

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METİN

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BAŞARANOĞLU

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Now showing 1 - 10 of 14

Open Access
Ovaries are more vulnerable than hepatocytes for insulin resistance and hyperinsulinemia
(2016-01-01) GULTEPE, Ilhami; Basaranoglu, METİN; SULEYMANOGLU, Yaser; Basaranoglu, GÖKÇEN; BEYAZIT, Fatma; BAŞARANOĞLU, METİN; BAŞARANOĞLU, GÖKÇEN
Background/Aims: Non-alcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS) are common metabolic disorders. We aimed to evaluate the underlying mechanisms in the development of NAFLD and PCOS.
Open Access
Role of Discipline and Educational Method on Vocational High School Students- Success in an Anesthesia Course
(2015-04-01) Basaranoglu, GÖKÇEN; Basaranoglu, METİN; BAŞARANOĞLU, GÖKÇEN; BAŞARANOĞLU, METİN
Objective: The goal of this study is to reveal the relationship between discipline and teaching method and between vocational high school technical students' success in an anesthesia course and levels of following the lessons. Methods: A questionnaire was filled out by first-year technical students in an anesthesia course for situational awareness evaluation at the beginning of the term. Oral presentations were supported by catechetics, reward systems, etc. to ensure active participation. Results: While the students' success rate was 91.9%, the dissatisfaction rate was 4%. The students stated that they were most satisfied (100%) with the rewarding part of the theoretical lessons. Conclusion: Anesthesiology requires discipline for achieving success. Students' course success on anesthesia can be enhanced using a student-centered learning and reward system.
Open Access
Rate and Predictors of Endoscopic Mucosal Healing in Biologic Naive Patients with Inflammatory Bowel Disease by Azathioprine Treatment: A Real World, 10 Years- Experience from a Single Centre in Turkey.
(2016-08-01T00:00:00Z) Basaranoglu, METİN; Ertan, A; Mathew, S; Senturk, H; Ala, A; Demirbag, AE; BAŞARANOĞLU, METİN; ŞENTÜRK, HAKAN
Background: There is increasing evidence that endoscopic mucosal healing (EMH) is a key target in inflammatory bowel disease (IBD) therapy. However, there is limited evidence of EMH rates with conventional IBD therapy outside of Western population groups. Ai̇m: To evaluate the role of azathioprine (AZA) in inducing EMH in IBD patients. Methods: Patients with inflammatory bowel disease were evaluated in terms of endoscopic mucosal healing and the incidence of surgical interventions during the azathioprine treatment between 1995 to 2014. Results: A total of 120 inflammatory bowel disease patients were enrolled. Endoscopic mucosal healing was found in 37% patients with inflammatory bowel disease (42% in chronic ulcerative colitis and 33% in Crohn's disease). Male gender had a negative impact on the efficacy of azathioprine (P<0.05). Responder inflammatory bowel disease patients were older (age at the IBD diagnose) than the nonresponder (P<0.05). Azathioprine therapy reduced the number of the surgical interventions (P<0.05). Conclusi̇on: We showed that azathioprine therapy significantly induced endoscopic mucosal healing in biologic naïve patients with active inflammatory bowel disease as well as decreasing the surgical interventions, with negative predictive factors identified by a younger age at IBD presentation and male gender.
Open Access
From fatty liver to fibrosis: A tale of -second hit-
(2013-02-28) Basaranoglu, METİN; Basaranoglu, GÖKÇEN; Senturk, HAKAN; BAŞARANOĞLU, METİN; BAŞARANOĞLU, GÖKÇEN; ŞENTÜRK, HAKAN
Although much is known about how fat accumulates in the liver, much remains unknown about how this causes sustained hepatocellular injury. The consequences of injury are recognized as nonalcoholic steatohepatitis (NASH) and progressive fibrosis. The accumulation of fat within the hepatocytes sensitizes the liver to injury from a variety of causes and the regenerative capacity of a fatty liver is impaired. An additional stressor is sometimes referred to as a “second hit” in a paradigm that identifies the accumulation of fat as the “first hit”. Possible candidates for the second hit include increased oxidative stress, lipid peroxidation and release of toxic products such as malondialdehyde and 4-hydroxynonenal, decreased antioxidants, adipocytokines, transforming growth factor (TGF)-β, Fas ligand, mitochondrial dysfunction, fatty acid oxidation by CYPs (CYP 2E1, 4A10 and 4A14), and peroxisomes, excess iron, small intestinal bacterial overgrowth, and the generation of gut-derived toxins such as lipopolysaccharide and ethanol. Oxidative stress is one of the most popular proposed mechanisms of hepatocellular injury. Previous studies have specifically observed increased plasma and tissue levels of oxidative stress markers and lipid peroxidation products, with reduced hepatic and plasma levels of antioxidants. There is also some indirect evidence of the benefit of antioxidants such as vitamin E, S-adenosylmethionine, betaine, phlebotomy to remove iron, and N-acetylcysteine in NASH. However, a causal relationship or a pathogenic link between NASH and oxidative stress has not been established so far. A number of sources of increased reactive oxygen species production have been established in NASH that include proinflammatory cytokines such as tumor necrosis factor (TNF)-α, iron overload, overburdened and dysfunctional mitochondria, CYPs, and peroxisomes. Briefly, the pathogenesis of NASH is multifactorial and excess intracellular fatty acids, oxidant stress, ATP depletion, and mitochondrial dysfunction are important causes of hepatocellular injury in the steatotic liver.
Open Access
Mass spectrometry-based untargeted metabolomics study of non-obese individuals with non-alcoholic fatty liver disease
(2023-06-01) Demirel M.; Köktaşoğlu F.; Özkan E.; Dulun Ağaç H.; Gül A. Z.; Sharifov R.; Sarıkaya U.; Başaranoğlu M.; Selek Ş.; DEMİREL, METİN; KÖKTAŞOĞLU, FATMANUR; DULUN AĞAÇ, HALİME; GÜL, AYŞE ZEHRA; SARIKAYA, UFUK; BAŞARANOĞLU, METİN; SELEK, ŞAHABETTİN
Objectives: Non-alcoholic fatty liver disease (NAFLD) is a disease characterized by the accumulation of excessive fat in the liver, which can lead to fibrosis and has an increasing prevalence. NAFLD requires non-invasive diagnostic biomarkers. While typically observed in overweight individuals, it can also occur in non-obese/non-overweight individuals. Comparative studies on non-obese NAFLD patients are scarce. This study aimed to conduct a using liquid chromatography-high resolution mass spectrometry (LC-MS/MS)-based metabolic profiling of non-obese NAFLD patients and healthy controls. Materials and methods: The patient group consisted of 27 individuals with NAFLD, while the healthy control group included 39 individuals. Both groups were between 18 and 40 years old, had a BMI of less than 25 and had alcohol consumption less than 20 g/week for men and 10 g/week for women. Serum samples were collected and analyzed using LC-MS/MS. The data were analyzed using the TidyMass and MetaboAnalyst. Results: The LC-MS/MS analyses detected significant changes in D-amino acid metabolism, vitamin B6 metabolism, apoptosis, mTOR signaling pathway, lysine degradation, and phenylalanine metabolism pathways in non-obese NAFLD patients. Significant changes were also observed in the metabolites D-pantothenic acid, hypoxanthine, citric acid, citramalic acid, L-phenylalanine, glutamine, and histamine-trifluoromethyl-toluidide, β-hydroxymyristic acid, DL-Lactic acid, and 3-methyl-2-oxopentanoic. Overall, the study provides valuable insights into the metabolic changes associated with non-obese NAFLD patients and can contribute to the development of non-invasive diagnostic biomarkers for NAFLD.
Open Access
Association of endoscopic variceal treatment with portal venous system thrombosis in liver cirrhosis: a case-control study
(2022-05-01T00:00:00Z) Wang, Le; Guo, Xiaozhong; Shao, Xiaodong; Xu, Xiangbo; Zheng, Kexin; Wang, Ran; Chawla, Saurabh; BAŞARANOĞLU, METİN; Qi, Xingshun; BAŞARANOĞLU, METİN
Background: The association of endoscopic variceal treatment (EVT) with portal venous system thrombosis (PVST) in liver cirrhosis is still unclear. Methods: PVST was assessed by contrast-enhanced CT or MRI in 406 cirrhotic patients from our prospective database. Case and control groups, which are defined as patients with and without PVST, respectively, were matched at a ratio of 1:1 according to age, gender, Child-Pugh class, and MELD score. History of EVT was reviewed. Logistic regression analysis was used to identify the risk factors for PVST. Odds ratios (ORs) were calculated. Subgroup analyses were further performed in terms of degree and location of PVST. Results: Overall, 109 patients each were included in case and control groups. The case group had a significantly higher proportion of patients who had undergone EVT than the control group (53.2% versus 18.3%; p < 0.001). In detail, the case group had significantly higher proportions of patients who had undergone EVT for controlling bleeding (45.9% versus 14.7%; p < 0.001), endoscopic variceal ligation (EVL) alone (19.3% versus 9.2%; p = 0.033), and EVL combined with endoscopic cyanoacrylate glue injection (24.8% versus 5.5%; p < 0.001). EVT was independently associated with PVST (OR = 4.258; p < 0.001). In subgroup analyses, EVT remained independently associated with partial PVST (OR = 10.063; p < 0.001), complete PVST/fibrotic cord (OR = 4.889; p = 0.008), thrombosis within main portal vein (OR = 5.985; p < 0.001), and thrombosis within superior mesenteric and splenic veins (OR = 5.747; p < 0.001). Conclusions: EVT may lead to a higher risk of PVST, especially more severe PVST, in liver cirrhosis. Screening for and prophylaxis of PVST after EVT should be further explored.
Open Access
Carbohydrate intake and nonalcoholic fatty liver disease: fructose as a weapon of mass destruction
(2015-04-01) Basaranoglu, METİN; Basaranoglu, GÖKÇEN; Bugianesi, Elisabetta; BAŞARANOĞLU, METİN; BAŞARANOĞLU, GÖKÇEN
Excessive accumulation of triglycerides (TG) in liver, in the absence of significant alcohol consumption is nonalcoholic fatty liver disease (NAFLD). NAFLD is a significant risk factor for developing cirrhosis and an independent predictor of cardiovascular disease. High fructose corn syrup (HFCS)-containing beverages were associated with metabolic abnormalities, and contributed to the development of NAFLD in human trials. Ingested carbohydrates are a major stimulus for hepatic de novo lipogenesis (DNL) and are more likely to directly contribute to NAFLD than dietary fat. Substrates used for the synthesis of newly made fatty acids by DNL are primarily glucose, fructose, and amino acids. Epidemiological studies linked HFCS consumption to the severity of fibrosis in patients with NAFLD. New animal studies provided additional evidence on the role of carbohydrate-induced DNL and the gut microbiome in NAFLD. The excessive consumption of HFCS-55 increased endoplasmic reticulum stress, activated the stress-related kinase, caused mitochondrial dysfunction, and increased apoptotic activity in the liver. A link between dietary fructose intake, increased hepatic glucose transporter type-5 (Glut5) (fructose transporter) gene expression and hepatic lipid peroxidation, MyD88, TNF-α levels, gut-derived endotoxemia, toll-like receptor-4, and NAFLD was reported. The lipogenic and proinflammatory effects of fructose appear to be due to transient ATP depletion by its rapid phosphorylation within the cell and from its ability to raise intracellular and serum uric acid levels. However, large prospective studies that evaluated the relationship between fructose and NAFLD were not performed yet
Open Access
Significant cohort of non-alcoholic fatty liver disease with portal vein thrombosis in transplant waiting list.
(2016-03-08T00:00:00Z) Senturk, H; Basaranoglu, METİN; Najjar, SM; Demirbag, AE; BAŞARANOĞLU, METİN; ŞENTÜRK, HAKAN
Aim: To characterize non-alcoholic fatty liver disease (NAFLD) presentation with esophageal varices. Methods: We carried out a retrospective cohort study on 258 patients with esophageal varices at a single tertiary referral center. These patients underwent diagnosis of several liver diseases, including: NAFLD-associated cirrhosis, hepatitis B, hepatitis C, Wilson disease, autoimune liver diseases, and others. Results: Of the 258 patients, 39% of patients exhibited esophageal varices due to NAFLD-associated cirrhosis. Of the 38 (14.7%) patients developed hepatocellular carcinoma during follow-up, 52% were due to hepatitis B, 26% due to hepatitis C and 13.2% due to NAFLD. Of the 258 patients, 50.0% with NAFLD, 33.3% with hepatitis B, 26.3% with hepatitis C, and 58.3% with other diseases were alive at the end of the 5-year period with a significant difference according to the Kaplan-Meier log Rank test (P = 0.040). Portal vein thrombosis was detected in 47.5% of patients with NAFLD, in 29% of patients with hepatitis B, in 17% of patients with hepatitis C, and in 62% of patients with other related diseases (P < 0.0001). Conclusion: Our study showed a proportionally greater elevation in liver transplant candidacy in patients with NAFLD and portal vein thrombosis. Older patients were more prone to developing cirrhosis, hepatocellular carcinoma and a high mortality rate. However, younger patients exhibited more portal vein thrombosis and gastric varices.
Open Access
Lean and Nonobese NAFLD/NASH From a Hepatologist-s Point of View
(2021-01-01T00:00:00Z) BAŞARANOĞLU, METİN; BAŞARANOĞLU, METİN
Open Access
Fructose as a key player in the development of fatty liver disease
(2013-02-01T00:00:00Z) BAŞARANOĞLU, METİN; BAŞARANOĞLU, Gökçen; SABUNCU, TEVFİK; ŞENTÜRK, HAKAN; BAŞARANOĞLU, METİN; BAŞARANOĞLU, GÖKÇEN; ŞENTÜRK, HAKAN
We aimed to investigate whether increased consumption of fructose is linked to the increased prevalence of fatty liver. The prevalence of nonalcoholic steatohepatitis (NASH) is 3% and 20% in nonobese and obese subjects, respectively. Obesity is a low-grade chronic inflammatory condition and obesity-related cytokines such as interleukin-6, adiponectin, leptin, and tumor necrosis factor-a may play important roles in the development of nonalcoholic fatty liver disease (NAFLD). Additionally, the prevalence of NASH associated with both cirrhosis and hepatocellular carcinoma was reported to be high among patients with type 2 diabetes with or without obesity. Our research group previously showed that consumption of fructose is associated with adverse alterations of plasma lipid profiles and metabolic changes in mice, the American Lifestyle-Induced Obesity Syndrome model, which included consumption of a high-fructose corn syrup in amounts relevant to that consumed by some Americans. The observation reinforces the concerns about the role of fructose in the obesity epidemic. Increased availability of fructose (e. g., high-fructose corn syrup) increases not only abnormal glucose flux but also fructose metabolism in the hepatocyte. Thus, the anatomic position of the liver places it in a strategic buffering position for absorbed carbohydrates and amino acids. Fructose was previously accepted as a beneficial dietary component because it does not stimulate insulin secretion. However, since insulin signaling plays an important role in central mechanisms of NAFLD, this property of fructose may be undesirable. Fructose has a selective hepatic metabolism, and provokes a hepatic stress response involving activation of c-Jun N-terminal kinases and subsequent reduced hepatic insulin signaling. As high fat diet alone produces obesity, insulin resistance, and some degree of fatty liver with minimal inflammation and no fibrosis, the fast food diet which includes fructose and fats produces a gene expression signature of increased hepatic fibrosis, inflammation, endoplasmic reticulum stress and lipoapoptosis. Hepatic de novo lipogenesis (fatty acid and triglyceride synthesis) is increased in patients with NAFLD. Stable-isotope studies showed that increased de novo lipogenesis (DNL) in patients with NAFLD contributed to fat accumulation in the liver and the development of NAFLD. Specifically, DNL was responsible for 26% of accumulated hepatic triglycerides and 15%-23% of secreted very low-density lipoprotein triglycerides in patients with NAFLD compared to an estimated less than 5% DNL in healthy subjects and 10% DNL in obese people with hyperinsulinemia. In conclusion, understanding the underlying causes of NAFLD forms the basis for rational preventive and treatment strategies of this major form of chronic liver disease. (C) 2013 Baishideng. All rights reserved.