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3. INNODIA Master Protocol for the evaluation of investigational medicinal products in children, adolescents and adults with newly diagnosed type 1 diabetes

Author

Dunger, David B., Bruggraber, Sylvaine F. A., Mander, Adrian P., Marcovecchio, M. Loredana, Tree, Timothy, Chmura, Piotr Jaroslaw, Knip, Mikael, Schulte, Anke M., Mathieu, Chantal, Mathieu, C., Gillard, P., Casteels, K., Overbergh, L., Dunger, D., Wallace, C., Evans, M., Thankamony, A., Hendriks, E., Bruggraber, S., Peakman, M., Tree, T., Morgan, N., Richardson, S., Todd, J., Wicker, L., Mander, A., Dayan, C., Alhadj Ali, M., Pieber, T., Eizirik, D., Cnop, M., Brunak, S., Pociot, F., Johannesen, J., Rossing, P., Legido Quigley, C., Mallone, R., Scharfmann, R., Boitard, C., Knip, M., Otonkoski, T., Veijola, R., Lahesmaa, R., Oresic, M., Toppari, J., Danne, T., Ziegler, A. G., Achenbach, P., Rodriguez-Calvo, T., Solimena, M., Bonifacio, E., Speier, S., Holl, R., Dotta, F., Chiarelli, F., Marchetti, P., Bosi, E., Cianfarani, S., Ciampalini, P., de Beaufort, C., Dahl-Jørgensen, K., Skrivarhaug, T., Joner, G., Krogvold, L., Jarosz-Chobot, P., Battelino, T., Thorens, B., Gotthardt, M., Roep, B., Nikolic, T., Zaldumbide, A., Lernmark, A., Lundgren, M., Costecalde, G., Strube, T., Schulte, A., Nitsche, A., von Herrath, M., Wesley, J., Napolitano-Rosen, A., Thomas, M., Schloot, N., Goldfine, A., Waldron-Lynch, F., Kompa, J., Vedala, A., Hartmann, N., Nicolas, G., van Rampelbergh, J., Bovy, N., Dutta, S., Soderberg, J., Ahmed, S., Martin, F., Agiostratidou, G., Koralova, A., Willemsen, R., Smith, A., Anand, B., Puthi, V., Zac-Varghese, S., Datta, V., Dias, R., Sundaram, P., Vaidya, B., Patterson, C., Owen, K., Piel, B., Heller, S., Randell, T., Gazis, T., Bismuth Reismen, E., Carel, J-C, Riveline, J-P, Gautier, J-F, Andreelli, F., Travert, F., Cosson, E., Penfornis, A., Petit, C., Feve, B., Lucidarme, N., Beressi, J-P, Ajzenman, C., Radu, A., Greteau-Hamoumou, S., Bibal, C., Meissner, T., Heidtmann, B., Toni, S., Rami-Merhar, B., Eeckhout, B., Peene, B., Vantongerloo, N., Maes, T., Gommers, L., Marcovecchio, M.L., Vela, J., Latres, E., Children's Hospital, and HUS Children and Adolescents

Subjects
Trials, Adult, Adolescent, SARS-CoV-2, Prevention, Beta-cell function, COVID-19, Medicine (miscellaneous), Beta-cell Function, C-peptide, Master Protocol, Phase 2, Type 1 Diabetes, Type 1 diabetes, Diabetes Mellitus, Type 1, Treatment Outcome, 3121 General medicine, internal medicine and other clinical medicine, Diabetes Mellitus, Type 1/diagnosis, Master protocol, Humans, Pharmacology (medical), Child, Biomarkers
Abstract

Background The INNODIA consortium has established a pan-European infrastructure using validated centres to prospectively evaluate clinical data from individuals with newly diagnosed type 1 diabetes combined with centralised collection of clinical samples to determine rates of decline in beta-cell function and identify novel biomarkers, which could be used for future stratification of phase 2 clinical trials. Methods In this context, we have developed a Master Protocol, based on the “backbone” of the INNODIA natural history study, which we believe could improve the delivery of phase 2 studies exploring the use of single or combinations of Investigational Medicinal Products (IMPs), designed to prevent or reverse declines in beta-cell function in individuals with newly diagnosed type 1 diabetes. Although many IMPs have demonstrated potential efficacy in phase 2 studies, few subsequent phase 3 studies have confirmed these benefits. Currently, phase 2 drug development for this indication is limited by poor evaluation of drug dosage and lack of mechanistic data to understand variable responses to the IMPs. Identification of biomarkers which might permit more robust stratification of participants at baseline has been slow. Discussion The Master Protocol provides (1) standardised assessment of efficacy and safety, (2) comparable collection of mechanistic data, (3) the opportunity to include adaptive designs and the use of shared control groups in the evaluation of combination therapies, and (4) benefits of greater understanding of endpoint variation to ensure more robust sample size calculations and future baseline stratification using existing and novel biomarkers.

Published
2022
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11. 3D FIB-SEM reconstruction of microtubule-organelle interaction in whole primary mouse β cells

Author

Müller, A., Schmidt, D., Xu, C.S., Pang, S., D'Costa, J.V., Kretschmar, S., Münster, C., Kurth, T., Jug, F., Weigert, M., Hess, H.F., and Solimena, M.

Subjects
Technology Platforms
Abstract

Microtubules play a major role in intracellular trafficking of vesicles in endocrine cells. Detailed knowledge of microtubule organization and their relation to other cell constituents is crucial for understanding cell function. However, their role in insulin transport and secretion is under debate. Here, we use FIB-SEM to image islet β cells in their entirety with unprecedented resolution. We reconstruct mitochondria, Golgi apparati, centrioles, insulin secretory granules, and microtubules of seven β cells, and generate a comprehensive spatial map of microtubule-organelle interactions. We find that microtubules form nonradial networks that are predominantly not connected to either centrioles or endomembranes. Microtubule number and length, but not microtubule polymer density, vary with glucose stimulation. Furthermore, insulin secretory granules are enriched near the plasma membrane, where they associate with microtubules. In summary, we provide the first 3D reconstructions of complete microtubule networks in primary mammalian cells together with evidence regarding their importance for insulin secretory granule positioning and thus their supportive role in insulin secretion.

Published
2021

14. Erniedrigte Insulin-Biogenese in Langerhans-Inseln aus Pankreasteilresektaten von Typ 2-Diabetikern

Author

Ehehalt, Florian, Knoch, K. P., Meisterfeld, R., Erdmann, K., Kersting, S., Bergert, H., Dittert, D. D., Saeger, H. D., Solimena, M., Bruch, H. P., editor, Büchler, M. W., editor, Buhr, H. J., editor, Hohenberger, W., editor, Klar, E., editor, Post, S., editor, Schilling, M., editor, Schumpelick, V., editor, Siewert, J. R., editor, Thiede, A., editor, Becker, H., editor, Bittner, R., editor, Függer, R., editor, Köckerling, F., editor, Saeger, H. D., editor, Zornig, C., editor, Hölscher, A., editor, Izbicki, J. R., editor, Jauch, K. W., editor, Senninger, N., editor, Allgayer, H., editor, Bruns, C. J., editor, Celik, I., editor, Fries, H., editor, Kalthoff, H., editor, Schackert, H. K., editor, Brückner, U. B., editor, Ertel, W., editor, Faist, E., editor, Holzheimer, R. G., editor, Holzmann, B., editor, Schade, U. F., editor, Vollmar, B., editor, Heidecke, C. D., editor, Menger, M. D., editor, Neugebauer, E., editor, Spiegel, H. U., editor, Germann, G., editor, Haas, N., editor, Langer, S., editor, Machens, H. G., editor, Stark, G. B., editor, Steinau, H. U., editor, Haverich, A., editor, Heberer, M., editor, Fitze, G., editor, Roth, H., editor, von Schweinitz, D., editor, Waag, K. L., editor, Altendorf-Hofmann, A., editor, Lehnert, T., editor, Lorenz, W., editor, Ohmann, C., editor, Bechstein, W. O., editor, Broelsch, C., editor, Hopt, U., editor, Klempnauer, J., editor, Fändrich, F., editor, Markus, B., editor, Minor, T., editor, Neuhaus, P., editor, Wonigeit, K., editor, Dralle, H., editor, Goretzki, P. E., editor, Rothmund, M., editor, Bühren, V., editor, Josten, C., editor, Muhr, G., editor, Nast-Kolb, D., editor, Stürmer, K. M., editor, Trentz, O., editor, Brunkwall, J., editor, Sandmann, W., editor, Schmitz-Rixen, T., editor, Storck, M., editor, Branscheid, D., editor, Dienemann, H., editor, Hirner, A., editor, Passlick, B., editor, Toomes, H., editor, Beyersdorf, F., editor, Hetzer, R., editor, Schäfers, H. J., editor, Steinsträßer, L., editor, Vogt, P., editor, Arbogast, R., editor, and Bauer, H., editor

Published
2008
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15. Gentransfer in isolierten Langerhans-Inseln mit einem lentiviralen Vektorsystem

Author

Meisterfeld, Ronny, Ehehalt, F., Knoch, K. -P., Wündrich, E., Schnittler, H. J., Saeger, H. D., Solimena, M., Bruch, H. P., editor, Büchler, M. W., editor, Buhr, H. J., editor, Hohenberger, W., editor, Klar, E., editor, Post, S., editor, Schilling, M., editor, Schumpelick, V., editor, Siewert, J. R., editor, Thiede, A., editor, Becker, H., editor, Bittner, R., editor, Függer, R., editor, Köckerling, F., editor, Saeger, H. D., editor, Zornig, C., editor, Hölscher, A., editor, Izbicki, J. R., editor, Jauch, K. W., editor, Senninger, N., editor, Allgayer, H., editor, Bruns, C. J., editor, Celik, I., editor, Fries, H., editor, Kalthoff, H., editor, Schackert, H. K., editor, Brückner, U. B., editor, Ertel, W., editor, Faist, E., editor, Holzheimer, R. G., editor, Holzmann, B., editor, Schade, U. F., editor, Vollmar, B., editor, Heidecke, C. D., editor, Menger, M. D., editor, Neugebauer, E., editor, Spiegel, H. U., editor, Germann, G., editor, Haas, N., editor, Langer, S., editor, Machens, H. G., editor, Stark, G. B., editor, Steinau, H. U., editor, Haverich, A., editor, Heberer, M., editor, Fitze, G., editor, Roth, H., editor, von Schweinitz, D., editor, Waag, K. L., editor, Altendorf-Hofmann, A., editor, Lehnert, T., editor, Lorenz, W., editor, Ohmann, C., editor, Bechstein, W. O., editor, Broelsch, C., editor, Hopt, U., editor, Klempnauer, J., editor, Fändrich, F., editor, Markus, B., editor, Minor, T., editor, Neuhaus, P., editor, Wonigeit, K., editor, Dralle, H., editor, Goretzki, P. E., editor, Rothmund, M., editor, Bühren, V., editor, Josten, C., editor, Muhr, G., editor, Nast-Kolb, D., editor, Stürmer, K. M., editor, Trentz, O., editor, Brunkwall, J., editor, Sandmann, W., editor, Schmitz-Rixen, T., editor, Storck, M., editor, Branscheid, D., editor, Dienemann, H., editor, Hirner, A., editor, Passlick, B., editor, Toomes, H., editor, Beyersdorf, F., editor, Hetzer, R., editor, Schäfers, H. J., editor, Steinsträßer, L., editor, Vogt, P., editor, Arbogast, R., editor, and Bauer, H., editor

Published
2008
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16. Schutz und Regeneration der Betazellen

Author

Solimena, M., Lickert, H., and Schürmann, A.

Abstract

Der Typ-1-Diabetes sowie das fortgeschrittene Stadium des Typ-2-Diabetes sind durch den Verlust oder die Fehlfunktion der Insulin-produzierenden Betazellen in der Bauchspeicheldrüse gekennzeichnet. Bislang gibt es keine Möglichkeit, das Fortschreiten des Betazellverlusts durch eine medikamentöse Behandlung aufzuhalten oder umzukehren. In dem Forschungsschwerpunkt Schutz und Regeneration der Betazellen arbeitet das Deutsche Zentrum für Diabetesforschung (DZD) u. a. an Verfahren, um die Insulin-produzierenden Betazellen besser zu schützen bzw. sie wiederherzustellen oder zu ersetzen.

Published
2021

17. The transCampus metabolic training programme explores the link of SARS-CoV-2 virus to metabolic disease

Author

Bornstein, S.R., Guan, K., Brunßen, C., Mueller, G., Kamvissi-Lorenz, V., Lechler, R., Trembath, R., Mayr, M., Poston, L., Sancho, R., Ahmed, S., Alfar, E., Aljani, B., Alves, T.C., Amiel, S., Andoniadou, C.L., Bandral, M., Belavgeni, A., Berger, I., Birkenfeld, A.L., Bonifacio, E., Chavakis, T., Chawla, P., Choudhary, P., Cujba, A.M., Delgadillo Silva, L.F., Demcollari, T., Drotar, D.M., Duin, S., El-Agroudy, N.N., El-Armouche, A., Eugster, A., Gado, M., Gavalas, A., Gelinsky, M., Guirgus, M., Hansen, S., Hanton, E., Hasse, M., Henneicke, H., Heller, C., Hempel, H., Hogstrand, C., Hopkins, D., Jarc, L., Jones, P.M., Kamel, M., Kämmerer, S., King, A.J.F., Kurzbach, A., Lambert, C., Latunde-Dada, Y., Lieberam, I., Liers, J., Li, J.W., Linkermann, A., Locke, S., Ludwig, B., Manea, T., Maremonti, F., Marinicova, Z., McGowan, B.M., Mickunas, M., Mingrone, G., Mohanraj, K., Morawietz, H., Ninov, N., Peakman, M., Persaud, S.J., Pietzsch, J., Cachorro, E., Pullen, T.J., Pyrina, I., Rubino, F., Santambrogio, A., Schepp, F., Schlinkert, P., Scriba, L.D., Siow, R., Solimena, M., Spagnoli, F.M., Speier, S., Stavridou, A., Steenblock, C., Strano, A., Taylor, P., Tiepner, A., Tonnus, W., Tree, T., Watt, F.E., Werdermann, M., Wilson, M., Yusuf, N., and Ziegler, C.G.

Subjects
0301 basic medicine, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Clinical Biochemistry, education, MEDLINE, Disease, Settore MED/17 - MALATTIE INFETTIVE, Biochemistry, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, Internal medicine, Pandemic, Diabetes Mellitus, medicine, Humans, Obesity, Metabolic disease, Pandemics, metabolic training programme, Medical education, Communicable disease, Scope (project management), SARS-CoV-2, Biochemistry (medical), COVID-19, General Medicine, 030104 developmental biology, Infectious disease (medical specialty), transCampus, Education, Medical, Continuing, Covid-19, Metabolic Training Programme, Transcampus, 030217 neurology & neurosurgery
Abstract

Currently, we are experiencing a true pandemic of a communicable disease by the virus SARS-CoV-2 holding the whole world firmly in its grasp. Amazingly and unfortunately, this virus uses a metabolic and endocrine pathway via ACE2 to enter our cells causing damage and disease. Our international research training programme funded by the German Research Foundation has a clear mission to train the best students wherever they may come from to learn to tackle the enormous challenges of diabetes and its complications for our society. A modern training programme in diabetes and metabolism does not only involve a thorough understanding of classical physiology, biology and clinical diabetology but has to bring together an interdisciplinary team. With the arrival of the coronavirus pandemic, this prestigious and unique metabolic training programme is facing new challenges but also new opportunities. The consortium of the training programme has recognized early on the need for a guidance and for practical recommendations to cope with the COVID-19 pandemic for the community of patients with metabolic disease, obesity and diabetes. This involves the optimal management from surgical obesity programmes to medications and insulin replacement. We also established a global registry analyzing the dimension and role of metabolic disease including new onset diabetes potentially triggered by the virus. We have involved experts of infectious disease and virology to our faculty with this metabolic training programme to offer the full breadth and scope of expertise needed to meet these scientific challenges. We have all learned that this pandemic does not respect or heed any national borders and that we have to work together as a global community. We believe that this transCampus metabolic training programme provides a prime example how an international team of established experts in the field of metabolism can work together with students from all over the world to address a new pandemic.Currently, we are experiencing a true pandemic of a communicable disease by the virus SARS-CoV-2 holding the whole world firmly in its grasp. Amazingly and unfortunately, this virus uses a metabolic and endocrine pathway via ACE2 to enter our cells causing damage and disease. Our international research training programme funded by the German Research Foundation has a clear mission to train the best students wherever they may come from to learn to tackle the enormous challenges of diabetes and its complications for our society. A modern training programme in diabetes and metabolism does not only involve a thorough understanding of classical physiology, biology and clinical diabetology but has to bring together an interdisciplinary team. With the arrival of the coronavirus pandemic, this prestigious and unique metabolic training programme is facing new challenges but also new opportunities. The consortium of the training programme has recognized early on the need for a guidance and for practical recommendations to cope with the COVID-19 pandemic for the community of patients with metabolic disease, obesity and diabetes. This involves the optimal management from surgical obesity programmes to medications and insulin replacement. We also established a global registry analyzing the dimension and role of metabolic disease including new onset diabetes potentially triggered by the virus. We have involved experts of infectious disease and virology to our faculty with this metabolic training programme to offer the full breadth and scope of expertise needed to meet these scientific challenges. We have all learned that this pandemic does not respect or heed any national borders and that we have to work together as a global community. We believe that this transCampus metabolic training programme provides a prime example how an international team of established experts in the field of metabolism can work together with students from all over the world to address a new pandemic.

Published
2021

19. Circadian, Sleep and Caloric Intake Phenotyping in Type 2 Diabetes Patients With Rare Melatonin Receptor 2 Mutations and Controls: A Pilot Study

Author

Imam, A., Winnebeck, E.C., Buchholz, N., Froguel, P., Bonnefond, A., Solimena, M., Ivanova, A., Bouvier, M., Plouffe, B., Charpentier, G., Karamitri, A., Jockers, R., Roenneberg, T., and Vetter, C.

Subjects
SDG 3 - Good Health and Well-being, diabetes, Physiology, Physiology (medical), MTNR1B, MT2, circadian misalignment, sleep, diet, Mtnr1b, Mt2, Sleep, Diet, Circadian Misalignment, Social Jetlag, Diabetes, social jetlag, Original Research
Abstract

Background: Melatonin modulates circadian rhythms in physiology and sleep initiation. Genetic variants of the MTNR1B locus, encoding the melatonin MT2 receptor, have been associated with increased type 2 diabetes (T2D) risk. Carriers of the common intronic MTNR1B rs10830963 T2D risk variant have modified sleep and circadian traits such as changes of the melatonin profile. However, it is currently unknown whether rare variants in the MT2 coding region are also associated with altered sleep and circadian phenotypes, including meal timing. Materials and Methods: In this pilot study, 28 individuals [50% male; 46–82 years old; 50% with rare MT2 mutations (T2D MT2)] wore actigraphy devices and filled out daily food logs for 4 weeks. We computed circadian, sleep, and caloric intake phenotypes, including sleep duration, timing, and regularity [assessed by the Sleep Regularity Index (SRI)]; composite phase deviations (CPD) as well a sleep timing-based proxy for circadian misalignment; and caloric intake patterns throughout the day. Using regression analyses, we estimated age- and sex-adjusted mean differences (MD) and 95% confidence intervals (95%CI) between the two patient groups. Secondary analyses also compare T2D MT2 to 15 healthy controls. Results: Patients with rare MT2 mutations had a later sleep onset (MD = 1.23, 95%CI = 0.42;2.04), and midsleep time (MD = 0.91, 95%CI = 0.12;1.70), slept more irregularly (MD in SRI = −8.98, 95%CI = −16.36;−1.60), had higher levels of behavioral circadian misalignment (MD in CPD = 1.21, 95%CI = 0.51;1.92), were more variable in regard to duration between first caloric intake and average sleep offset (MD = 1.08, 95%CI = 0.07;2.08), and had more caloric episodes in a 24 h day (MD = 1.08, 95%CI = 0.26;1.90), in comparison to T2D controls. Secondary analyses showed similar patterns between T2D MT2 and non-diabetic controls. Conclusion: This pilot study suggests that compared to diabetic controls, T2D MT2 patients display a number of adverse sleep, circadian, and caloric intake phenotypes, including more irregular behavioral timing. A prospective study is needed to determine the role of these behavioral phenotypes in T2D onset and severity, especially in view of rare MT2 mutations.

Published
2020
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20. The transCampus Metabolic Training Programme Explores the Link of SARS-CoV-2 Virus to Metabolic Disease

Author

Bornstein, S. R., Guan, K., Brunbetaen, C., Mueller, G., Kamvissi-Lorenz, V., Lechler, R., Trembath, R., Mayr, M., Poston, L., Sancho, R., Ahmed, Sadek, Alfar, E., Aljani, B., Alves, T. C., Amiel, S., Andoniadou, C. L., Bandral, M., Belavgeni, A., Berger, I., Birkenfeld, A., Bonifacio, E., Chavakis, T., Chawla, P., Choudhary, P., Cujba, A. M., Delgadillo Silva, L. F., Demcollari, T., Drotar, D. M., Duin, S., El-Agroudy, N. N., El-Armouche, A., Eugster, A., Gado, M., Gavalas, A., Gelinsky, M., Guirgus, M., Hansen, S., Hanton, E., Hasse, M., Henneicke, H., Heller, C., Hempel, H., Hogstrand, C., Hopkins, D., Jarc, L., Jones, P. M., Kamel, M., Kammerer, S., King, A. J. F., Kurzbach, A., Lambert, C., Latunde-Dada, Y., Lieberam, I., Liers, J., Li, J. W., Linkermann, A., Locke, S., Ludwig, B., Manea, T., Maremonti, F., Marinicova, Z., Mcgowan, B. M., Mickunas, M., Mingrone, Geltrude, Mohanraj, K., Morawietz, H., Ninov, N., Peakman, M., Persaud, S. J., Pietzsch, J., Cachorro, E., Pullen, T. J., Pyrina, I., Rubino, F., Santambrogio, Alberto, Schepp, F., Schlinkert, P., Scriba, L. D., Siow, R., Solimena, M., Spagnoli, F. M., Speier, S., Stavridou, A., Steenblock, C., Strano, A., Taylor, P., Tiepner, A., Tonnus, W., Tree, T., Watt, F., Werdermann, M., Wilson, M., Yusuf, N., Ziegler, C. G., Ahmed S., Mingrone G. (ORCID:0000-0003-2021-528X), Santambrogio A., Bornstein, S. R., Guan, K., Brunbetaen, C., Mueller, G., Kamvissi-Lorenz, V., Lechler, R., Trembath, R., Mayr, M., Poston, L., Sancho, R., Ahmed, Sadek, Alfar, E., Aljani, B., Alves, T. C., Amiel, S., Andoniadou, C. L., Bandral, M., Belavgeni, A., Berger, I., Birkenfeld, A., Bonifacio, E., Chavakis, T., Chawla, P., Choudhary, P., Cujba, A. M., Delgadillo Silva, L. F., Demcollari, T., Drotar, D. M., Duin, S., El-Agroudy, N. N., El-Armouche, A., Eugster, A., Gado, M., Gavalas, A., Gelinsky, M., Guirgus, M., Hansen, S., Hanton, E., Hasse, M., Henneicke, H., Heller, C., Hempel, H., Hogstrand, C., Hopkins, D., Jarc, L., Jones, P. M., Kamel, M., Kammerer, S., King, A. J. F., Kurzbach, A., Lambert, C., Latunde-Dada, Y., Lieberam, I., Liers, J., Li, J. W., Linkermann, A., Locke, S., Ludwig, B., Manea, T., Maremonti, F., Marinicova, Z., Mcgowan, B. M., Mickunas, M., Mingrone, Geltrude, Mohanraj, K., Morawietz, H., Ninov, N., Peakman, M., Persaud, S. J., Pietzsch, J., Cachorro, E., Pullen, T. J., Pyrina, I., Rubino, F., Santambrogio, Alberto, Schepp, F., Schlinkert, P., Scriba, L. D., Siow, R., Solimena, M., Spagnoli, F. M., Speier, S., Stavridou, A., Steenblock, C., Strano, A., Taylor, P., Tiepner, A., Tonnus, W., Tree, T., Watt, F., Werdermann, M., Wilson, M., Yusuf, N., Ziegler, C. G., Ahmed S., Mingrone G. (ORCID:0000-0003-2021-528X), and Santambrogio A.

Abstract

Currently, we are experiencing a true pandemic of a communicable disease by the virus SARS-CoV-2 holding the whole world firmly in its grasp. Amazingly and unfortunately, this virus uses a metabolic and endocrine pathway via ACE2 to enter our cells causing damage and disease. Our international research training programme funded by the German Research Foundation has a clear mission to train the best students wherever they may come from to learn to tackle the enormous challenges of diabetes and its complications for our society. A modern training programme in diabetes and metabolism does not only involve a thorough understanding of classical physiology, biology and clinical diabetology but has to bring together an interdisciplinary team. With the arrival of the coronavirus pandemic, this prestigious and unique metabolic training programme is facing new challenges but also new opportunities. The consortium of the training programme has recognized early on the need for a guidance and for practical recommendations to cope with the COVID-19 pandemic for the community of patients with metabolic disease, obesity and diabetes. This involves the optimal management from surgical obesity programmes to medications and insulin replacement. We also established a global registry analyzing the dimension and role of metabolic disease including new onset diabetes potentially triggered by the virus. We have involved experts of infectious disease and virology to our faculty with this metabolic training programme to offer the full breadth and scope of expertise needed to meet these scientific challenges. We have all learned that this pandemic does not respect or heed any national borders and that we have to work together as a global community. We believe that this transCampus metabolic training programme provides a prime example how an international team of established experts in the field of metabolism can work together with students from all over the world to address a new pandemic.

Published
2021

25. Fourth meeting of the European Neurological Society 25–29 June 1994 Barcelona, Spain: Abstracts of Symposia and free communications

Author

Harms, L., Bock, A., JÄnisch, W., Valdueza, J., Weber, J., Link, I., De Keyser, J., Goossens, A., Wilczak, N., Vedeler, C., Bjorge, L., Uvestad, E., Conti, G., Williams, K., Ginsberg, L., Rafique, S., Rapoport, S. I., Gershfeld, N. L., De La Meilleure, G., Crevits, L., Faiss, J. H., Heye, N., Blanke, J., Sackmann, A., Kastrup, O., Doornbos, R., van der Worp, H. B., Kappelle, L. J., Bar, P. R., Davie, C. A., Barker, G. J., Brenton, D., Miller, D. H., Thompson, A. J., Block, F., Schwarz, M., Delodovici, L., Baruzzi, F., Bonaldi, G., Dario, A., Marra, A., Mercuri, A., Dworzak, F., Cavallari, P., Confalonieri, P., Zuffi, M., Antozzi, C., Cornelio, F., Baldissera, F., Chassande, B., Ameri, A., Eymard, B., Poisson, M., Vérier, A., Brunet, P., Congia, S., Murgia, P. L., Cannas, A., Borghero, G., Uselli, S., Mellino, G., Ferrai, R., Lampis, R., Massa, R., Muzzetto, B., Giannini, F., Rossi, S., Cioni, R., d'Aniello, C., Guarneri, A., Battistini, N., Ceriani, F., Del Santo, A., Poloni, M., Campo, J. F., Iglesias, F., Guitera, M. V., Farinas, C., Pascual, J., Leno, C., Berciano, J., Thorpe, I. W., Kendall, B. E., McDonald, W. I., Moulignier, A., Dromer, F., Baudrimont, M., Dupont, B., Gozlan, J., El Amrani, M., Petit, J. C., Roullet, E., Sterzi, R., Causaran, R., Protti, A., Riva, M., Erminio, F., Arena, O., Villa, F., Maccagnano, E., Miletta, M., Spinelli, F., Ben-Hur, T., Weidenfeldl, J., Rao, N. S., Chari, C. C., Laforet, P., Matheron, S., Adams, D., Chemouilli, Ph., Desi, M., Said, G., Davous, P., Lionnet, F., Pulik, M., Genet, P., Rozenberg, F., Cartier, L. M., Castillo, J. L., Cea, J. G., Villagra, R., de Saint Martin, L., Mahieux, F., Manifacier, M. J., Mattos, K., Queiros, C., Publio, L., Vinhas, V., PeÇanha-Martins, A. 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H., Mobner, R., Fassbender, K., Kuhnen, J., Schwartz, A., Hennerici, M., Miller, A., Lider, O., Abramsky, O., Weiner, H. L., Offner, H., Vanderbark, A. A., Paoino, E., Fainardi, E., Addonizio, M. C., Ruppi, P., Tola, M. R., Granieri, E., Carreras, M., Sazdovitch, V., Joutel, A., Verdier-taillefer, M. H., Heinzlef, O., Radder, C., Tournier-Lasserve, E., Brenner, R. E., Munro, P. M. G., Williams, S. C. R., Bell, J. D., Hawkins, C. P., Filippi, M., Campi, A., Dousset, V., Canal, N., Comi, G., Zhu, J., Weber, F., Retska, R., List, J., Zhang, L., Brock, M., Taphoorn, M. J. B., Heimans, J. J., van der Veen, E. A., Karim, A. B. M. F., Sarazin, M., Argentino, N., Delattre, J. Y., Derkinderen, P., Buchwald, B., Schroter, G., Serve, G., Franke, C. H., Conrad, B., Kitchen, N. D., Thomas, D. G. T., Forman, A. D., Ang, Kie- Kian, Price, R., Stephens, C., Salmaggi, A., Nermni, R., Silvani, A., Forno, M. 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A., Rothstein, T. L., Gibson J. M., Morrison P. M., Collins A. D., Eiselt, M., Wagnur, H., Zwiener, U., Schindler, T., Efendi, H., Ertekin, C., Erfas, M., Larsson, L. E., Sirin, H., AraÇ, N., Toygar, A., Demir, Y., Seddigh, S., Vogt, T. H., Hundemer, H., Visbeck, A., Pastena, L., Faralli, F., Mainardi, G., Gagliardi, R., Linden, D., Berlit, P., Lopez, O. L., Becker, J. T., Jungreis, C., Brenner, R., Rezek, D., Dekesky, S. T., Estol, C., Boller, F., Fernandez, J. M., Mederer, S., Batlle, J., Turon, A., Codina, A., Hitzenberger, P., Vila, N., Valls-SolÇ, J., Chamorro, A., Pouget, J., Schmied, A., Morin, D., Azulay, J. Ph., Vedel, J. P., Montalt, J., Escudero, J., Barona, R., Campos, A., Varli, K., Ertem, E., Uludag, B., Yagiz, A., Privorkin, Z., Steinvil, Y., Kott, E., Combarros, O., Sanchez-Pernaute, R., Orizaola, P., Mokrusch, Th., Kutluaye, E., Selcuki, D., Ertikin, C., Zettl, U., Gold, R., Harvey, G. K., Hartung, H. P., Toyka, K. V., Wokke, J. H. J., Oey, P. L., Ippel, P. F., Jansen, G. H., Franssen, H., Toyooka, K., Fujimura, H., Ueno, S., Yoshikawa, H., Yorifuji, S., Yanagihara, T., Talamon, C., Tzourio, C., Kiefer, R., Jung, S., Toyka, K., Ruolt, I., Tranchant, C., Mohr, M., Warter, J. M., Younger, D. S., Rosoklija, G., Hays, A. P., Kurita, R., Hasegawa, O., Matsumto, M., Komiyama, A., Nara, Y., Oueslati, S., Belal, S., Turki, I., Ben Hamida, C., Hentati, F., Ben Hamida, M., Kwiecinski, H., Krolicki, L., Domzal-Stryga, A., Dellemijn, P. L. I., van Deventer, P., van Moll, B., Drogendijk, T., Vecht, Ch. J., Nemni S., Amadio, Fazio, R., Galardin, G., Delodovici, M. L., Peghi, E., Monticelli, M. L., Sessa, A., Viguera, M. L., Palomar, M., Gamez, J., Cervera, C., Navarro, C., Serena, J., Duran, I., Fernandez, A. L., Comabella, M., Nos, C., Rio, J., Montalban, J., Navarro, X., Verdu, E., Darbra, S., Buti, M., Mrabet, A., Fredj, M., Gouider, R., Tounsi, H., Khalfallah, N., Haddad, A., Dbaiss, T., Ghnassia, R., Rouillet, E., Chedru, F., Porsche, H., Strenge, H., Li, S. W., Young, Y. P., Garcia, A. A., Baron, P., Scarpini, E., Bianchi, R., Conti, A., Livraghi, S., Rees, J. H., Gregson, N. A., Hughes, R. A. C., Sedano, M. J., Calleja, J., Canga, E., Bahou, Y., Biary, N., Al Deeb, S. M., Guern, E. L. E., Gugenheim, M., Tardieu, S., Aisonobe, T. M., Agid, Y., Bouche, P., Brice, A., Rautenstrauss, B., Nelis, E., Grehl, H., Van Broeckhoven, C., Pfeiffer, R. A., Liehr, T., Ganzmann, E., Gehring, C., Neundörfer, B., Geremia, L., Doronzo, R., Sacilotto, G., Sergi, P., Pastorino, G. C., Scarlato, G., Planté-Bordeneuve, V., Mantel, A., Baas, F., Moser, H., Antonini, A., Psylla, M., Günther, I., Vontobell, P., Beer, H. F., Leenders, K. L., Chaudhuri, K. Ray, Parker, J., Pye, I. F., Millac, P. A. H., Abbott, R. J., Sutter, M., Albani, C., de Rijk, M. C., Breteler, M. M. B., Graveland, G. A., van der Mechè, F. G. A., Hofman, A., Keipes, M., Hilger, Ch., Diederich, N., Metz, H., Hentges, F., Pollak, P., Benabid, A. L., Limousin, P., Hoffmann, D., Benazzouz, A., Perret, J., Laihinen, A., Rinne, J. O., Ruottinen, H., Nagren, K., Lehikoinen, P., Oikonen, V., Ruotsalainen, U., Rinne, U. K., Cocozza, S., Pizzuti, A., Cavalcanti, F., Monticelli, A., Pianese, L., Redolfi, E., Paiau, F., Di Donato, S., Pandolfo, M., Palau, F., Monros, E., De Michele, G., Smeyers, P., Lopez-ArLandis, J., Uilchez, J., Filla, A., Genis, D., Matilla, T., Volpini, V., Blanchs, M. I., Davalos, A., Molins, A., Rosell, J., Estivill, X., De Jonghe, P., Smeyers, G., Krols, L., Mercelis, R., Hazan, J., Weissenbach, J., Martin, J. J., Warner, T. A. T., Williams, L., Orb, A. S., Harding, A. E., Giunti, P., Sweeney, M. G., Spadaro, M., Jodice, C., Novelletto, A., Malaspina, P., Frontali, M., Salmon, E., Gregoire, Del Fiore, Comar, Franck, G., Scheltens, P. H., Siegfried, K., Dartigues, E., De Deyn, P., Horn, R., Nelson, I., Hanna, M. G., Morgan-Hughes, J. A., Collinge, J., Palmer, M. S., Campbell, T., Mahal, S., Sidle, K., Humphreys, C., Tavitian, B., Pappata, S., Jobert, A., Crouzel, A. M., DiGiamberardino, L., Steimetz, G., Barbanti, P., Fabbrini, G., Salvatore, M., Buzzi, M. G., Di Piero, V., Petraroli, R., Sbriccoli, A., Pocchiari, M., Macchi, G., Lenzi, G. L., Spiegel, R., Maguire, P., Schmid, W., Ott, A., Bots, M. L., Grobbe, D. E., Hofman, A., Howard, R. S., Russell, S., Losseff, N., Hirsch, N. P., Couderc, R., Bailleul, S., Nargeot, M. C., Touchon, J., Picot, M. C., Rizzo, M., Watson, G., McGehee, D., Dingus, T., Kappos, L., Radü, E. W., Haas, J., Hartard, C. H., Spuler, S., Yousry, T., Voltz, R., Scheller, A., Holler, E., Hohlfeld, R., Scolding, N. J., Sussman, J., Kolar, O. J., Farlow, M. R., Rice, P. H., Zipp, F., Sotgiu, S., Weiss, E. H., Wekerle, H., Chalmers, R., Robertson, N., Compston, D. A. S., Martino, G., Clementi, E., Brambilla, E., Moiola, L., Martinelli, V., Colombo, B., Poggi, A., Rovaris, M., Grimaldi, L. M. E., Roth, M. P., Descoins, P., Ballivet, S., Ruidavets, J. B., Waubant, E., Nogueira, L., Cambon-Thomsen, A., Clanet, M., Leppert, D., Hauser, S., Lugaresi, A., Tartaro, A., D'aurelio, P., Befalo, L. L. O., Thomas, A., Malatesta, G., Gambi, D., Benedikz, J. E. G., Magnusson, H., Poser, C. M., Guomundsson, G., Bates, T. E., Davies, S. E. C., Clark, J. B., Landon, D. N., ùther, J. R., Rautenberg, W., Overgaard, K., Sereghy, T., Pedersen, H., Boysen, G., Diez-Tejedor, E., Carceller, F., Gutierrez, M., Lopez-Pajares, R., Roda, J. M., Chandra, B., Ricart, W., Gonzalez-Huix, F., Molina, A., Rundek, T., Demarin, V., De Reuck, J., Boon, P., Decoq, D., Strijckmans, K., Goethals, P., Lemahieu, I., Nibbio, A., Chabriat, H., Vahedi, K., Nagy, T., Verin, M., Mas, J. L., Julien, J., Ducrocq, X., Iba-Zizen, M. T., Cabanis, E. A., Bousser, M. G., Rolland, Y., Landgraf, F., Bompais, B., Lemaitre, M. H., Edan, G., Vorstrup, S., Knudsen, L., Olsen, K. Skovgaard, Videbaek, C., Schroeder, T., van Gijn, J., Jansen, H. M. L., Pruim, J., Paans, A. M. J., Willemsen, A. T. M., Hew, J. M., vd Vliet, A. M., Haaxma, R., Vaalburg, W., Minderhoud, J. M., Korf, J., Soudain, S. E., Ho, T. W., Mishu, B., Li, C. Y., Nachainkin, I., Gao, C. Y., Cornblath, D. R., Griffin, J. W., Asbury, A. K., Blaser, M. J., McKhann, G. M., Ho, T., Macko, C., Xue, P., Stadlan, E. M., Ramos-Alvarez, M., Valenciano, L., Visser, L. H., van der Meché, F. G. A., van Darn, P. A., Meulstee, J., Schmitz, P. I. M., Jacobs, B., Oomes, P. G., Kleyweg, R. P., Jacobs, B. C., Endtz, H. P., van Doorn, P. A., van der Mech, F. G. A., Van den Berg, L. H., Mollee, I., Logtenberg, T., Thomas, P. K., Plant, G., Baxter, P. J., Luis, R. Santiago, Matsumoto, M., Notermans, N. C., Wokke, J. H. J., Lokhorst, H. M., van der Graaf, Y., Jennekens, F. G. I., Azulay, J. P., Bille-Turg, F., Valentin, P., Farnarier, G. G., Pellissier, J. F., Serratrice, G., Quasthoff, S., Schneider, U., Grafe, P., Hilkens, P. H. E., Moll, J. W. B., van der Burg, M. E. L., Planting, A. S. T., van Putten, W. L. J., van den Bent, M. J., Birklein, F., Spitzer, A., Lang, E., Neundorfer, B., Diehl, R. R., Lücke, D., Smith, G. D. P., Mathias, C. J., Serra, J., Campera, M., Ochoa, J. L., Ray Chaudhuri, K., Pavitt, D., Alam, M., Handwerker, H. O., Bleasdale-Barr, K., Smith, G., Murray, N. M. F., Hawkins, P., Pepys, M., Gellera, C., DiDonato, S., Taroni, F., Uncini, A., Di Muzio, A., Servidei, S., Silvestri, G., Lodi, R., Iotti, S., Barbiroli, B., Morrissey, S. P., Borruat, F. X., Francis, D., Mosely, I., Hansen, H. C., Helmke, K., Kunze, K., Sadzot, B., Maquet, P., Lemaire, Plenevaux, Damhaut, Sommer, C., Myers, R. R., Berta, E., Mantegazza, R., Argov, Z., Shapira, Y., Wirguin, I., Beuuer, J., Franke, C., Roberts, M., Willison, H., Vincent, A., Newsom-Davis, J., Morrison, K. E., Damels, R., Francis, M., Campbell, L., Davies, K. E., Kohler, W., Bucka, C., Hertel, G., Kanovsky, P., Auer, D., Ackermann, H., Klose, U., Naegele, Th., Bien, S., Voigt, K., Fink, G. R., Stephan, K. M., Wise, R. J. S., Mullatti, N., Hewer, L., Frackowiak, R. S. J., Weiller, C. S., Rijnites, M., Jueptner, M., Bauermann, T., Krams, M., Diener, H. C., van Walderveen, M. A. A., Barkhof, F., Hommes, O. R., Valk, J., Willmer, J. P., Guzman, D. A., Passingham, R. E., Silbersweig, D., Ceballos-Baumann, A., Frith, C. D., Frackowiak, R., Lucas, C. H., Goullard, L., Marchau, M. J., Godefroy, O., Rondepierre, P. H., Chamas, E., Mounier-Vehier, F., Leys, D., Renato, J., Verdugo, M. S. C., Campero, M., Jose, L., Ochoa, D. S. C., Vivancos, F., Tejedor, E. Diez, Martinez, N., Roda, J., Frank, A., Barreiro, P., Satoh, Y., Nagata, K., Maeda, T., Hirata, Y., YalÇinerner, B., Ozkara, C., Ozer, F., Ozer, S., Hanoglu, L., Zunker, P., Pozo, J. L., Oberwittler, C., Schick, A., Buschmann, H. -Ch., Ringelstein, E. Bernd, Lara, M., Anzola, G. P., Magoni, M., Volta, G. Dalla, Tarasov, A., Feigin, V., Beaudry, M. G., Carrier, S., Chicoutimi, Henriques, I. L., Bogoussslavsky, J., van Melle, G., Mathieu, J., Perusse, L., Allard, P., Prevost, C., Cantin, L., Bouchard, J. M., De Braekeleer, M., Agbo, C., Neau, J. P., Tantot, A. M., Dary-Auriol, M., Ingrand, P., Gil, R., Baltadjiev, D., Zekin, D., Sabey, K., Gennaula, C. P., Pope, B. A., Caparros-Lefebvre, D., Girard-Buttaz, I., Pruvo, J. P., Petit, H., Hipola, D., Martin, M., Giménez-Roldan, S., Ivanez, V., Japaridze, G., Carrasco, J. L., Picomell, I., Herranz, J. L., Macias, J. A., Nieto, M., Noya, M., Oller, L., Kiteva-Trencevska, G., Delgado, M. R., Liu, H., Luengo, A., Parra, J., Colas, J., Fernandez, M. J., Manzanares, R., Kornhuber, M. E., Malashkhia, V., Orkodashili, G., Martinez, M., Bonaventura, I., Porta, G., Martinez, I., Fernandez, A., Aguilar, M., Masnou, P., Drouet, A., Dreyfus, M., Cartron, J., Morel-Kopp, M. C., Tchernia, G., Kaplan, C., Lammers, M. W., Hekster, Y. A., Keyser, A., Meinardi, H., Renier, W. O., Boon, P. A. J. M., Have, M. D., Kint, B., Cruz, P., Cadilha, A., Almeida, R., Goncalves, M., Pimenta, M., Ramos, L. M. P., Polder, T. W., Broere, C. A., Polman, L., Rother, I., Rother, M., Schlaug, G., Arnold, S., Holthausen, H., Wunderlich, G., Ebner, A., Luders, H., Witte, O. W., Seitz, R. J., Serra, L. L., Gallicchio, B., Rotondi, F., Wieshmann, U., Meierkord, H., Sabev, K., Di Carlo, V., Gueguen, B., Derouesné, Ch., Ancri, D., Bourdel, M. C., Guillou, S., Aliaga, R., Chornet, M. A., Rodrigo, A., Pascual, A. Pascual -Leone, Catala, M. D., Pascual-Leone, A., Benbadis, S. R., Dinner, D. S., Chelune, G. J., Lüders, H. O., Piedmonte, M. R., Blanco, T., Lopez, M. P., Romero, B., Deltoro, A., Pascual, A., Pascual, Leone, Bolgert, F., Josse, M. O., Tassan, P., Touze, E., Laplane, D., Godenberg, F., Brizioli, E., Del Gobbo, M., Pelliccioni, G., Scarpino, O., Durak, H., Damlacik, G., Tunca, Z., Fidaner, H., Yurekli, Y., Yemez, B., Kaygisiz, A., Anllo, E. A., Esperet, E., Giovagnoli, A. R., Casazza, M., Spreafico, R., Avanzini, G., Mascheroni, S., Vecchio, I., Tornali, C., Antonuzzo, A., Grasso, A. A., Bella, R., Pennisi, G., Raffaele, R., Broeckx, J., Schildermans, F., Hospers, W., Deberdt, W., Carney, J. M., Aksenova, M., Chen, M. S., Juncadella, M., Busquets, N., De la Fuente, I., Rodriguez, A., Rubio, F., Soler, R., Khati, C., Pillon, B., Deweer, B., Malapani, C., Malichard, N., Dubois, B., Rancurel, G., Lopez, D. L., Jungreia, G., DeKosky, S. T., Boiler, F., Weiller, C., Rijntjes, M., Mueller, S. P., Maguire, E. 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M., Pleiffer, G., Kunre, K., Dieterich, M., Brandt, Th., Guarino, M., Stracciari, A., Pazzaglia, P., D'Alessandro, R., Santilli, I., Donato, M., The European Velnacrine Study Group, The Dutch Guillain-Barré study group, The COP-1 Multicenter Clinical and Research Group Study, and European Study Group

Published
1994
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27. Association of GAD-65, but not of GAD-67, with Golgi complex of transfected Chinese hamster ovary cells mediated by the N-terminal region

Author

Solimena, M., Aggujaro, D., Muntzel, C., Dirxx, R., Butler, M., Camilli, P. de, and Hayday, A.

Subjects
Glutamate decarboxylase -- Research, Golgi apparatus -- Analysis, Science and technology
Abstract

The subcellular structure of glutamic acid decarboxylase (GAD) and its underlying mechanisms were studied. This involved the cloning of GAD-65, its comparison to GAD-67 in transfected fibroblasts and the transfection of a chimeric GAD-65-GAD-67 gene targeted towards the Golgi complex. It was found that a response required for the chimeric association also exists within the N-terminal domain of GAD-65.

Published
1993

30. Functional circadian and sleep phenotyping of type 2 diabetes patients with melatonin receptor 2 mutations and controls: a pilot study

Author

Imam, A., primary, Winnebeck, E., additional, Buchholz, N., additional, Froguel, P., additional, Bonnefond, A., additional, Solimena, M., additional, Ivanova, A., additional, Bouvier, M., additional, Plouffe, B., additional, Charpentier, G., additional, Karamitri, A., additional, Jockers, R., additional, Roenneberg, T., additional, and Vetter, C., additional

Published
2019
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35. A Global Approach for Quantitative Super Resolution and Electron Microscopy on Cryo and Epoxy Sections Using Self-labeling Protein Tags

Author

Müller A, Martin Neukam, Ivanova A, Sönmez A, Münster C, Kretschmar S, Kalaidzidis Y, Kurth T, Jm, Verbavatz, and Solimena M

Subjects
Staining and Labeling, Epoxy Resins, Science, Recombinant Fusion Proteins, Green Fluorescent Proteins, Organelles, Super-resolution microscopy, Transmission electron microscopy, TU Dresden, Publishing Funds, Organellen, Super-Auflösungsmikroskopie, Transmissionselektronenmikroskopie, TU Dresden, Publikationsfonds, Article, Fixatives, Luminescent Proteins, Mice, Microscopy, Electron, Transmission, Microscopy, Fluorescence, Insulin-Secreting Cells, Freezing, ddc:520, Medicine, Animals, Frozen Sections, Insulin, Cells, Cultured, Cryoultramicrotomy
Abstract

Correlative light and electron microscopy (CLEM) is a powerful approach to investigate the molecular ultrastructure of labeled cell compartments. However, quantitative CLEM studies are rare, mainly due to small sample sizes and the sensitivity of fluorescent proteins to strong fixatives and contrasting reagents for EM. Here, we show that fusion of a self-labeling protein to insulin allows for the quantification of age-distinct insulin granule pools in pancreatic beta cells by a combination of super resolution and transmission electron microscopy on Tokuyasu cryosections. In contrast to fluorescent proteins like GFP organic dyes covalently bound to self-labeling proteins retain their fluorescence also in epoxy resin following high pressure freezing and freeze substitution, or remarkably even after strong chemical fixation. This enables for the assessment of age-defined granule morphology and degradation. Finally, we demonstrate that this CLEM protocol is highly versatile, being suitable for single and dual fluorescent labeling and detection of different proteins with optimal ultrastructure preservation and contrast.

Published
2017

36. Decreased STARD10 expression is associated with defective insulin secretion in humans and mice

Author

Carrat, GR, Hu, M, Nguyen-Tu, M-S, Chabosseau, P, Gaulton, KJ, van de Bunt, M, Siddiq, A, Falchi, M, Thurner, M, Canouil, M, Pattou, F, Leclerc, I, Pullen, TJ, Cane, MC, Prabhala, P, Greenwald, W, Schulte, A, Marchetti, P, Ibberson, M, MacDonald, PE, Manning Fox, JE, Gloyn, AL, Froguel, P, Solimena, M, McCarthy, M, Rutter, GA, Commission of the European Communities, Medical Research Council (MRC), Société Francophone du Diabète, and Wellcome Trust

Subjects
endocrine system diseases, Medical and Health Sciences, Mice, Insulin-Secreting Cells, Insulin Secretion, RISK VARIANTS, 2.1 Biological and endogenous factors, Homeostasis, GWAS, Genetics(clinical), genetics, Aetiology, Cloning, Molecular, Genetics (clinical), IN-VIVO, Genetics & Heredity, diabetes, islet, GTPase-Activating Proteins, Adaptor Proteins, 11 Medical And Health Sciences, Biological Sciences, secretion, Liver, GTTT-REPEAT, Life Sciences & Biomedicine, Type 2, Proinsulin, ARAP1, insulin, mouse, STARD10, Adaptor Proteins, Signal Transducing, Alleles, Animals, Carrier Proteins, Diabetes Mellitus, Type 2, Gene Expression Regulation, Genetic Variation, Humans, Insulin, Phosphoproteins, Quantitative Trait Loci, Transcriptome, Genetics, Article, GENETIC ARCHITECTURE, TYPE-2, Diabetes Mellitus, GLYCEMIC TRAITS, ddc:610, GENOME-WIDE ASSOCIATION, Metabolic and endocrine, Science & Technology, TRANSFER PROTEIN, Human Genome, Signal Transducing, Molecular, 06 Biological Sciences, DIABETES SUSCEPTIBILITY LOCI, PANCREATIC BETA-CELL, Cloning
Abstract

Genetic variants near ARAP1 (CENTD2) and STARD10 influence type 2 diabetes (T2D) risk. The risk alleles impair glucose-induced insulin secretion and, paradoxically but characteristically, are associated with decreased proinsulin:insulin ratios, indicating improved proinsulin conversion. Neither the identity of the causal variants nor the gene(s) through which risk is conferred have been firmly established. Whereas ARAP1 encodes a GTPase activating protein, STARD10 is a member of the steroidogenic acute regulatory protein (StAR)-related lipid transfer protein family. By integrating genetic fine-mapping and epigenomic annotation data and performing promoter-reporter and chromatin conformational capture (3C) studies in β cell lines, we localize the causal variant(s) at this locus to a 5 kb region that overlaps a stretch-enhancer active in islets. This region contains several highly correlated T2D-risk variants, including the rs140130268 indel. Expression QTL analysis of islet transcriptomes from three independent subject groups demonstrated that T2D-risk allele carriers displayed reduced levels of STARD10 mRNA, with no concomitant change in ARAP1 mRNA levels. Correspondingly, β-cell-selective deletion of StarD10 in mice led to impaired glucose-stimulated Ca(2+) dynamics and insulin secretion and recapitulated the pattern of improved proinsulin processing observed at the human GWAS signal. Conversely, overexpression of StarD10 in the adult β cell improved glucose tolerance in high fat-fed animals. In contrast, manipulation of Arap1 in β cells had no impact on insulin secretion or proinsulin conversion in mice. This convergence of human and murine data provides compelling evidence that the T2D risk associated with variation at this locus is mediated through reduction in STARD10 expression in the β cell.

Published
2017
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43. Stability and targeting of proICA512/IA-2 to insulin secretory granules requires beta4-sheet mediated dimerization of its ectodomain in the endoplasmic reticulum

Author

Torkko, J., Primo, M., Dirkx, R., Friedrich, A., Viehrig, A., Vergari, E., Borgonovo, B., Sonmez, A., Wegbrod, C., Lachnit, M., Munster, C., Sica, Mauricio, Emárcora, M., and Solimena, M.

Subjects
endocrine system, endoplasmic reticulum, Biología Celular, Microbiología, β4- sheet mediated dimerization, type-1 diabetes autoantigen ICA512/IA-2/RPTPN, insulin secretory granules, ectodomain, tyrosine 30 phosphatase
Abstract

The type 1 diabetes autoantigen ICA512/IA-2/RPTPN is a receptor protein tyrosine phosphatase of the insulin secretory granules (SGs) which regulates the size of granule stores, possibly via cleavage/signaling of its cytosolic tail. The role of its extracellular region remains unknown. Structural studies indicated that β2- or β4-strands in the mature ectodomain (ME ICA512) form dimers in vitro. Here we show that ME ICA512 prompts proICA512 dimerization in the endoplasmic reticulum. Perturbation of ME ICA512 β2-strand N-glycosylation upon S508A replacement allows for proICA512 dimerization, O-glycosylation, targeting to granules, and conversion, which are instead precluded upon G553D replacement in the ME ICA512 β4-strand. S508A/G553D and N506A/G553D double mutants dimerize but remain in the endoplasmic reticulum. Removal of the N-terminal fragment (ICA512-NTF) preceding ME ICA512 allows an ICA512-ΔNTF G553D mutant to exit the endoplasmic reticulum, and ICA512-ΔNTF is constitutively delivered to the cell surface. The signal for SG sorting is located within the NTF RESP18 homology domain (RESP18-HD), whereas soluble NTF is retained in the endoplasmic reticulum. Hence, we propose that the ME ICA512 β2-strand fosters proICA512 dimerization until NTF prevents N506 glycosylation. Removal of this constraint allows for proICA512 β4-strand-induced dimerization, exit from the endoplasmic reticulum, O-glycosylation, and RESP18-HD-mediated targeting to granules.

Published
2015

44. Dynamik der Blutzuckerregulation nach partieller Pankreasresektion – eine prospektive Beobachtungsstudie

Author

Ehehalt, F, Sturm, D, Distler, M, Saeger, HD, Solimena, M, Kersting, S, and Grützmann, R

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Einleitung: Eine chirurgische Reduktion des Bauchspeicheldrüsen-Parenchyms führt zu einer Reduktion der insulin- und glukagonproduzierenden Zellen und stellt damit einen Eingriff in den Blutzuckerhaushalt dar. Der Einfluss einer partiellen Pankreasresektion auf die Blutzuckerregulation [for full text, please go to the a.m. URL], 130. Kongress der Deutschen Gesellschaft für Chirurgie

Published
2013
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45. Creating a 'Transcampus' in diabetes research between King's College London and the Technische Universität Dresden: update on islet biology and transplantation

Author

Bornstein, Sr, Amiel, Sa, Rubino, F, Mingrone, Geltrude, Kamvissi, V, Solimena, M, Bonifacio, E, Jones, P, Schwarz, P, Birkenfeld, Al, Behrens, A, Barthel, A, Lechler, R, Peakman, M., Mingrone, Geltrude (ORCID:0000-0003-2021-528X), Bornstein, Sr, Amiel, Sa, Rubino, F, Mingrone, Geltrude, Kamvissi, V, Solimena, M, Bonifacio, E, Jones, P, Schwarz, P, Birkenfeld, Al, Behrens, A, Barthel, A, Lechler, R, Peakman, M., and Mingrone, Geltrude (ORCID:0000-0003-2021-528X)

Abstract

n/a

Published
2015

46. Sudden death and paroxysmal autonomic dysfunction in stiff-man syndrome

Author

Mitsumoto H, Estes Ml, De Camilli P, Solimena M, Schwartzman Mj, La Franchise Ef, and Samuel M. Chou

Subjects
Adult, Spasm, medicine.medical_specialty, Neurology, Autopsy, Sudden death, Tachypnea, Autoimmune Diseases, Death, Sudden, Internal medicine, medicine, Humans, Autoantibodies, Cause of death, Autoimmune disease, business.industry, Syndrome, Receptors, GABA-A, medicine.disease, Spinal cord, Muscle Rigidity, Surgery, medicine.anatomical_structure, Autonomic Nervous System Diseases, nervous system, Gliosis, Cardiology, Female, Neurology (clinical), medicine.symptom, business
Abstract

Two women with typical stiff-man syndrome (SMS) developed increasingly frequent attacks of muscle spasms with severe paroxysmal autonomic dysfunctions such as transient hyperpyrexia, diaphoresis, tachypnea, tachycardia, pupillary dilation, and arterial hypertension. Autoantibodies to GABA-ergic neurons were identified in the serum of both patients and in the cerebrospinal fluid of one. Both died suddenly and unexpectedly. General autopsy did not reveal the cause of death. Neuropathological studies revealed perivascular gliosis in the spinal cord and brain stem of one patient and lymphocytic perivascular infiltration in the spinal cord, brain stem, and basal ganglia of the other. The occurrence of a chronic inflammatory reaction in one of the two patients supports the idea that an autoimmune disease against GABA-ergic neurons may be involved in SMS. A review of the literature indicates that functional impairment in SMS is severe and prognosis is unpredictable because of the potential for sudden and unexpected death. Both muscular abnormalities and autonomic dysfunctions may result from autoimmunity directed against GABA-ergic neurons.

Published
1991
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49. Creating a “Transcampus” in Diabetes Research Between King’s College London and the Technische Universität Dresden: Update on Islet Biology and Transplantation

Author

Bornstein, S., additional, Amiel, S., additional, Rubino, F., additional, Mingrone, G., additional, Kamvissi, V., additional, Solimena, M., additional, Bonifacio, E., additional, Jones, P., additional, Schwarz, P., additional, Birkenfeld, A., additional, Behrens, A., additional, Barthel, A., additional, Lechler, R., additional, and Peakman, M., additional

Published
2014
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