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706 results on '"Donath, Marc Y."'

152. OP0030 RANDOMIZED CONTROLLED 24-WEEK TRIAL EVALUATING THE SAFETY AND EFFICACY OF BLINDED TAPERING VERSUS CONTINUATION OF LONG-TERM PREDNISONE (5 MG/D) IN PATIENTS WITH RHEUMATOID ARTHRITIS WHO ACHIEVED LOW DISEASE ACTIVITY OR REMISSION ON TOCILIZUMAB

Author

Burmester, Gerd Rüdiger, primary, Buttgereit, Frank, additional, Bernasconi, Corrado, additional, Alvaro-Gracia, Jose-Maria, additional, Castro, Nidia, additional, Dougados, Maxime, additional, Gabay, Cem, additional, Jacob, M., additional, Laar, van, additional, Michael Nebesky, J., additional, Pethoe-Schramm, Attila, additional, Salvarani, Carlo, additional, Donath, Marc Y., additional, and John, Markus R., additional

Published
2019
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157. Treatment of Primary Aldosteronism With mTORC1 Inhibitors

Author

Trinh, Beckey, primary, Hepprich, Matthias, additional, Betz, Matthias J, additional, Burkard, Thilo, additional, Cavelti-Weder, Claudia, additional, Seelig, Eleonora, additional, Meienberg, Fabian, additional, Kratschmar, Denise V, additional, Beuschlein, Felix, additional, Reincke, Martin, additional, Odermatt, Alex, additional, Hall, Michael N, additional, Donath, Marc Y, additional, and Swierczynska, Marta M, additional

Published
2019
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160. Proteomic Landscape of Aldosterone-Producing Adenoma

Author

Swierczynska, Marta M., primary, Betz, Matthias J., additional, Colombi, Marco, additional, Dazert, Eva, additional, Jenö, Paul, additional, Moes, Suzette, additional, Pfaff, Cécile, additional, Glatz, Katharina, additional, Reincke, Martin, additional, Beuschlein, Felix, additional, Donath, Marc Y., additional, and Hall, Michael N., additional

Published
2019
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164. β Cell-Specific Deletion of the IL-1 Receptor Antagonist Impairs β Cell Proliferation and Insulin Secretion

Author

Böni-Schnetzler, Marianne, primary, Häuselmann, Stéphanie P., additional, Dalmas, Elise, additional, Meier, Daniel T., additional, Thienel, Constanze, additional, Traub, Shuyang, additional, Schulze, Friederike, additional, Steiger, Laura, additional, Dror, Erez, additional, Martin, Praxedis, additional, Herrera, Pedro L., additional, Gabay, Cem, additional, and Donath, Marc Y., additional

Published
2018
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165. Glucose-induced [beta] cell production of IL-1[beta] contributes to glucotoxicity in human pancreatic islets

Author

Maedler, Kathrin, Sergeev, Pavel, Ris, Frederic, Oberholzer, Jose, Joller-Jemelka, Helen I., Spinas, Giatgen A., Kaiser, Nurit, Halban, Philippe A., and Donath, Marc Y.

Subjects
Health care industry
Abstract

The editors recently became aware that three images in Figure 4F of this article are duplicated in a 2002 Proceedings of the National Academy of Science of the United States [...]

Published
2017
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166. Fas (CD95) in adipocytes mediates adipose tissue inflammation and contributes to liver and whole-body insulin resistance

Author

Wueest Stephan, Rapold Reto A, Schumann Desiree M, Rytka Julia M, Schildknecht Anita, Nov Ori, Chervonsky Alexander V, Rudich Assaf, Schoenle Eugen J, Donath Marc Y, and Konrad Daniel

Abstract

Adipose tissue inflammation is linked to the pathogenesis of insulin resistance. In addition to exerting death promoting effects the death receptor Fas (also known as CD95) can activate inflammatory pathways in several cell lines and tissues although little is known about the metabolic consequence of Fas activation in adipose tissue. We therefore sought to investigate the contribution of Fas in adipocytes to obesity associated metabolic dysregulation. Fas expression was markedly increased in the adipocytes of common genetic and diet induced mouse models of obesity and insulin resistance as well as in the adipose tissue of obese and type 2 diabetic patients. Mice with Fas deficiency either in all cells or specifically in adipocytes (the latter are referred to herein as AFasKO mice) were protected from deterioration of glucose homeostasis induced by high fat diet (HFD). Adipocytes in AFasKO mice were more insulin sensitive than those in wild type mice and mRNA levels of proinflammatory factors were reduced in white adipose tissue. Moreover AFasKO mice were protected against hepatic steatosis and were more insulin sensitive both at the whole body level and in the liver. Thus Fas in adipocytes contributes to adipose tissue inflammation hepatic steatosis and insulin resistance induced by obesity and may constitute a potential therapeutic target for the treatment of insulin resistance and type 2 diabetes.

Published
2010
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168. The Role of Inflammation in β-cell Dedifferentiation

Author

Nordmann, Thierry M., primary, Dror, Erez, additional, Schulze, Friederike, additional, Traub, Shuyang, additional, Berishvili, Ekaterine, additional, Barbieux, Charlotte, additional, Böni-Schnetzler, Marianne, additional, and Donath, Marc Y., additional

Published
2017
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172. Pancreatic α Cell-Derived Glucagon-Related Peptides Are Required for β Cell Adaptation and Glucose Homeostasis

Author

Traub, Shuyang, primary, Meier, Daniel T., additional, Schulze, Friederike, additional, Dror, Erez, additional, Nordmann, Thierry M., additional, Goetz, Nicole, additional, Koch, Norina, additional, Dalmas, Elise, additional, Stawiski, Marc, additional, Makshana, Valmir, additional, Thorel, Fabrizio, additional, Herrera, Pedro L., additional, Böni-Schnetzler, Marianne, additional, and Donath, Marc Y., additional

Published
2017
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175. Identification of a SIRT1 Mutation in a Family with Type 1 Diabetes

Author

Biason-Lauber, Anna, Böni-Schnetzler, Marianne, Hubbard, Basil P., Bouzakri, Karim, Brunner, Andrea, Cavelti-Weder, Claudia, Keller, Cornelia, Meyer-Böni, Monika, Meier, Daniel T., Brorsson, Caroline, Timper, Katharina, Leibowitz, Gil, Patrignani, Andrea, Bruggmann, Remy, Boily, Gino, Zulewski, Henryk, Geier, Andreas, Cermak, Jennifer M., Elliott, Peter, Ellis, James L., Westphal, Christoph, Knobel, Urs, Eloranta, Jyrki J., Kerr-Conte, Julie, Pattou, François, Konrad, Daniel, Matter, Christian M., Fontana, Adriano, Rogler, Gerhard, Schlapbach, Ralph, Regairaz, Camille, Carballido, José M., Glaser, Benjamin, McBurney, Michael W., Pociot, Flemming, Sinclair, David A., and Donath, Marc Y.

Published
2013
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177. Expression of Concern. Low Concentration of Interleukin-1β Induces FLICE-Inhibitory Protein–Mediated β-Cell Proliferation in Human Pancreatic Islets. Diabetes 2006;55:2713–2722; DOI: 10.2337/db05-1430

Author

Maedler, Kathrin, primary, Schumann, Desiree M., additional, Sauter, Nadine, additional, Ellingsgaard, Helga, additional, Bosco, Domenico, additional, Baertschiger, Reto, additional, Iwakura, Yoichiro, additional, Oberholzer, José, additional, Wollheim, Claes B., additional, Gauthier, Benoit R., additional, and Donath, Marc Y., additional

Published
2016
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179. Glucose-Dependent Insulinotropic Peptide Stimulates Glucagon-Like Peptide 1 Production by Pancreatic Islets via Interleukin 6, Produced by α Cells

Author

Timper, Katharina, primary, Dalmas, Elise, additional, Dror, Erez, additional, Rütti, Sabine, additional, Thienel, Constanze, additional, Sauter, Nadine S., additional, Bouzakri, Karim, additional, Bédat, Benoit, additional, Pattou, Francois, additional, Kerr-Conte, Julie, additional, Böni-Schnetzler, Marianne, additional, and Donath, Marc Y., additional

Published
2016
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180. Glucose-dependent insulinotropic peptide (GIP) stimulates Glucagon-like peptide (GLP)-1 from human and mouse pancreatic islets partly via alpha-cell-derived IL-6

Author

Timper, Katharina, primary, Dalmas, Elise, additional, Dror, Erez, additional, Rutti, Sabine, additional, Thienel, Constanze, additional, Sauter, Nadine S., additional, Bouzakri, Karim, additional, Bedat, Benoit, additional, Pattou, Francois, additional, Kerr-Conte, Julie, additional, Boni-Schnetzler, Marianne, additional, and Donath, Marc Y., additional

Published
2016
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181. Development of an Interleukin-1β Vaccine in Patients with Type 2 Diabetes

Author

Cavelti-Weder, Claudia, primary, Timper, Katharina, additional, Seelig, Eleonora, additional, Keller, Cornelia, additional, Osranek, Martin, additional, Lässing, Ute, additional, Spohn, Gunther, additional, Maurer, Patrik, additional, Müller, Philipp, additional, Jennings, Gary T, additional, Willers, Joerg, additional, Saudan, Philippe, additional, Donath, Marc Y, additional, and Bachmann, Martin F, additional

Published
2016
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184. How biologics targeting the IL-1 system are being considered for the treatment of type 2 diabetes

Author

Böni-Schnetzler Marianne and Donath Marc Y

Subjects
Clinical Trials as Topic, Interleukin 1 Receptor Antagonist Protein, Diabetes Mellitus, Type 2, Reviews, Humans, Antibodies, Blocking, Interleukin-1
Abstract

Metabolic diseases are associated with activation of the innate immune system in various tissues and characterised by elevated inflammatory factors and the presence of immune cells. Type 2 diabetes develops when islet beta cells are deficient in producing sufficient insulin to overcome peripheral insulin resistance. Intra islet IL 1ß activity diminishes beta cell function and survival and governs islet inflammation. Targeting the IL 1 system with the IL 1 receptor antagonist IL1Ra improved insulin secretion glycemia and reduced systemic inflammation in a proof of concept study with patients with type 2 diabetes. Currently long lasting and specific IL 1ß blocking antibodies are evaluated in clinical trials and this may lead to a novel cytokine based treatment for type 2 diabetes. © 2012 The Authors. British Journal of Clinical Pharmacology © 2012 The British Pharmacological Society.

Published
2012

185. Β-Cell Glucotoxicity in the Psammomys obesus Model of Type 2 Diabetes

Author

Leibowitz, Gil, Yuli, Michal, Donath, Marc Y., Nesher, Rafael, Melloul, Danielle, Cerasi, Erol, Gross, David J., and Kaiser, Nurit

Subjects
Biological transport -- Physiological aspects, Insulin -- Physiological aspects, Glucose metabolism -- Physiological aspects, Type 2 diabetes -- Development and progression, Hyperglycemia -- Development and progression, Health, Physiological aspects, Development and progression
Abstract

Deficient insulin secretion and relative hyperproinsulinemia are characteristic features of type 2 diabetes. The gerbil Psammomys obesus appears to be an ideal natural model of the human disease because it [...]

Published
2001

191. Aging correlates with decreased beta-cell proliferative capacity and enhanced sensitivity to apoptosis: a potential role for Fas and pancreatic duodenal homeobox-1

Author

Maedler, Kathrin, Schumann, Desiree, Schulthess, Fabienne, Oberholzer, José, Bosco, Domenico, Berney, Thierry, and Donath, Marc Y

Subjects
Adult, Male, endocrine system, Fas Ligand Protein, ddc:617, Adolescent, Homeodomain Proteins/physiology, Middle Aged, Glucose/pharmacology, Membrane Glycoproteins/physiology, Aging/physiology, Rats, Rats, Sprague-Dawley, Apoptosis/drug effects/physiology, Insulin-Secreting Cells/cytology, Tumor Necrosis Factors/physiology, Animals, Humans, Trans-Activators/physiology, Antigens, CD95/physiology, Cells, Cultured, Aged, Cell Proliferation
Abstract

Type 2 diabetes is characterized by a deficit in beta-cell mass, and its incidence increases with age. Here, we analyzed beta-cell turnover in islets from 2- to 3- compared with 7- to 8-month-old rats and in human islets from 53 organ donors with ages ranging from 17 to 74 years. In cultured islets from 2- to 3-month-old rats, the age at which rats are usually investigated, increasing glucose from 5.5 to 11.1 mmol/l decreased beta-cell apoptosis, which was augmented when glucose was further increased to 33.3 mmol/l. In parallel, beta-cell proliferation was increased by both 11.1 and 33.3 mmol/l glucose compared with 5.5 mmol/l. In contrast, in islets from 7- to 8-month-old rats and from adult humans, increasing glucose concentrations from 5.5 to 33.3 mmol/l induced a linear increase in beta-cell death and a decrease in proliferation. Additionally, in cultivated human islets, age correlated positively with the sensitivity to glucose-induced beta-cell apoptosis and negatively to baseline proliferation. In rat islets, constitutive expression of Fas ligand and glucose-induced Fas receptor expression were observed only in 7- to 8-month-old but not in 2- to 3-month-old islets, whereas no age-dependent changes in the Fas/Fas ligand system could be detected in human islets. However, pancreatic duodenal homeobox (PDX)-1 expression decreased with age in pancreatic tissue sections of rats and humans. Furthermore, older rat islets were more sensitive to the high-glucose-mediated decrease in PDX-1 expression than younger islets. Therefore, differences in glucose sensitivity between human and 2- to 3-month-old rat islets may be due to both differences in age and in the genetic background. These data provide a possible explanation for the increased incidence of type 2 diabetes at an older age and support the use of islets from older rats as a more appropriate model to study glucose-induced beta-cell apoptosis.

Published
2006

193. Angiotensin II Induces Interleukin-1β–Mediated Islet Inflammation and β-Cell Dysfunction Independently of Vasoconstrictive Effects

Author

Sauter, Nadine S., primary, Thienel, Constanze, additional, Plutino, Yuliya, additional, Kampe, Kapil, additional, Dror, Erez, additional, Traub, Shuyang, additional, Timper, Katharina, additional, Bédat, Benoit, additional, Pattou, Francois, additional, Kerr-Conte, Julie, additional, Jehle, Andreas W., additional, Böni-Schnetzler, Marianne, additional, and Donath, Marc Y., additional

Published
2014
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195. Interleukin-6 contributes to early fasting-induced free fatty acid mobilization in mice

Author

Wueest, Stephan, primary, Item, Flurin, additional, Boyle, Christina N., additional, Jirkof, Paulin, additional, Cesarovic, Nikola, additional, Ellingsgaard, Helga, additional, Böni-Schnetzler, Marianne, additional, Timper, Katharina, additional, Arras, Margarete, additional, Donath, Marc Y., additional, Lutz, Thomas A., additional, Schoenle, Eugen J., additional, and Konrad, Daniel, additional

Published
2014
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200. Interleukin-1 antagonism in type 1 diabetes of recent onset:two multicentre, randomised, double-blind, placebo-controlled trials

Author

Moran, Antoinette, Bundy, Brian, Becker, Dorothy J, DiMeglio, Linda A, Gitelman, Stephen E, Goland, Robin, Greenbaum, Carla J, Herold, Kevan C, Marks, Jennifer B, Raskin, Philip, Sanda, Srinath, Schatz, Desmond, Wherrett, Diane K, Wilson, Darrell M, Krischer, Jeffrey P, Skyler, Jay S, Pickersgill, Linda, de Koning, Eelco, Ziegler, Anette-G, Böehm, Bernhard, Badenhoop, Klaus, Schloot, Nanette, Bak, Jens Friis, Pozzilli, Paolo, Mauricio, Didac, Donath, Marc Y, Castaño, Luis, Wägner, Ana, Lervang, Hans Henrik, Perrild, Hans, Mandrup-Poulsen, Thomas, Moran, Antoinette, Bundy, Brian, Becker, Dorothy J, DiMeglio, Linda A, Gitelman, Stephen E, Goland, Robin, Greenbaum, Carla J, Herold, Kevan C, Marks, Jennifer B, Raskin, Philip, Sanda, Srinath, Schatz, Desmond, Wherrett, Diane K, Wilson, Darrell M, Krischer, Jeffrey P, Skyler, Jay S, Pickersgill, Linda, de Koning, Eelco, Ziegler, Anette-G, Böehm, Bernhard, Badenhoop, Klaus, Schloot, Nanette, Bak, Jens Friis, Pozzilli, Paolo, Mauricio, Didac, Donath, Marc Y, Castaño, Luis, Wägner, Ana, Lervang, Hans Henrik, Perrild, Hans, and Mandrup-Poulsen, Thomas

Abstract

Innate immunity contributes to the pathogenesis of autoimmune diseases, such as type 1 diabetes, but until now no randomised, controlled trials of blockade of the key innate immune mediator interleukin-1 have been done. We aimed to assess whether canakinumab, a human monoclonal anti-interleukin-1 antibody, or anakinra, a human interleukin-1 receptor antagonist, improved β-cell function in recent-onset type 1 diabetes.

Published
2013

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