Search

Your search keyword '"Demir, Münevver"' showing total 394 results
Start Over Author "Demir, Münevver"
394 results on '"Demir, Münevver"'

1. Interleukin‐18 signaling promotes activation of hepatic stellate cells in mouse liver fibrosis

Author

Knorr, Jana, Kaufmann, Benedikt, Inzaugarat, Maria Eugenia, Holtmann, Theresa Maria, Geisler, Lukas, Hundertmark, Jana, Kohlhepp, Marlene Sophia, Boosheri, Laela M, Chilin‐Fuentes, Daisy R, Birmingham, Amanda, Fisch, Kathleen M, Schilling, Joel D, Loosen, Sven H, Trautwein, Christian, Roderburg, Christoph, Demir, Münevver, Tacke, Frank, Hoffman, Hal M, Feldstein, Ariel E, and Wree, Alexander

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Immunology, Liver Disease, Digestive Diseases, Nutrition, Chronic Liver Disease and Cirrhosis, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Oral and gastrointestinal, Mice, Animals, Inflammasomes, Hepatic Stellate Cells, Interleukin-18, NLR Family, Pyrin Domain-Containing 3 Protein, Liver Cirrhosis, Fibrosis, Carrier Proteins, Liver, Medical Biochemistry and Metabolomics, Gastroenterology & Hepatology, Clinical sciences
Abstract

Background and aimsNucleotide-binding oligomerization domain-like receptor-family pyrin domain-containing 3 (NLRP3) inflammasome activation has been shown to result in liver fibrosis. Mechanisms and downstream signaling remain incompletely understood. Here, we studied the role of IL-18 in hepatic stellate cells (HSCs), and its impact on liver fibrosis.Approach and resultsWe observed significantly increased serum levels of IL-18 (128.4 pg/ml vs. 74.9 pg/ml) and IL-18 binding protein (BP; 46.50 ng/ml vs. 15.35 ng/ml) in patients with liver cirrhosis compared with healthy controls. Single cell RNA sequencing data showed that an immunoregulatory subset of murine HSCs highly expresses Il18 and Il18r1 . Treatment of cultured primary murine HSC with recombinant mouse IL-18 accelerated their transdifferentiation into myofibroblasts. In vivo , IL-18 receptor-deficient mice had reduced liver fibrosis in a model of fibrosis induced by HSC-specific NLRP3 overactivation. Whole liver RNA sequencing analysis from a murine model of severe NASH-induced fibrosis by feeding a choline-deficient, L-amino acid-defined, high fat diet showed that genes related to IL-18 and its downstream signaling were significantly upregulated, and Il18-/- mice receiving this diet for 10 weeks showed protection from fibrotic changes with decreased number of alpha smooth muscle actin-positive cells and collagen deposition. HSC activation triggered by NLRP3 inflammasome activation was abrogated when IL-18 signaling was blocked by its naturally occurring antagonist IL-18BP. Accordingly, we observed that the severe inflammatory phenotype associated with myeloid cell-specific NLRP3 gain-of-function was rescued by IL-18BP.ConclusionsOur study highlights the role of IL-18 in the development of liver fibrosis by its direct effect on HSC activation identifying IL-18 as a target to treat liver fibrosis.

Published
2023

4. The fecal mycobiome in non-alcoholic fatty liver disease ☆

Author

Demir, Münevver, Lang, Sonja, Hartmann, Phillipp, Duan, Yi, Martin, Anna, Miyamoto, Yukiko, Bondareva, Marina, Zhang, Xinlian, Wang, Yanhan, Kasper, Philipp, Bang, Corinna, Roderburg, Christoph, Tacke, Frank, Steffen, Hans-Michael, Goeser, Tobias, Kruglov, Andrey, Eckmann, Lars, Stärkel, Peter, Fouts, Derrick E, and Schnabl, Bernd

Subjects
Substance Misuse, Nutrition, Alcoholism, Alcohol Use and Health, Chronic Liver Disease and Cirrhosis, Hepatitis, Digestive Diseases, Liver Disease, 2.1 Biological and endogenous factors, Aetiology, Oral and gastrointestinal, Good Health and Well Being, Animals, Feces, Gastrointestinal Microbiome, Humans, Liver, Mice, Mycobiome, Non-alcoholic Fatty Liver Disease, Saccharomyces cerevisiae, Fungi, microbiota, microbiome, metagenomics, gut pathogens, NAFLD, NASH, Clinical Sciences, Public Health and Health Services, Gastroenterology & Hepatology
Abstract

Background & aimsStudies investigating the gut-liver axis have largely focused on bacteria, whereas little is known about commensal fungi. We characterized fecal fungi in patients with non-alcoholic fatty liver disease (NAFLD) and investigated their role in a fecal microbiome-humanized mouse model of Western diet-induced steatohepatitis.MethodsWe performed fungal internal transcribed spacer 2 sequencing using fecal samples from 78 patients with NAFLD, 16 controls and 73 patients with alcohol use disorder. Anti-Candida albicans (C. albicans) IgG was measured in blood samples from 17 controls and 79 patients with NAFLD. Songbird, a novel multinominal regression tool, was used to investigate mycobiome changes. Germ-free mice were colonized with feces from patients with non-alcoholic steatohepatitis (NASH), fed a Western diet for 20 weeks and treated with the antifungal amphotericin B.ResultsThe presence of non-obese NASH or F2-F4 fibrosis was associated with a distinct fecal mycobiome signature. Changes were characterized by an increased log-ratio for Mucor sp./Saccharomyces cerevisiae (S. cerevisiae) in patients with NASH and F2-F4 fibrosis. The C. albicans/S. cerevisiae log-ratio was significantly higher in non-obese patients with NASH when compared with non-obese patients with NAFL or controls. We observed a different fecal mycobiome composition in patients with NAFLD and advanced fibrosis compared to those with alcohol use disorder and advanced fibrosis. Plasma anti-C. albicans IgG was increased in patients with NAFLD and advanced fibrosis. Gnotobiotic mice, colonized with human NASH feces and treated with amphotericin B were protected from Western diet-induced steatohepatitis.ConclusionsNon-obese patients with NAFLD and more advanced disease have a different fecal mycobiome composition to those with mild disease. Antifungal treatment ameliorates diet-induced steatohepatitis in mice. Intestinal fungi could be an attractive target to attenuate NASH.Lay summaryNon-alcoholic fatty liver disease is one of the most common chronic liver diseases and is associated with changes in the fecal bacterial microbiome. We show that patients with non-alcoholic fatty liver disease and more severe disease stages have a specific composition of fecal fungi and an increased systemic immune response to Candida albicans. In a fecal microbiome-humanized mouse model of Western diet-induced steatohepatitis, we show that treatment with antifungals reduces liver damage.

Published
2022

5. Colesevelam ameliorates non-alcoholic steatohepatitis and obesity in mice

Author

Hartmann, Phillipp, Duan, Yi, Miyamoto, Yukiko, Demir, Münevver, Lang, Sonja, Hasa, Elda, Stern, Patrick, Yamashita, Dennis, Conrad, Mary, Eckmann, Lars, and Schnabl, Bernd

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Hepatitis, Chronic Liver Disease and Cirrhosis, Digestive Diseases, Nutrition, Liver Disease, Genetics, Obesity, Aetiology, 2.1 Biological and endogenous factors, Metabolic and endocrine, Oral and gastrointestinal, Good Health and Well Being, Animals, Bile Acids and Salts, Colesevelam Hydrochloride, Disease Models, Animal, Humans, Liver, Mice, Mice, Inbred C57BL, Non-alcoholic Fatty Liver Disease, Bile acid sequestrants, Humanized mice, Non-alcoholic fatty liver disease, Experimental liver disease, Liver inflammation, Liver steatosis, Liver fibrosis, Insulin resistance, Western diet, Rodents, Gastroenterology & Hepatology, Clinical sciences
Abstract

BackgroundObesity, non-alcoholic fatty liver disease (NAFLD) and its more advanced form non-alcoholic steatohepatitis (NASH) are important causes of morbidity and mortality worldwide. Bile acid dysregulation is a pivotal part in their pathogenesis. The aim of this study was to evaluate the bile acid sequestrant colesevelam in a microbiome-humanized mouse model of diet-induced obesity and steatohepatitis.MethodsGerm-free C57BL/6 mice were associated with stool from patients with NASH and subjected to 20 weeks of Western diet feeding with and without colesevelam.ResultsColesevelam reduced Western diet-induced body and liver weight gain in microbiome-humanized mice compared with controls. It ameliorated Western diet-induced hepatic inflammation, steatosis, fibrosis and insulin resistance. Colesevelam increased de novo bile acid synthesis and decreased hepatic cholesterol content in microbiome-humanized mice fed a Western diet. It further induced the gene expression of the antimicrobials Reg3g and Reg3b in the distal small intestine and decreased plasma levels of LPS.ConclusionsColesevelam ameliorates Western diet-induced steatohepatitis and obesity in microbiome-humanized mice.

Published
2022

6. Soluble urokinase plasminogen activator receptor levels predict survival in patients with portal hypertension undergoing TIPS

Author

Loosen, Sven H., Benz, Fabian, Mohr, Raphael, Reuken, Philipp A., Wirtz, Theresa H., Junker, Lioba, Jansen, Christian, Meyer, Carsten, Praktiknjo, Michael, Wree, Alexander, Reißing, Johanna, Demir, Münevver, Gu, Wenyi, Vucur, Mihael, Schierwagen, Robert, Stallmach, Andreas, Kunstein, Anselm, Bode, Johannes, Trautwein, Christian, Tacke, Frank, Luedde, Tom, Bruns, Tony, Trebicka, Jonel, and Roderburg, Christoph

Published
2024
Full Text
View/download PDF

9. Combined analysis of gut microbiota, diet and PNPLA3 polymorphism in biopsy‐proven non‐alcoholic fatty liver disease

Author

Lang, Sonja, Martin, Anna, Zhang, Xinlian, Farowski, Fedja, Wisplinghoff, Hilmar, Vehreschild, Maria JGT, Krawczyk, Marcin, Nowag, Angela, Kretzschmar, Anne, Scholz, Claus, Kasper, Philipp, Roderburg, Christoph, Mohr, Raphael, Lammert, Frank, Tacke, Frank, Schnabl, Bernd, Goeser, Tobias, Steffen, Hans‐Michael, and Demir, Münevver

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Chronic Liver Disease and Cirrhosis, Liver Disease, Nutrition, Digestive Diseases, Prevention, Genetics, Aetiology, 2.1 Biological and endogenous factors, Metabolic and endocrine, Inflammatory and immune system, Oral and gastrointestinal, Good Health and Well Being, Aged, Biopsy, Cross-Sectional Studies, Diet, Gastrointestinal Microbiome, Humans, Lipase, Liver, Membrane Proteins, Non-alcoholic Fatty Liver Disease, Polymorphism, Single Nucleotide, microbiome, microbiota, NAFLD, NASH, nutrition, PNPLA3, PNPLA3, Gastroenterology & Hepatology, Clinical sciences
Abstract

Background and aimsNon-alcoholic fatty liver disease (NAFLD) is a global health burden. Risk factors for disease severity include older age, increased body mass index (BMI), diabetes, genetic variants, dietary factors and gut microbiota alterations. However, the interdependence of these factors and their individual impact on disease severity remain unknown.MethodsIn this cross-sectional study, we performed 16S gene sequencing using fecal samples, collected dietary intake, PNPLA3 gene variants and clinical and liver histology parameters in a well-described cohort of 180 NAFLD patients. Principal component analyses were used for dimensionality reduction of dietary and microbiota data. Simple and multiple stepwise ordinal regression analyses were performed.ResultsComplete data were available for 57 NAFLD patients. In the simple regression analysis, features associated with the metabolic syndrome had the highest importance regarding liver disease severity. In the multiple regression analysis, BMI was the most important factor associated with the fibrosis stage (OR per kg/m2 : 1.23, 95% CI 1.10-1.37, P

Published
2021

11. A global research priority agenda to advance public health responses to fatty liver disease

Author

Lazarus, Jeffrey V., Mark, Henry E., Allen, Alina M., Arab, Juan Pablo, Carrieri, Patrizia, Noureddin, Mazen, Alazawi, William, Alkhouri, Naim, Alqahtani, Saleh A., Arrese, Marco, Bataller, Ramon, Berg, Thomas, Brennan, Paul N., Burra, Patrizia, Castro-Narro, Graciela E., Cortez-Pinto, Helena, Cusi, Kenneth, Dedes, Nikos, Duseja, Ajay, Francque, Sven M., Hagström, Hannes, Huang, Terry T-K., Wajcman, Dana Ivancovsky, Kautz, Achim, Kopka, Christopher J., Krag, Aleksander, Miller, Veronica, Newsome, Philip N., Rinella, Mary E., Romero, Diana, Sarin, Shiv Kumar, Silva, Marcelo, Spearman, C. Wendy, Tsochatzis, Emmanuel A., Valenti, Luca, Villota-Rivas, Marcela, Zelber-Sagi, Shira, Schattenberg, Jörn M., Wong, Vincent Wai-Sun, Younossi, Zobair M., Aberg, Fredrik, Adams, Leon, Al-Naamani, Khalid, Albadawy, Reda M., Alexa, Zinaida, Allison, Michael, Alnaser, Faisal A., Alswat, Khalid, Alvares-da-Silva, Mario Reis, Alvaro, Domenico, Alves-Bezerra, Michele, Andrade, Raul J., Anstee, Quentin M., Awuku, Yaw Asante, Baatarkhuu, Oidov, Baffy, Gyorgy, Bakieva, Shokhista, Bansal, Meena B., Barouki, Robert, Batterham, Rachel L., Behling, Cynthia, Belfort-DeAguiar, Renata, Berzigotti, Annalisa, Betel, Michael, Bianco, Cristiana, Bosi, Emanuele, Boursier, Jerome, Brunt, Elizabeth M., Bugianesi, Elisabetta, Byrne, Christopher J., Cabrera Cabrejos, Maria Cecilia, Caldwell, Stephen, Carr, Rotonya, Castellanos Fernández, Marlen Ivón, Castera, Laurent, Castillo-López, Maria Gabriela, Caussy, Cyrielle, Cerda-Reyes, Eira, Ceriello, Antonio, Chan, Wah- Kheong, Chang, Yoosoo, Charatcharoenwitthaya, Phunchai, Chavez-Tapia, Norberto, Chung, Raymond T., Colombo, Massimo, Coppell, Kirsten, Cotrim, Helma P., Craxi, Antonio, Crespo, Javier, Dassanayake, Anuradha, Davidson, Nicholas O., De Knegt, Robert, de Ledinghen, Victor, Demir, Münevver, Desalegn, Hailemichael, Diago, Moises, Dillon, John F., Dimmig, Bruce, Dirac, M. Ashworth, Dirchwolf, Melisa, Dufour, Jean-François, Dvorak, Karel, Ekstedt, Mattias, El-Kassas, Mohamed, Elsanousi, Osama M., Elsharkawy, Ahmed M., Elwakil, Reda, Eskridge, Wayne, Eslam, Mohammed, Esmat, Gamal, Fan, Jian- Gao, Ferraz, Maria Lucia, Flisiak, Robert, Fortin, Davide, Fouad, Yasser, Freidman, Scott L., Fuchs, Michael, Gadano, Adrian, Gastaldelli, Amalia, Geerts, Anja, Geier, Andreas, George, Jacob, Gerber, Lynn H., Ghazinyan, Hasmik, Gheorghe, Liana, Kile, Denise Giangola, Girala, Marcos, Boon Bee, George Goh, Goossens, Nicolas, Graupera, Isabel, Grønbæk, Henning, Hamid, Saeed, Hebditch, Vanessa, Henry, Zachary, Hickman, Ingrid J., Hobbs, L. Ansley, Hocking, Samantha L., Hofmann, Wolf Peter, Idilman, Ramazan, Iruzubieta, Paula, Isaacs, Scott, Isakov, Vasily A., Ismail, Mona H., Jamal, Mohammad H., Jarvis, Helen, Jepsen, Peter, Jornayvaz, François, Sudhamshu, K.C., Kakizaki, Satoru, Karpen, Saul, Kawaguchi, Takumi, Keating, Shelley E., Khader, Yousef, Kim, Seung Up, Kim, Won, Kleiner, David E., Koek, Ger, Joseph Komas, Narcisse Patrice, Kondili, Loreta A., Koot, Bart G., Korenjak, Marko, Kotsiliti, Eleni, Koulla, Yiannoula, Kugelmas, Carina, Kugelmas, Marcelo, Labidi, Asma, Lange, Naomi F., Lavine, Joel E., Lazo, Mariana, Leite, Nathalie, Lin, Han-Chieh, Lkhagvaa, Undram, Long, Michelle T., Lopez-Jaramillo, Patricio, Lozano, Adelina, Macedo, Maria Paula, Malekzadeh, Reza, Marchesini, Giulio, Marciano, Sebastian, Martinez, Kim, Martínez Vázquez, Sophia E., Mateva, Lyudmila, Mato, José M., Nlombi, Charles Mbendi, McCary, Alexis Gorden, McIntyre, Jeff, McKee, Martin, Mendive, Juan M., Mikolasevic, Ivana, Miller, Pamela S., Milovanovic, Tamara, Milton, Terri, Moreno-Alcantar, Rosalba, Morgan, Timothy R., Motala, Ayesha, Muris, Jean, Musso, Carla, Nava-González, Edna J., Negro, Francesco, Nersesov, Alexander V., Neuschwander-Tetri, Brent A., Nikolova, Dafina, Norris, Suzanne, Novak, Katja, Ocama, Ponsiano, Ong, Janus P., Ong-Go, Arlinking, Onyekwere, Charles, Padilla, Martin, Pais, Raluca, Pan, Calvin, Panduro, Arturo, Panigrahi, Manas K., Papatheodoridis, Georgios, Paruk, Imran, Patel, Keyur, Gonçalves, Carlos Penha, Figueroa, Marlene Pérez, Pérez-Escobar, Juanita, Pericàs, Juan M., Perseghin, Gianluca, Pessoa, Mário Guimarães, Petta, Salvatore, Marques Souza de Oliveira, Claudia Pinto, Prabhakaran, Dorairaj, Pyrsopoulous, Nikolaos, Rabiee, Atoosa, Ramji, Alnoor, Ratziu, Vlad, Ravendhran, Natarajan, Ray, Katrina, Roden, Michael, Romeo, Stefano, Romero-Gómez, Manuel, Rotman, Yaron, Rouabhia, Samir, Rowe, Ian A., Sadirova, Shakhlo, Alkhatry, Maryam Salem, Salupere, Riina, Satapathy, Sanjaya K., Schwimmer, Jeffrey B., Sebastiani, Giada, Seim, Lynn, Seki, Yosuke, Serme, Abdel Karim, Shapiro, David, Sharvadze, Lali, Shaw, Jonathan E., Shawa, Isaac Thom, Shenoy, Thrivikrama, Shibolet, Oren, Shimakawa, Yusuke, Shubrook, Jay H., Singh, Shivaram Prasad, Sinkala, Edford, Skladany, Lubomir, Skrypnyk, Igor, Song, Myeong Jun, Sookoian, Silvia, Sridharan, Kannan, Stefan, Norbert, Stine, Jonathan G., Stratakis, Nikolaos, Sheriff, Dhastagir Sultan, Sundaram, Shikha S., Svegliati-Baroni, Gianluca, Swain, Mark G., Tacke, Frank, Taheri, Shahrad, Tan, Soek-Siam, Tapper, Elliot B., Targher, Giovanni, Tcaciuc, Eugen, Thiele, Maja, Tiniakos, Dina, Tolmane, Ieva, Torre, Aldo, Torres, Esther A., Treeprasertsuk, Sombat, Trenell, Michael, Turcan, Svetlana, Turcanu, Adela, Valantinas, Jonas, van Kleef, Laurens A., Velarde Ruiz Velasco, Jose Antonio, Vesterhus, Mette, Vilar-Gomez, Eduardo, Waked, Imam, Wattacheril, Julia, Wedemeyer, Heiner, Wilkins, Fonda, Willemse, José, Wong, Robert J., Yilmaz, Yusuf, Yki-Järvinen, Hannele, Yu, Ming-Lung, Yumuk, Volkan, Zeybel, Müjdat, Zheng, Kenneth I., Zheng, Ming-Hua, and Huang, Terry T.-K.

Published
2023
Full Text
View/download PDF

12. Intestinal Virome Signature Associated With Severity of Nonalcoholic Fatty Liver Disease

Author

Lang, Sonja, Demir, Münevver, Martin, Anna, Jiang, Lu, Zhang, Xinlian, Duan, Yi, Gao, Bei, Wisplinghoff, Hilmar, Kasper, Philipp, Roderburg, Christoph, Tacke, Frank, Steffen, Hans-Michael, Goeser, Tobias, Abraldes, Juan G, Tu, Xin M, Loomba, Rohit, Stärkel, Peter, Pride, David, Fouts, Derrick E, and Schnabl, Bernd

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Nutrition and Dietetics, Chronic Liver Disease and Cirrhosis, Digestive Diseases, Clinical Research, Liver Disease, Oral and gastrointestinal, Infection, Adult, Aged, Case-Control Studies, Cross-Sectional Studies, Feces, Female, Gastrointestinal Microbiome, Humans, Intestines, Liver Cirrhosis, Male, Middle Aged, Non-alcoholic Fatty Liver Disease, Prospective Studies, Severity of Illness Index, Virome, Young Adult, Microbiota, Biomarker, Prognostic Factor, Progression, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology, Clinical sciences, Nutrition and dietetics
Abstract

Background & aimsAlterations in the gut microbiome have been associated with the severity of nonalcoholic fatty liver disease (NAFLD). Previous studies focused exclusively on the bacteria in the microbiome; we investigated changes in the viral microbiome (virome) in patients with NAFLD.MethodsIn a prospective, cross-sectional, observational study, we extracted RNA and DNA virus-like particles from fecal samples from 73 patients with NAFLD: 29 patients had an NAFLD Activity Score (NAS) of 0-4, 44 patients had an NAS of 5-8 or liver cirrhosis (LCI), 37 patients had F0-F1 fibrosis, and 36 patients had F2-F4 fibrosis. As controls, 9 individuals without liver disease and 13 patients with mild primary biliary cholangitis were included in the analysis. We performed shotgun metagenomic sequencing of virus-like particles.ResultsPatients with NAFLD and NAS 5-8/LCI had a significant decrease in intestinal viral diversity compared with patients with NAFLD and NAS 0-4 or control individuals. The presence of more advanced NAFLD was associated with a significant reduction in the proportion of bacteriophages compared with other intestinal viruses. Using multivariate logistic regression analysis with leave-1-out cross validation, we developed a model, including a viral diversity index and simple clinical variables, that identified patients with NAS 5-8/LCI with an area under the curve of 0.95 (95% confidence interval, 0.91-0.99) and F2-F4 fibrosis with an area under the curve of 0.88 (95% confidence interval, 0.80-0.95). Addition of data on viral diversity significantly improved multivariate models, including those based on only clinical parameters or bacterial diversity.ConclusionsIn a study of fecal viromes from patients with NAFLD and control individuals, we associated histologic markers of NAFLD severity with significant decreases in viral diversity and proportion of bacteriophages. We developed a model based on fecal viral diversity and clinical data that identifies patients with severe NAFLD and fibrosis more accurately than models based only on clinical or bacterial data.

Published
2020

14. Treating hepatitis D with bulevirtide – Real-world experience from 114 patients

Author

Dietz-Fricke, Christopher, Tacke, Frank, Zöllner, Caroline, Demir, Münevver, Schmidt, Hartmut H., Schramm, Christoph, Willuweit, Katharina, Lange, Christian M., Weber, Sabine, Denk, Gerald, Berg, Christoph P., Grottenthaler, Julia M., Merle, Uta, Olkus, Alexander, Zeuzem, Stefan, Sprinzl, Kathrin, Berg, Thomas, van Bömmel, Florian, Wiegand, Johannes, Herta, Toni, Seufferlein, Thomas, Zizer, Eugen, Dikopoulos, Nektarios, Thimme, Robert, Neumann-Haefelin, Christoph, Galle, Peter R., Sprinzl, Martin, Lohse, Ansgar W., Schulze zur Wiesch, Julian, Kempski, Jan, Geier, Andreas, Reiter, Florian P., Schlevogt, Bernhard, Gödiker, Juliana, Hofmann, Wolf Peter, Buggisch, Peter, Kahlhöfer, Julia, Port, Kerstin, Maasoumy, Benjamin, Cornberg, Markus, Wedemeyer, Heiner, and Deterding, Katja

Published
2023
Full Text
View/download PDF

15. Natürlicher Verlauf

Author

Demir, Münevver, Steffen, Hans-Michael, Geier, Andreas, editor, Canbay, Ali, editor, and Lammert, Frank, editor

Published
2022
Full Text
View/download PDF

18. TOP-003-YI Model for end-stage liver disease score-based liver allocation is associated with reduced survival in low donation countries-a comparative analysis between Germany and the USA

Author

Wiering, Leke, primary, Aigner, Annette, additional, van Rosmalen, Marieke, additional, Globke, Brigitta, additional, Raschzok, Nathanael, additional, Schöning, Wenzel, additional, Lurje, Georg, additional, Demir, Münevver, additional, Tacke, Frank, additional, Pratschke, Johann, additional, Öllinger, Robert, additional, and Ritschl, Paul, additional

Published
2024
Full Text
View/download PDF

21. Efficacy of finerenone in patients with type 2 diabetes, chronic kidney disease and altered markers of liver steatosis and fibrosis: A FIDELITY subgroup analysis

Author

Perakakis, Nikolaos; https://orcid.org/0000-0002-2319-6603, Bornstein, Stefan R; https://orcid.org/0000-0002-5211-2536, Birkenfeld, Andreas L; https://orcid.org/0000-0003-1407-9023, Linkermann, Andreas; https://orcid.org/0000-0001-6287-9725, Demir, Münevver, Anker, Stefan D, Filippatos, Gerasimos; https://orcid.org/0000-0002-5640-0332, Pitt, Bertram, Rossing, Peter; https://orcid.org/0000-0002-1531-4294, Ruilope, Luis M, Kolkhof, Peter, Lawatscheck, Robert, Scott, Charlie, Bakris, George L; https://orcid.org/0000-0003-1183-1267, FIDELIO-DKD and FIGARO-DKD investigators, Perakakis, Nikolaos; https://orcid.org/0000-0002-2319-6603, Bornstein, Stefan R; https://orcid.org/0000-0002-5211-2536, Birkenfeld, Andreas L; https://orcid.org/0000-0003-1407-9023, Linkermann, Andreas; https://orcid.org/0000-0001-6287-9725, Demir, Münevver, Anker, Stefan D, Filippatos, Gerasimos; https://orcid.org/0000-0002-5640-0332, Pitt, Bertram, Rossing, Peter; https://orcid.org/0000-0002-1531-4294, Ruilope, Luis M, Kolkhof, Peter, Lawatscheck, Robert, Scott, Charlie, Bakris, George L; https://orcid.org/0000-0003-1183-1267, and FIDELIO-DKD and FIGARO-DKD investigators

Abstract

AIM Investigating the effect of finerenone on liver function, cardiovascular and kidney composite outcomes in patients with chronic kidney disease and type 2 diabetes, stratified by their risk of liver steatosis, inflammation and fibrosis. MATERIALS AND METHODS Post hoc analysis stratified patients (N = 13 026) by liver fibrosis and enzymes: high risk of steatosis (hepatic steatosis index >36); elevated transaminases [alanine transaminase (ALT) >33 (males) and >25 IU/L (females)]; and fibrosis-4 (FIB-4) index scores >3.25, >2.67 and >1.30. Liver enzymes were assessed by changes in ALT, aspartate aminotransferase and gamma-glutamyl transferase. Composite kidney outcome was defined as onset of kidney failure, sustained estimated glomerular filtration rate decline ≥57% from baseline over ≥4 weeks or kidney death. Composite cardiovascular outcome was defined as cardiovascular death, non-fatal myocardial infarction, non-fatal stroke or hospitalization for heart failure. RESULTS ALT, aspartate aminotransferase and gamma-glutamyl transferase levels were consistent between treatment groups and remained stable throughout. Finerenone consistently reduced the risk of composite kidney outcome, irrespective of altered liver tests. Higher FIB-4 score was associated with higher incidence rates of composite cardiovascular outcome. Finerenone reduced the risk of composite cardiovascular outcome versus placebo in FIB-4 subgroups by 52% (>3.25), 39% (>2.67) and 24% (>1.30) (p values for interaction = .01, .13 and .03, respectively). CONCLUSIONS Finerenone has neutral effects on liver parameters in patients with chronic kidney disease and type 2 diabetes. Finerenone showed robust and consistent kidney benefits in patients with altered liver tests, and profound cardiovascular benefits even in patients with higher FIB-4 scores who were at high risk of developing cardiovascular complications.

Published
2024

22. Efficacy of finerenone in patients with type 2 diabetes, chronic kidney disease and altered markers of liver steatosis and fibrosis:A FIDELITY subgroup analysis

Author

Perakakis, Nikolaos, Bornstein, Stefan R, Birkenfeld, Andreas L, Linkermann, Andreas, Demir, Münevver, Anker, Stefan D, Filippatos, Gerasimos, Pitt, Bertram, Rossing, Peter, Ruilope, Luis M, Kolkhof, Peter, Lawatscheck, Robert, Scott, Charlie, Bakris, George L, Perakakis, Nikolaos, Bornstein, Stefan R, Birkenfeld, Andreas L, Linkermann, Andreas, Demir, Münevver, Anker, Stefan D, Filippatos, Gerasimos, Pitt, Bertram, Rossing, Peter, Ruilope, Luis M, Kolkhof, Peter, Lawatscheck, Robert, Scott, Charlie, and Bakris, George L

Abstract

AIM: Investigating the effect of finerenone on liver function, cardiovascular and kidney composite outcomes in patients with chronic kidney disease and type 2 diabetes, stratified by their risk of liver steatosis, inflammation and fibrosis.MATERIALS AND METHODS: Post hoc analysis stratified patients (N = 13 026) by liver fibrosis and enzymes: high risk of steatosis (hepatic steatosis index >36); elevated transaminases [alanine transaminase (ALT) >33 (males) and >25 IU/L (females)]; and fibrosis-4 (FIB-4) index scores >3.25, >2.67 and >1.30. Liver enzymes were assessed by changes in ALT, aspartate aminotransferase and gamma-glutamyl transferase. Composite kidney outcome was defined as onset of kidney failure, sustained estimated glomerular filtration rate decline ≥57% from baseline over ≥4 weeks or kidney death. Composite cardiovascular outcome was defined as cardiovascular death, non-fatal myocardial infarction, non-fatal stroke or hospitalization for heart failure.RESULTS: ALT, aspartate aminotransferase and gamma-glutamyl transferase levels were consistent between treatment groups and remained stable throughout. Finerenone consistently reduced the risk of composite kidney outcome, irrespective of altered liver tests. Higher FIB-4 score was associated with higher incidence rates of composite cardiovascular outcome. Finerenone reduced the risk of composite cardiovascular outcome versus placebo in FIB-4 subgroups by 52% (>3.25), 39% (>2.67) and 24% (>1.30) (p values for interaction = .01, .13 and .03, respectively).CONCLUSIONS: Finerenone has neutral effects on liver parameters in patients with chronic kidney disease and type 2 diabetes. Finerenone showed robust and consistent kidney benefits in patients with altered liver tests, and profound cardiovascular benefits even in patients with higher FIB-4 scores who were at high risk of developing cardiovascular complications.

Published
2024

23. Amendment „Neue Nomenklatur zur MASLD (Metabolic Dysfunction Associated Steatotic Liver Disease; metabolische Dysfunktion assoziierte steatotische Lebererkrankung) " zur S2k-Leitlinie „Nicht-alkoholische Fettlebererkrankung" (v.2.0/April 2022) der Deutschen Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS)

Author

Roeb, Elke, Canbay, Ali, Bantel, Heike, Bojunga, Jörg, de Laffolie, Jan, Demir, Münevver, Denzer, Ulrike W., Geier, Andreas, Hofmann, Wolf Peter, Hudert, Christian, Karlas, Thomas, Krawczyk, Marcin, Longerich, Thomas, Lüdde, Tom, Roden, Michael, Schattenberg, Jörn M., Sterneck, Martina, Tannapfel, Andrea, Lorenz, Pia, and Tacke, Frank

Published
2024
Full Text
View/download PDF

28. Norursodeoxycholic acid versus placebo in the treatment of non-alcoholic fatty liver disease: a double-blind, randomised, placebo-controlled, phase 2 dose-finding trial

Author

Vogel, Wolfgang, Aigner, Elmar, Datz, Christian, Tilg, Herbert, Gerken, Guido, Rust, Christian, Cordes, Hans-Jörg, Steib, Christian, Pathil-Warth, Anita, Prinz, MD, Christian, Lammert, Frank, Antoni, Christoph, Klausmann, Gerhard, Häussinger, Dieter, Zipprich, Alexander, Traussnigg, Stefan, Schattenberg, Jörn M, Demir, Münevver, Wiegand, Johannes, Geier, Andreas, Teuber, Gerlinde, Hofmann, Wolf Peter, Kremer, Andreas E, Spreda, Frank, Kluwe, Johannes, Petersen, Jörg, Boettler, Tobias, Rainer, Florian, Halilbasic, Emina, Greinwald, Roland, Pröls, Markus, Manns, Michael P, Fickert, Peter, and Trauner, Michael

Published
2019
Full Text
View/download PDF

30. Efficacy of finerenone in patients with type 2 diabetes, chronic kidney disease and altered markers of liver steatosis and fibrosis: A FIDELITY subgroup analysis.

Author

Perakakis, Nikolaos, Bornstein, Stefan R., Birkenfeld, Andreas L., Linkermann, Andreas, Demir, Münevver, Anker, Stefan D., Filippatos, Gerasimos, Pitt, Bertram, Rossing, Peter, Ruilope, Luis M., Kolkhof, Peter, Lawatscheck, Robert, Scott, Charlie, and Bakris, George L.

Subjects
HEPATIC fibrosis, TYPE 2 diabetes, CHRONIC kidney failure, ASPARTATE aminotransferase, GAMMA-glutamyltransferase, ALANINE aminotransferase, LIVER enzymes
Abstract

Aim: Investigating the effect of finerenone on liver function, cardiovascular and kidney composite outcomes in patients with chronic kidney disease and type 2 diabetes, stratified by their risk of liver steatosis, inflammation and fibrosis. Materials and Methods: Post hoc analysis stratified patients (N = 13 026) by liver fibrosis and enzymes: high risk of steatosis (hepatic steatosis index >36); elevated transaminases [alanine transaminase (ALT) >33 (males) and >25 IU/L (females)]; and fibrosis‐4 (FIB‐4) index scores >3.25, >2.67 and >1.30. Liver enzymes were assessed by changes in ALT, aspartate aminotransferase and gamma‐glutamyl transferase. Composite kidney outcome was defined as onset of kidney failure, sustained estimated glomerular filtration rate decline ≥57% from baseline over ≥4 weeks or kidney death. Composite cardiovascular outcome was defined as cardiovascular death, non‐fatal myocardial infarction, non‐fatal stroke or hospitalization for heart failure. Results: ALT, aspartate aminotransferase and gamma‐glutamyl transferase levels were consistent between treatment groups and remained stable throughout. Finerenone consistently reduced the risk of composite kidney outcome, irrespective of altered liver tests. Higher FIB‐4 score was associated with higher incidence rates of composite cardiovascular outcome. Finerenone reduced the risk of composite cardiovascular outcome versus placebo in FIB‐4 subgroups by 52% (>3.25), 39% (>2.67) and 24% (>1.30) (p values for interaction =.01,.13 and.03, respectively). Conclusions: Finerenone has neutral effects on liver parameters in patients with chronic kidney disease and type 2 diabetes. Finerenone showed robust and consistent kidney benefits in patients with altered liver tests, and profound cardiovascular benefits even in patients with higher FIB‐4 scores who were at high risk of developing cardiovascular complications. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

37. Improvements in ALT levels during Bulevirtide treatment for hepatitis D are seen regardless of virologic response

Author

Dietz-Fricke, Christopher, primary, Tacke, Frank, additional, Zöllner, Caroline, additional, Demir, Münevver, additional, Schmidt, Hartmut, additional, Schramm, Christoph, additional, Willuweit, Katharina, additional, Lange, Christian M., additional, Weber, Sabine, additional, Denk, Gerald, additional, Berg, Christoph, additional, Grottenthaler, Julia, additional, Merle, Uta, additional, Olkus, Alexander, additional, Zeuzem, Stefan, additional, Sprinzl, Kathrin, additional, Berg, Thomas, additional, van Bömmel, Florian, additional, Wiegand, Johannes, additional, Herta, Toni, additional, Seufferlein, Thomas, additional, Zizer, Eugen, additional, Dikopoulos, Nektarios, additional, Thimme, Robert, additional, Neumann-Haefelin, Christoph, additional, Galle, Peter, additional, Sprinzl, Martin, additional, Lohse, Ansgar W., additional, Kempski, Jan, additional, zur Wiesch, Julian Schulze, additional, Geier, Andreas, additional, Reiter, Florian P, additional, Schlevogt, Bernhard, additional, Goediker, Juliana, additional, Hofmann, Wolf Peter, additional, Buggisch, Peter, additional, Kahlhöfer, Julia, additional, Port, Kerstin, additional, Maasoumy, Benjamin, additional, Cornberg, Markus, additional, Wedemeyer, Heiner, additional, and Deterding, Katja, additional

Published
2023
Full Text
View/download PDF

39. Soluble urokinase plasminogen activator receptor is a biomarker for outcome in decompensated liver cirrhosis and acute-on-chronic liver failure

Author

Lamatsch, Sven, primary, Hassan, Mohsin, additional, de la Peña-Ramirez, Carlos, additional, Kappert, Kai, additional, Mohr, Raphael, additional, Demir, Münevver, additional, Phan, Minh, additional, Andreola, Fausto, additional, Veelken, Rhea, additional, Aehling, Niklas F, additional, Fischer, Janett, additional, Mookerjee, Raj, additional, Berg, Thomas, additional, Jalan, Rajiv, additional, Tacke, Frank, additional, and Engelmann, Cornelius, additional

Published
2023
Full Text
View/download PDF

42. Liver fat as risk factor of hepatic and cardiometabolic diseases

Author

Demir, Münevver, Bornstein, Stefan R; https://orcid.org/0000-0002-5211-2536, Mantzoros, Christos S, Perakakis, Nikolaos; https://orcid.org/0000-0002-2319-6603, Demir, Münevver, Bornstein, Stefan R; https://orcid.org/0000-0002-5211-2536, Mantzoros, Christos S, and Perakakis, Nikolaos; https://orcid.org/0000-0002-2319-6603

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a disorder characterized by excessive accumulation of fat in the liver that can progress to liver inflammation (non-alcoholic steatohepatitis [NASH]), liver fibrosis, and cirrhosis. Although most efforts for drug development are focusing on the treatment of the latest stages of NAFLD, where significant fibrosis and NASH are present, findings from studies suggest that the amount of liver fat may be an important independent risk factor and/or predictor of development and progression of NAFLD and metabolic diseases. In this review, we first describe the current tools available for quantification of liver fat in humans and then present the clinical and pathophysiological evidence that link liver fat with NAFLD progression as well as with cardiometabolic diseases. Finally, we discuss current pharmacological and non-pharmacological approaches to reduce liver fat and present open questions that have to be addressed in future studies.

Published
2023

43. The fecal mycobiome in non-alcoholic fatty liver disease.

Author

Demir, Münevver, Demir, Münevver, Lang, Sonja, Hartmann, Phillipp, Duan, Yi, Martin, Anna, Miyamoto, Yukiko, Bondareva, Marina, Zhang, Xinlian, Wang, Yanhan, Kasper, Philipp, Bang, Corinna, Roderburg, Christoph, Tacke, Frank, Steffen, Hans-Michael, Goeser, Tobias, Kruglov, Andrey, Eckmann, Lars, Stärkel, Peter, Fouts, Derrick E, Schnabl, Bernd, Demir, Münevver, Demir, Münevver, Lang, Sonja, Hartmann, Phillipp, Duan, Yi, Martin, Anna, Miyamoto, Yukiko, Bondareva, Marina, Zhang, Xinlian, Wang, Yanhan, Kasper, Philipp, Bang, Corinna, Roderburg, Christoph, Tacke, Frank, Steffen, Hans-Michael, Goeser, Tobias, Kruglov, Andrey, Eckmann, Lars, Stärkel, Peter, Fouts, Derrick E, and Schnabl, Bernd

Abstract

Background & aimsStudies investigating the gut-liver axis have largely focused on bacteria, whereas little is known about commensal fungi. We characterized fecal fungi in patients with non-alcoholic fatty liver disease (NAFLD) and investigated their role in a fecal microbiome-humanized mouse model of Western diet-induced steatohepatitis.MethodsWe performed fungal internal transcribed spacer 2 sequencing using fecal samples from 78 patients with NAFLD, 16 controls and 73 patients with alcohol use disorder. Anti-Candida albicans (C. albicans) IgG was measured in blood samples from 17 controls and 79 patients with NAFLD. Songbird, a novel multinominal regression tool, was used to investigate mycobiome changes. Germ-free mice were colonized with feces from patients with non-alcoholic steatohepatitis (NASH), fed a Western diet for 20 weeks and treated with the antifungal amphotericin B.ResultsThe presence of non-obese NASH or F2-F4 fibrosis was associated with a distinct fecal mycobiome signature. Changes were characterized by an increased log-ratio for Mucor sp./Saccharomyces cerevisiae (S. cerevisiae) in patients with NASH and F2-F4 fibrosis. The C. albicans/S. cerevisiae log-ratio was significantly higher in non-obese patients with NASH when compared with non-obese patients with NAFL or controls. We observed a different fecal mycobiome composition in patients with NAFLD and advanced fibrosis compared to those with alcohol use disorder and advanced fibrosis. Plasma anti-C. albicans IgG was increased in patients with NAFLD and advanced fibrosis. Gnotobiotic mice, colonized with human NASH feces and treated with amphotericin B were protected from Western diet-induced steatohepatitis.ConclusionsNon-obese patients with NAFLD and more advanced disease have a different fecal mycobiome composition to those with mild disease. Antifungal treatment ameliorates diet-induced steatohepatitis in mice. Intestinal fungi could be an attractive target to attenuate NAS

Published
2022

44. Maternal exercise conveys protection against NAFLD in the offspring via hepatic metabolic programming

Author

Bae-Gartz, Inga, Kasper, Philipp, Großmann, Nora, Breuer, Saida, Janoschek, Ruth, Kretschmer, Tobias, Appel, Sarah, Schmitz, Lisa, Vohlen, Christina, Quaas, Alexander, Schweiger, Michal R., Grimm, Christina, Fischer, Axel, Ferrari, Nina, Graf, Christine, Frese, Christian K., Lang, Sonja, Demir, Münevver, Schramm, Christoph, Fink, Gregor, Goeser, Tobias, Dötsch, Jörg, and Hucklenbruch-Rother, Eva

Published
2020
Full Text
View/download PDF

49. Cenicriviroc for the treatment of COVID-19: first interim results of a randomised, placebo-controlled, investigator-initiated, double-blind phase II trial

Author

Kurth, Florian, primary, Helbig, Elisa T., additional, Lippert, Lena J., additional, Thibeault, Charlotte, additional, Barbone, Gianluca, additional, Eckart, Marius A., additional, Kluge, Martin, additional, Puengel, Tobias, additional, Demir, Münevver, additional, Röhle, Robert, additional, Keller, Theresa, additional, Ruwwe-Glösenkamp, Christoph, additional, Witzenrath, Martin, additional, Suttorp, Norbert, additional, von Kalle, Christof, additional, Sander, Leif E., additional, Jochum, Christoph, additional, and Tacke, Frank, additional

Published
2023
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results