Search

Your search keyword '"Birkenfeld"' showing total 4,592 results
Start Over Author "Birkenfeld"

Refine your results

more »

more »

more »

more »

more »

more »

more »
4,592 results on '"Birkenfeld"'

152. Proteinuric chronic kidney disease is associated with altered red blood cell lifespan, deformability and metabolism

Author

Bissinger, Rosi, Nemkov, Travis, D'Alessandro, Angelo, Grau, Marijke, Dietz, Thomas, Bohnert, Bernhard N., Essigke, Daniel, Wörn, Matthias, Schaefer, Lina, Xiao, Mengyun, Beirne, Jonathan M., Kalo, M. Zaher, Schork, Anja, Bakchoul, Tamam, Omage, Kingsley, Kong, Lingsi, Gonzalez-Menendez, Irene, Quintanilla-Martinez, Leticia, Fehrenbacher, Birgit, Schaller, Martin, Dhariwal, Achal, Birkenfeld, Andreas L., Grahammer, Florian, Qadri, Syed M., and Artunc, Ferruh

Published
2021
Full Text
View/download PDF

153. COVID-19 and metabolic disease: mechanisms and clinical management

Author

Steenblock, Charlotte, Schwarz, Peter E H, Ludwig, Barbara, Linkermann, Andreas, Zimmet, Paul, Kulebyakin, Konstantin, Tkachuk, Vsevolod A, Markov, Alexander G, Lehnert, Hendrik, de Angelis, Martin Hrabě, Rietzsch, Hannes, Rodionov, Roman N, Khunti, Kamlesh, Hopkins, David, Birkenfeld, Andreas L, Boehm, Bernhard, Holt, Richard I G, Skyler, Jay S, DeVries, J Hans, Renard, Eric, Eckel, Robert H, Alberti, K George M M, Geloneze, Bruno, Chan, Juliana C, Mbanya, Jean Claude, Onyegbutulem, Henry C, Ramachandran, Ambady, Basit, Abdul, Hassanein, Mohamed, Bewick, Gavin, Spinas, Giatgen A, Beuschlein, Felix, Landgraf, Rüdiger, Rubino, Francesco, Mingrone, Geltrude, and Bornstein, Stefan R

Published
2021
Full Text
View/download PDF

158. Improving insulin sensitivity, liver steatosis and fibrosis in type 2 diabetes by a food-based digital education-assisted lifestyle intervention program: a feasibility study

Author

Zaharia, Oana P., Kupriyanova, Yuliya, Karusheva, Yanislava, Markgraf, Daniel F., Kantartzis, Konstantinos, Birkenfeld, Andreas L., Trenell, Michael, Sahasranaman, Aarti, Cheyette, Chris, Kössler, Theresa, Bódis, Kálmán, Burkart, Volker, Hwang, Jong-Hee, Roden, Michael, Szendroedi, Julia, and Pesta, Dominik H.

Published
2021
Full Text
View/download PDF

174. Potential for a precision measurement of solar pp neutrinos in the Serappis experiment

Author

Bieger, Lukas, Birkenfeld, Thilo, Blum, David, Depnering, Wilfried, Enqvist, Timo, Enzmann, Heike, Gao, Feng, Genster, Christoph, Göttel, Alexandre, Grewing, Christian, Gromov, Maxim, Hackspacher, Paul, Hagner, Caren, Heinz, Tobias, Kampmann, Philipp, Karagounis, Michael, Kruth, Andre, Kuusiniemi, Pasi, Lachenmaier, Tobias, Liebau, Daniel, Liu, Runxuan, Loo, Kai, Ludhova, Livia, Meyhöfer, David, Müller, Axel, Muralidharan, Pavithra, Oberauer, Lothar, Othegraven, Rainer, Parkalian, Nina, Pei, Yatian, Pilarczyk, Oliver, Rebber, Henning, Robens, Markus, Roth, Christian, Sawatzki, Julia, Schweizer, Konstantin, Settanta, Giulio, Slupecki, Maciej, Smirnov, Oleg, Stahl, Achim, Steiger, Hans, Steinmann, Jochen, Sterr, Tobias, Stock, Matthias Raphael, Tang, Jian, Theisen, Eric, Tietzsch, Alexander, Trzaska, Wladyslaw, van den Boom, Johannes, van Waasen, Stefan, Vollbrecht, Cornelius, Wiebusch, Christopher, Wonsak, Bjoern, Wurm, Michael, Wysotzki, Christian, Xu, Yu, Yegin, Ugur, Zambanini, Andre, and Züfle, Jan

Published
2022
Full Text
View/download PDF

176. Optimization of the JUNO liquid scintillator composition using a Daya Bay antineutrino detector

Author

Abusleme, A., Adam, T., Ahmad, S., Aiello, S., Akram, M., Ali, N., An, F.P., An, G.P., An, Q., Andronico, G., Anfimov, N., Antonelli, V., Antoshkina, T., Asavapibhop, B., de André, J.P.A.M., Babic, A., Balantekin, A.B., Baldini, W., Baldoncini, M., Band, H.R., Barresi, A., Baussan, E., Bellato, M., Bernieri, E., Biare, D., Birkenfeld, T., Bishai, M., Blin, S., Blum, D., Blyth, S., Bordereau, C., Brigatti, A., Brugnera, R., Budano, A., Burgbacher, P., Buscemi, M., Bussino, S., Busto, J., Butorov, I., Cabrera, A., Cai, H., Cai, X., Cai, Y.K., Cai, Z.Y., Cammi, A., Campeny, A., Cao, C.Y., Cao, G.F., Cao, J., Caruso, R., Cerna, C., Chang, J.F., Chang, Y., Chen, H.S., Chen, P.A., Chen, P.P., Chen, S.M., Chen, S.J., Chen, X.R., Chen, Y.W., Chen, Y.X., Chen, Y., Chen, Z., Cheng, J., Cheng, Y.P., Cheng, Z.K., Chepurnov, A., Cherwinka, J.J., Chiarello, F., Chiesa, D., Chimenti, P., Chu, M.C., Chukanov, A., Chuvashova, A., Clementi, C., Clerbaux, B., Di Lorenzo, S. Conforti, Corti, D., Costa, S., Dal Corso, F., Cummings, J.P., Dalager, O., De La Taille, C., Deng, F.S., Deng, J.W., Deng, Z., Deng, Z.Y., Depnering, W., Diaz, M., Ding, X.F., Ding, Y.Y., Dirgantara, B., Dmitrievsky, S., Diwan, M.V., Dohnal, T., Donchenko, G., Dong, J.M., Dornic, D., Doroshkevich, E., Dove, J., Dracos, M., Druillole, F., Du, S.X., Dusini, S., Dvorak, M., Dwyer, D.A., Enqvist, T., Enzmann, H., Fabbri, A., Fajt, L., Fan, D.H., Fan, L., Fang, C., Fang, J., Fatkina, A., Fedoseev, D., Fekete, V., Feng, L.C., Feng, Q.C., Fiorentini, G., Ford, R., Formozov, A., Fournier, A., Franke, S., Gallo, J.P., Gan, H.N., Gao, F., Garfagnini, A., Göttel, A., Genster, C., Giammarchi, M., Giaz, A., Giudice, N., Giuliani, F., Gonchar, M., Gong, G.H., Gong, H., Gorchakov, O., Gornushkin, Y., Grassi, M., Grewing, C., Gromov, M., Gromov, V., Gu, M.H., Gu, W.Q., Gu, X.F., Gu, Y., Guan, M.Y., Guardone, N., Gul, M., Guo, C., Guo, J.Y., Guo, L., Guo, W.L., Guo, X.H., Guo, Y.H., Guo, Z., Haacke, M., Hackenburg, R.W., Hackspacher, P., Hagner, C., Han, R., Han, Y., Hans, S., He, M., He, W., Heeger, K.M., Heinz, T., Heng, Y.K., Herrera, R., Higuera, A., Hong, D.J., Hor, Y.K., Hou, S.J., Hsiung, Y.B., Hu, B.Z., Hu, H., Hu, J.R., Hu, J., Hu, S.Y., Hu, T., Hu, Z.J., Huang, C.H., Huang, G.H., Huang, H.X., Huang, Q.H., Huang, W.H., Huang, X.T., Huang, Y.B., Huber, P., Hui, J.Q., Huo, L., Huo, W.J., Huss, C., Hussain, S., Insolia, A., Ioannisian, A., Ioannisyan, D., Isocrate, R., Jaffe, D.E., Jen, K.L., Ji, X.L., Ji, X.P., Ji, X.Z., Jia, H.H., Jia, J.J., Jian, S.Y., Jiang, D., Jiang, X.S., Jin, R.Y., Jing, X.P., Johnson, R.A., Jollet, C., Jones, D., Joutsenvaara, J., Jungthawan, S., Kalousis, L., Kampmann, P., Kang, L., Karagounis, M., Kazarian, N., Kettell, S.H., Khan, A., Khan, W., Khosonthongkee, K., Kinz, P., Kohn, S., Korablev, D., Kouzakov, K., Kramer, M., Krasnoperov, A., Krokhaleva, S., Krumshteyn, Z., Kruth, A., Kutovskiy, N., Kuusiniemi, P., Lachacinski, B., Lachenmaier, T., Landini, C., Langford, T.J., Lee, J., Lee, J.H.C., Lefevre, F., Lei, L., Lei, R., Leitner, R., Leung, J., Li, D.M., Li, F., Li, H.T., Li, H.L., Li, J., Li, J.J., Li, J.Q., Li, K.J., Li, M.Z., Li, N., Li, Q.J., Li, R.H., Li, S.C., Li, S.F., Li, S.J., Li, T., Li, W.D., Li, W.G., Li, X.M., Li, X.N., Li, X.L., Li, X.Q., Li, Y., Li, Y.F., Li, Z.B., Li, Z.Y., Liang, H., Liang, J.J., Liebau, D., Limphirat, A., Limpijumnong, S., Lin, C.J., Lin, G.L., Lin, S.X., Lin, T., Lin, Y.H., Ling, J.J., Link, J.M., Lippi, I., Littenberg, L., Littlejohn, B.R., Liu, F., Liu, H., Liu, H.B., Liu, H.D., Liu, H.J., Liu, H.T., Liu, J.C., Liu, J.L., Liu, M., Liu, Q., Liu, R.X., Liu, S.Y., Liu, S.B., Liu, S.L., Liu, X.W., Liu, Y., Lokhov, A., Lombardi, P., Loo, K., Lorenz, S., Lu, C., Lu, H.Q., Lu, J.B., Lu, J.G., Lu, S.X., Lu, X.X., Lubsandorzhiev, B., Lubsandorzhiev, S., Ludhova, L., Luk, K.B., Luo, F.J., Luo, G., Luo, P.W., Luo, S., Luo, W.M., Lyashuk, V., Ma, Q.M., Ma, S., Ma, X.B., Ma, X.Y., Ma, Y.Q., Malyshkin, Y., Mantovani, F., Mao, Y.J., Mari, S.M., Marini, F., Marium, S., Marshall, C., Martellini, C., Martin-Chassard, G., Caicedo, D.A. Martinez, Martini, A., Martino, J., Mayilyan, D., McDonald, K.T., McKeown, R.D., Müller, A., Meng, G., Mednieks, I., Meng, Y., Meregaglia, A., Meroni, E., Meyhöfer, D., Mezzetto, M., Miller, J., Miramonti, L., Monforte, S., Montini, P., Montuschi, M., Morozov, N., Muralidharan, P., Napolitano, J., Nastasi, M., Naumov, D.V., Naumova, E., Nemchenok, I., Nikolaev, A., Ning, F.P., Ning, Z., Nunokawa, H., Oberauer, L., Ochoa-Ricoux, J.P., Olshevskiy, A., Ortica, F., Pan, H.R., Paoloni, A., Park, J., Parkalian, N., Parmeggiano, S., Patton, S., Payupol, T., Pec, V., Pedretti, D., Pei, Y.T., Pelliccia, N., Peng, A.G., Peng, H.P., Peng, J.C., Perrot, F., Petitjean, P.A., Rico, L.F. Pineres, Popov, A., Poussot, P., Pratumwan, W., Previtali, E., Pun, C.S.J., Qi, F.Z., Qi, M., Qian, S., Qian, X., Qian, X.H., Qiao, H., Qin, Z.H., Qiu, S.K., Rajput, M., Ranucci, G., Raper, N., Re, A., Rebber, H., Rebii, A., Ren, B., Ren, J., Reveco, C.M., Rezinko, T., Ricci, B., Robens, M., Roche, M., Rodphai, N., Rohwer, L., Romani, A., Rosero, R., Roskovec, B., Roth, C., Ruan, X.C., Ruan, X.D., Rujirawat, S., Rybnikov, A., Sadovsky, A., Saggese, P., Salamanna, G., Sangka, A., Sanguansak, N., Sawangwit, U., Sawatzki, J., Sawy, F., Schever, M., Schuler, J., Schwab, C., Schweizer, K., Selivanov, D., Selyunin, A., Serafini, A., Settanta, G., Settimo, M., Shahzad, M., Shi, G., Shi, J.Y., Shi, Y.J., Shutov, V., Sidorenkov, A., Šimkovic, F., Sirignano, C., Siripak, J., Sisti, M., Slupecki, M., Smirnov, M., Smirnov, O., Sogo-Bezerra, T., Songwadhana, J., Soonthornthum, B., Sotnikov, A., Sramek, O., Sreethawong, W., Stahl, A., Stanco, L., Stankevich, K., Štefánik, D., Steiger, H., Steiner, H., Steinmann, J., Stender, M., Strati, V., Studenikin, A., Sun, G.X., Sun, L.T., Sun, J.L., Sun, S.F., Sun, X.L., Sun, Y.J., Sun, Y.Z., Suwonjandee, N., Szelezniak, M., Tang, J., Tang, Q., Tang, X., Tietzsch, A., Tkachev, I., Tmej, T., Treskov, K., Troni, G., Trzaska, W., Tse, W.-H., Tull, C.E., Tuve, C., van Waasen, S., Boom, J. van den, Vassilopoulos, N., Vedin, V., Verde, G., Vialkov, M., Viaud, B., Viren, B., Volpe, C., Vorobel, V., Votano, L., Walker, P., Wang, C., Wang, C.H., Wang, E., Wang, G.L., Wang, J., Wang, K.Y., Wang, L., Wang, M.F., Wang, M., Wang, N.Y., Wang, R.G., Wang, S.G., Wang, W., Wang, W.S., Wang, X., Wang, X.Y., Wang, Y., Wang, Y.F., Wang, Y.G., Wang, Y.M., Wang, Y.Q., Wang, Z., Wang, Z.M., Wang, Z.Y., Watcharangkool, A., Wei, H.Y., Wei, L.H., Wei, W., Wei, Y.D., Wen, L.J., Whisnant, K., White, C.G., Wiebusch, C., Wong, S.C.F., Wong, H.L.H., Wonsak, B., Worcester, E., Wu, C.H., Wu, D.R., Wu, F.L., Wu, Q., Wu, W.J., Wu, Z., Wurm, M., Wurtz, J., Wysotzki, C., Xi, Y.F., Xia, D.M., Xie, Y.G., Xie, Z.Q., Xing, Z.Z., Xu, D.L., Xu, F.R., Xu, H.K., Xu, J.L., Xu, J., Xu, M.H., Xu, T., Xu, Y., Xue, T., Yan, B.J., Yan, X.B., Yan, Y.P., Yang, A.B., Yang, C.G., Yang, H., Yang, J., Yang, L., Yang, X.Y., Yang, Y.F., Yang, Y.Z., Yao, H.F., Yasin, Z., Ye, J.X., Ye, M., Yegin, U., Yeh, M., Yermia, F., Yi, P.H., You, Z.Y., Young, B.L., Yu, B.X., Yu, C.X., Yu, C.Y., Yu, H.Z., Yu, M., Yu, X.H., Yu, Z.Y., Yuan, C.Z., Yuan, Y., Yuan, Z.X., Yuan, Z.Y., Yue, B.B., Zafar, N., Zambanini, A., Zeng, P., Zeng, S., Zeng, T.X., Zeng, Y.D., Zhan, L., Zhang, C., Zhang, F.Y., Zhang, G.Q., Zhang, H.H., Zhang, H.Q., Zhang, J., Zhang, J.B., Zhang, J.W., Zhang, P., Zhang, Q.M., Zhang, T., Zhang, X.M., Zhang, X.T., Zhang, Y., Zhang, Y.H., Zhang, Y.M., Zhang, Y.P., Zhang, Y.X., Zhang, Y.Y., Zhang, Z.J., Zhang, Z.P., Zhang, Z.Y., Zhao, F.Y., Zhao, J., Zhao, R., Zhao, S.J., Zhao, T.C., Zheng, D.Q., Zheng, H., Zheng, M.S., Zheng, Y.H., Zhong, W.R., Zhou, J., Zhou, L., Zhou, N., Zhou, S., Zhou, X., Zhu, J., Zhu, K.J., Zhuang, H.L., Zong, L., and Zou, J.H.

Published
2021
Full Text
View/download PDF

178. Molecular biomarkers of complex traits

Author

Zeggini, Eleftheria (Prof. Dr.), Zeggini, Eleftheria (Prof. Dr.);Wurst, Wolfgang (Prof. Dr.);Birkenfeld, Andreas (Prof. Dr.), Png, Yunting Grace, Zeggini, Eleftheria (Prof. Dr.), Zeggini, Eleftheria (Prof. Dr.);Wurst, Wolfgang (Prof. Dr.);Birkenfeld, Andreas (Prof. Dr.), and Png, Yunting Grace

Abstract

The causal mechanisms behind complex diseases like type 2 diabetes and Alzheimer’s disease remain elusive. Protein levels that are perturbed in disease can inform pathophysiology and represent valuable biomarkers and drug targets. In this thesis, I aim to understand the genetic regulation underlying >400 serum proteins (protein quantitative trait loci [pQTLs]), using whole genome sequence data from two isolated Greek populations (N~3,000). Through causal inference analysis, we highlight protein-disease relationships that may be translated into the clinic., Die ursächlichen Mechanismen, die komplexen Krankheiten wie Typ-2-Diabetes und Alzheimer zugrunde liegen, sind nach wie vor unklar. Proteinspiegel, die bei Krankheiten gestört sind, können Aufschluss über die Pathophysiologie geben und stellen wertvolle Biomarker und Ziele von Medikamenten dar. In dieser Arbeit möchte ich die genetische Regulierung von >400 Serumproteinen (protein quantitative trait loci [pQTLs]) untersuchen, indem ich Sequenzdaten von Gesamtgenomen von zwei isolierten griechischen Populationen (N~3.000) verwende. Durch eine Analyse der kausalen Inferenz heben wir Beziehungen zwischen Proteinen und Krankheiten hervor, die in der klinischen Anwendung nützlich sein können.

Published
2024

179. Intrapartale Mikroblutanalyse - noch zeitgemäß?

Author

Birkenfeld, Anika and Birkenfeld, Anika

Abstract

In der vorliegenden retrospektiven Arbeit wurden zwei Patientinnenkollektive gebildet, es wurden alle Frauen eingeschlossen, die zwischen dem 01.01.2011 und dem 31.12.2020 entbunden wurden. Ausgeschlossen wurden die Frauen, die vor der 34+0 Schwangerschaftswoche geboren haben und alle primären Sectios. Die Patientinnengruppen wurde betrachtet hinsichtlich des Geburtsmodus abhängig ob eine MBU durchgeführt wurde oder nicht. Die Daten der Arbeit zeigen, dass die korrekte Durchführung der MBU durch geschultes Personal, ein gutes Instrument ergänzend zum CTG ist. Die Entscheidung zur Weiterführung oder Forcierung der Geburt wird erleichtert und das Ergebnis kann zur Senkung der Sectiorate beitragen und zu einer Verbesserung des neonatalen Outcomes führen. Daher stellt die MBU in der Geburtshilfe aktuell und auch in Zukunft eine sinnvolle Untersuchung dar.

Published
2024

180. 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

181. Outcomes With Finerenone in Patients With Chronic Kidney Disease and Type 2 Diabetes by Baseline Insulin Resistance

Author

Ebert, Thomas, Anker, Stefan D, Ruilope, Luis M, Fioretto, Paola, Fonseca, Vivian, Umpierrez, Guillermo E, Birkenfeld, Andreas L, Lawatscheck, Robert, Scott, Charlie, Rohwedder, Katja, Rossing, Peter, Ebert, Thomas, Anker, Stefan D, Ruilope, Luis M, Fioretto, Paola, Fonseca, Vivian, Umpierrez, Guillermo E, Birkenfeld, Andreas L, Lawatscheck, Robert, Scott, Charlie, Rohwedder, Katja, and Rossing, Peter

Abstract

OBJECTIVE: To explore whether insulin resistance, assessed by estimated glucose disposal rate (eGDR), is associated with cardiorenal risk and whether it modifies finerenone efficacy.RESEARCH DESIGN AND METHODS: In FIDELITY (N = 13,026), patients with type 2 diabetes, either 1) urine albumin-to-creatinine ratio (UACR) of ≥30 to <300 mg/g and estimated glomerular filtration rate (eGFR) of ≥25 to ≤90 mL/min/1.73 m2 or 2) UACR of ≥300 to ≤5,000 mg/g and eGFR of ≥25 mL/min/1.73 m2, who also received optimized renin-angiotensin system blockade, were randomized to finerenone or placebo. Outcomes included cardiovascular (cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure) and kidney (kidney failure, sustained decrease of ≥57% in eGFR from baseline, or renal death) composites. eGDR was calculated using waist circumference, hypertension status, and glycated hemoglobin for 12,964 patients.RESULTS: Median eGDR was 4.1 mg/kg/min. eGDR

Published
2024

182. 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

183. Exercise restores brain insulin sensitivity in sedentary adults who are overweight and obese

Author

Stephanie Kullmann, Thomas Goj, Ralf Veit, Louise Fritsche, Lore Wagner, Patrick Schneeweiss, Miriam Hoene, Christoph Hoffmann, Jürgen Machann, Andreas Niess, Hubert Preissl, Andreas L. Birkenfeld, Andreas Peter, Hans-Ulrich Häring, Andreas Fritsche, Anja Moller, Cora Weigert, and Martin Heni

Subjects
Metabolism, Neuroscience, Medicine
Abstract

BACKGROUND Insulin resistance of the brain can unfavorably affect long-term weight maintenance and body fat distribution. Little is known if and how brain insulin sensitivity can be restored in humans. We aimed to evaluate the effects of an exercise intervention on insulin sensitivity of the brain and how this relates to exercise-induced changes in whole-body metabolism and behavior.METHODS In this clinical trial, sedentary participants who were overweight and obese underwent an 8-week supervised aerobic training intervention. Brain insulin sensitivity was assessed in 21 participants (14 women, 7 men; age range 21–59 years; BMI range 27.5–45.5 kg/m2) using functional MRI, combined with intranasal administration of insulin, before and after the intervention.RESULTS The exercise program resulted in enhanced brain insulin action to the level of a person of healthy weight, demonstrated by increased insulin-induced striatal activity and strengthened hippocampal functional connectivity. Improved brain insulin action correlated with increased mitochondrial respiration in skeletal muscle, reductions in visceral fat and hunger, as well as improved cognition. Mediation analyses suggest that improved brain insulin responsiveness helps mediate the peripheral exercise effects leading to healthier body fat distribution and reduced perception of hunger.CONCLUSION Our study demonstrates that an 8-week exercise intervention in sedentary individuals can restore insulin action in the brain. Hence, the ameliorating benefits of exercise toward brain insulin resistance may provide an objective therapeutic target in humans in the challenge to reduce diabetes risk factors.TRIAL REGISTRATION ClinicalTrials.gov (NCT03151590).FUNDING BMBF/DZD 01GI0925.

Published
2022
Full Text
View/download PDF

186. Therapie des Typ-2-Diabetes

Author

Landgraf, Rüdiger, Aberle, Jens, Birkenfeld, Andreas L., Gallwitz, Baptist, Kellerer, Monika, Klein, Harald H., Müller-Wieland, Dirk, Nauck, Michael A., Reuter, Hans-Martin, and Siegel, Erhard

Published
2021
Full Text
View/download PDF

188. Lipidtherapie bei Patienten mit Diabetes mellitus: Eine gemeinsame Stellungnahme der Kommission Fettstoffwechsel sowie der AG Herz und Diabetes der Deutschen Diabetes Gesellschaft (DDG), der Sektion Diabetologie und Stoffwechsel der Deutschen Gesellschaft für Endokrinologie (DGE), der AG Herz und Diabetes der Deutschen Gesellschaft für Kardiologie (DGK) und der gemeinsamen AG Herz – Hormone – Diabetes der DGK, DGE und DDG

Author

Parhofer, Klaus G., Birkenfeld, Andreas L., Krone, Wilhelm, Lehrke, Michael, Marx, Nikolaus, Merkel, Martin, Schütt, Katharina S., Zirlik, Andreas, and Müller-Wieland, Dirk

Published
2021
Full Text
View/download PDF

190. Efficacy and Safety of the Combination of Palmitoylethanolamide, Superoxide Dismutase, Alpha Lipoic Acid, Vitamins B12, B1, B6, E, Mg, Zn and Nicotinamide for 6 Months in People with Diabetic Neuropathy.

Author

Didangelos, Triantafyllos, Karlafti, Eleni, Kotzakioulafi, Evangelia, Giannoulaki, Parthena, Kontoninas, Zisis, Kontana, Anastasia, Evripidou, Polykarpos, Savopoulos, Christos, Birkenfeld, Andreas L., and Kantartzis, Konstantinos

Abstract

Aim: To investigate the efficacy of Palmitoylethanolamide (PEA, 300 mg), Superoxide Dismutase (SOD, 70 UI), Alpha Lipoic Acid (ALA, 300 mg), vitamins B6 (1.5 mg), B1 (1.1 mg), B12 (2.5 mcg), E (7.5 mg), nicotinamide (9 mg), and minerals (Mg 30 mg, Zn 2.5 mg) in one tablet in people with Diabetic Neuropathy (DN). Patients–methods: In the present pilot study, 73 people (age 63.0 ± 9.9 years, 37 women) with type 2 Diabetes Mellitus (DMT2) (duration 17.5 ± 7.3 years) and DN were randomly assigned to receive either the combination of ten elements (2 tablets/24 h) in the active group (n = 36) or the placebo (n = 37) for 6 months. We used the Michigan Neuropathy Screening Instrument Questionnaire and Examination (MNSIQ and MNSIE), measured vibration perception threshold (VPT) with biothesiometer, and Cardiovascular Autonomic Reflex Tests (CARTs). Nerve function was assessed by DPN Check [sural nerve conduction velocity (SNCV) and amplitude (SNAP)]. Sudomotor function was assessed with SUDOSCAN, which measures electrochemical skin conductance in hands and feet (ESCH and ESCF). Pain score (PS) was assessed with Pain DETECT questionnaire. Quality of life was assessed by questionnaire. Results: In the active group, there was a large improvement of pain (PS from 20.9 to 13.9, p < 0.001). There was also a significant improvement of vitamin B12 (B12) levels, MNSIQ, SNCV, VPT, and ESCF (222.1 vs. 576.3 pg/ mL, p < 0.001; 6.1 vs. 5.9, p = 0.017; 28.8 vs. 30.4, p = 0.001; 32.1 vs. 26.7, p = 0.001; and 72.2 vs. 74.8, p < 0.001 respectively). In the placebo group, neither pain (21.6 vs. 21.7, p = 0.870) or any other aforementioned parameters changed significantly, and MNSIE worsened (2.9 vs. 3.4, p < 0.001). As a result, changes from baseline to follow-up in pain, B12 levels, VPT, and MNSIQ differed significantly between the two groups (p < 0.001, 0.025, 0.009, and <0.001, respectively). CARTs, SNAP, ESCH did not significantly change in either of the two groups. Conclusions: The combination of the ten elements in one tablet for 6 months at a daily dose of two tablets in people with DN significantly improves pain, vibration perception threshold, and B12 levels. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

191. The role of adipose tissue dysfunction in hepatic insulin resistance and T2D.

Author

Sancar, Gencer and Birkenfeld, Andreas L.

Subjects
*TYPE 2 diabetes, *INSULIN resistance, *ADIPOSE tissues, *LIVER diseases, *HOMEOSTASIS
Abstract

The root cause of type 2 diabetes (T2D) is insulin resistance (IR), defined by the failure of cells to respond to circulating insulin to maintain lipid and glucose homeostasis. While the causes of whole-body insulin resistance are multifactorial, a major contributing factor is dysregulation of liver and adipose tissue function. Adipose dysfunction, particularly adipose tissue-IR (adipo-IR), plays a crucial role in the development of hepatic insulin resistance and the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) in the context of T2D. In this review, we will focus on molecular mechanisms of hepatic insulin resistance and its association with adipose tissue function. A deeper understanding of the pathophysiological mechanisms of the transition from a healthy state to insulin resistance, impaired glucose tolerance, and T2D may enable us to prevent and intervene in the progression to T2D. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

192. Changes in lean body mass with glucagon‐like peptide‐1‐based therapies and mitigation strategies.

Author

Neeland, Ian J., Linge, Jennifer, and Birkenfeld, Andreas L.

Subjects
MUSCLE mass, WEIGHT loss, LEAN body mass, TYPE 2 diabetes, INSULIN sensitivity
Abstract

Weight loss induced by glucagon‐like peptide‐1 receptor agonists (GLP‐1RAs) and dual glucagon‐like peptide‐1 receptor (GLP‐1R)/glucose‐dependent insulinotropic polypeptide receptor agonists is coming closer to the magnitudes achieved with surgery. However, with greater weight loss there is concern about potential side effects on muscle quantity (mass), health and function. There is heterogeneity in the reported effects of GLP‐1‐based therapies on lean mass changes in clinical trials: in some studies, reductions in lean mass range between 40% and 60% as a proportion of total weight lost, while other studies show lean mass reductions of approximately 15% or less of total weight lost. There are several potential reasons underlying this heterogeneity, including population, drug‐specific/molecular, and comorbidity effects. Furthermore, changes in lean mass may not always reflect changes in muscle mass as the former measure includes not only muscle but also organs, bone, fluids, and water in fat tissue. Based on contemporary evidence with the addition of magnetic resonance imaging‐based studies, skeletal muscle changes with GLP‐1RA treatments appear to be adaptive: reductions in muscle volume seem to be commensurate with what is expected given ageing, disease status, and weight loss achieved, and the improvement in insulin sensitivity and muscle fat infiltration likely contributes to an adaptive process with improved muscle quality, lowering the probability for loss in strength and function. Nevertheless, factors such as older age and severity of disease may influence the selection of appropriate candidates for these therapies due to risk of sarcopenia. To further improve muscle health during weight loss, several pharmacological treatments to maintain or improve muscle mass designed in combination with GLP‐1‐based therapies are under development. Future research on GLP‐1‐based and other therapies designed for weight loss should focus on more accurate and meaningful assessments of muscle mass, composition, as well as function, mobility or strength, to better define their impact on muscle health for the substantial number of patients who will likely be taking these medications well into the future. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

194. Effects of ACLY Inhibition on Body Weight Distribution: A Drug Target Mendelian Randomization Study.

Author

Gill, Dipender, Dib, Marie-Joe, Gill, Rubinder, Bornstein, Stefan R., Burgess, Stephen, and Birkenfeld, Andreas L.

Subjects
TYPE 2 diabetes, WAIST-hip ratio, LDL cholesterol, BODY mass index, SINGLE nucleotide polymorphisms
Abstract

Background: Adenosine triphosphate-citrate lyase (ACLY) inhibition has proven clinically efficacious for low-density lipoprotein cholesterol (LDL-c) lowering and cardiovascular disease (CVD) risk reduction. Clinical and genetic evidence suggests that some LDL-c lowering strategies, such as 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) inhibition with statin therapy increase body weight and the risk of developing type 2 diabetes mellitus (T2DM). However, whether ACLY inhibition affects metabolic risk factors is currently unknown. We aimed to investigate the effects of ACLY inhibition on glycaemic and anthropometric traits using Mendelian randomization (MR). Methods: As genetic instruments for ACLY inhibition, we selected weakly correlated single-nucleotide polymorphisms at the ACLY gene associated with lower ACLY gene expression in the eQTLGen study (N = 31,684) and lower LDL-c levels in the Global Lipid Genetic Consortium study (N = 1.65 million). Two-sample Mendelian randomization was employed to investigate the effects of ACLY inhibition on T2DM risk, and glycaemic and anthropometric traits using summary data from large consortia, with sample sizes ranging from 151,013 to 806,834 individuals. Findings for genetically predicted ACLY inhibition were compared to those obtained for genetically predicted HMGCR inhibition using the same instrument selection strategy and outcome data. Results: Primary MR analyses showed that genetically predicted ACLY inhibition was associated with lower waist-to-hip ratio (β per 1 standard deviation lower LDL-c: −1.17; 95% confidence interval (CI): −1.61 to −0.73; p < 0.001) but not with risk of T2DM (odds ratio (OR) per standard deviation lower LDL-c: 0.74, 95% CI = 0.25 to 2.19, p = 0.59). In contrast, genetically predicted HMGCR inhibition was associated with higher waist-to-hip ratio (β = 0.15; 95%CI = 0.04 to 0.26; p = 0.008) and T2DM risk (OR = 1.73, 95% CI = 1.27 to 2.36, p < 0.001). The MR analyses considering secondary outcomes showed that genetically predicted ACLY inhibition was associated with a lower waist-to-hip ratio adjusted for body mass index (BMI) (β = −1.41; 95%CI = −1.81 to −1.02; p < 0.001). In contrast, genetically predicted HMGCR inhibition was associated with higher HbA1c (β = 0.19; 95%CI = 0.23 to 0.49; p < 0.001) and BMI (β = 0.36; 95%CI = 0.23 to 0.49; p < 0.001). Conclusions: Human genetic evidence supports the metabolically favourable effects of ACLY inhibition on body weight distribution, in contrast to HMGCR inhibition. These findings should be used to guide and prioritize ongoing clinical development efforts. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

195. Amiloride versus furosemide for the treatment of edema in patients with nephrotic syndrome: A pilot study (AMILOR).

Author

Schork, Anja, Vogel, Elisabeth, Bohnert, Bernhard N., Essigke, Daniel, Wörn, Matthias, Fischer, Imma, Heyne, Nils, Birkenfeld, Andreas L., and Artunc, Ferruh

Subjects
NEPHROTIC syndrome, AMILORIDE, FUROSEMIDE, SODIUM channels, EDEMA
Abstract

Aim: In rodent models of nephrotic syndrome (NS), edema formation was prevented by blockade of the epithelial sodium channel ENaC with amiloride. However, apart from case reports, there is no evidence favoring ENaC blockade in patients with NS. Methods: The monocentric randomized controlled AMILOR study investigated the antiedematous effect of amiloride (starting dose 5 mg/day, max. 15 mg/day) in comparison to standard therapy with the loop diuretic furosemide (40 mg/day, max. 120 mg/day) over 16 days. Overhydration (OH) was measured by bioimpedance spectroscopy (BCM, Fresenius). Depending on the OH response, diuretic dose was adjusted on days 2, 5, 8 and 12, and if necessary, hydrochlorothiazide (HCT) was added from d8 (12.5 mg/day, max. 25 mg/day). The primary endpoint was the decrease in OH on d8. The study was terminated prematurely due to insufficient recruitment and a low statistical power due to a low actual effect size. Results: Median baseline OH was +26.4 (interquartile range 15.5–35.1)% extracellular water (ECW) in the amiloride arm and + 27.9 (24.1–29.4)% ECW in the furosemide arm and decreased by 1.95 (0.80–6.40) and 5.15 (0.90–8.30)% ECW after 8 days, respectively, and by 10.10 (1.30–14.40) and 7.40 (2.80–10.10)% ECW after 16 days, respectively. OH decrease on d8 and d16 was not significantly different between both arms. Conclusion: The AMILOR study is the first randomized controlled pilot study suggesting a similar antiedematous effect as furosemide. Further studies are required to better define the role of amiloride in NS (EudraCT 2019‐002607‐18). [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

197. Damping signatures at JUNO, a medium-baseline reactor neutrino oscillation experiment

Author

Wang, Jun, Liao, Jiajun, Wang, Wei, Abusleme, Angel, Adam, Thomas, Ahmad, Shakeel, Ahmed, Rizwan, Aiello, Sebastiano, Akram, Muhammad, An, Fengpeng, An, Qi, Andronico, Giuseppe, Anfimov, Nikolay, Antonelli, Vito, Antoshkina, Tatiana, Asavapibhop, Burin, Athayde Marcondes de André, João Pedro, Auguste, Didier, Babic, Andrej, Balashov, Nikita, Baldini, Wander, Barresi, Andrea, Basilico, Davide, Baussan, Eric, Bellato, Marco, Bergnoli, Antonio, Birkenfeld, Thilo, Blin, Sylvie, Blum, David, Blyth, Simon, Bolshakova, Anastasia, Bongrand, Mathieu, Bordereau, Clément, Breton, Dominique, Brigatti, Augusto, Brugnera, Riccardo, Bruno, Riccardo, Budano, Antonio, Buscemi, Mario, Busto, Jose, Butorov, Ilya, Cabrera, Anatael, Cai, Hao, Cai, Xiao, Cai, Yanke, Cai, Zhiyan, Callegari, Riccardo, Cammi, Antonio, Campeny, Agustin, Cao, Chuanya, Cao, Guofu, Cao, Jun, Caruso, Rossella, Cerna, Cédric, Chang, Jinfan, Chang, Yun, Chen, Pingping, Chen, Po-An, Chen, Shaomin, Chen, Xurong, Chen, Yi-Wen, Chen, Yixue, Chen, Yu, Chen, Zhang, Cheng, Jie, Cheng, Yaping, Chetverikov, Alexey, Chiesa, Davide, Chimenti, Pietro, Chukanov, Artem, Claverie, Gérard, Clementi, Catia, Clerbaux, Barbara, Conforti Di Lorenzo, Selma, Corti, Daniele, Corso, Flavio Dal, Dalager, Olivia, De La Taille, Christophe, Deng, Jiawei, Deng, Zhi, Deng, Ziyan, Depnering, Wilfried, Diaz, Marco, Ding, Xuefeng, Ding, Yayun, Dirgantara, Bayu, Dmitrievsky, Sergey, Dohnal, Tadeas, Dolzhikov, Dmitry, Donchenko, Georgy, Dong, Jianmeng, Doroshkevich, Evgeny, Dracos, Marcos, Druillole, Frédéric, Du, Ran, Du, Shuxian, Dusini, Stefano, Dvorak, Martin, Enqvist, Timo, Enzmann, Heike, Fabbri, Andrea, Fajt, Lukas, Fan, Donghua, Fan, Lei, Fang, Jian, Fang, Wenxing, Fargetta, Marco, Fedoseev, Dmitry, Fekete, Vladko, Feng, Li-Cheng, Feng, Qichun, Ford, Richard, Fournier, Amélie, Gan, Haonan, Gao, Feng, Garfagnini, Alberto, Gavrikov, Arsenii, Giammarchi, Marco, Giaz, Agnese, Giudice, Nunzio, Gonchar, Maxim, Gong, Guanghua, Gong, Hui, Gornushkin, Yuri, Göttel, Alexandre, Grassi, Marco, Grewing, Christian, Gromov, Vasily, Gu, Minghao, Gu, Xiaofei, Gu, Yu, Guan, Mengyun, Guardone, Nunzio, Gul, Maria, Guo, Cong, Guo, Jingyuan, Guo, Wanlei, Guo, Xinheng, Guo, Yuhang, Hackspacher, Paul, Hagner, Caren, Han, Ran, Han, Yang, Hassan, Muhammad Sohaib, He, Miao, He, Wei, Heinz, Tobias, Hellmuth, Patrick, Heng, Yuekun, Herrera, Rafael, Hor, YuenKeung, Hou, Shaojing, Hsiung, Yee, Hu, Bei-Zhen, Hu, Hang, Hu, Jianrun, Hu, Jun, Hu, Shouyang, Hu, Tao, Hu, Zhuojun, Huang, Chunhao, Huang, Guihong, Huang, Hanxiong, Huang, Wenhao, Huang, Xin, Huang, Xingtao, Huang, Yongbo, Hui, Jiaqi, Huo, Lei, Huo, Wenju, Huss, Cédric, Hussain, Safeer, Ioannisian, Ara, Isocrate, Roberto, Jelmini, Beatrice, Jen, Kuo-Lun, Jeria, Ignacio, Ji, Xiaolu, Ji, Xingzhao, Jia, Huihui, Jia, Junji, Jian, Siyu, Jiang, Di, Jiang, Wei, Jiang, Xiaoshan, Jin, Ruyi, Jing, Xiaoping, Jollet, Cécile, Joutsenvaara, Jari, Jungthawan, Sirichok, Kalousis, Leonidas, Kampmann, Philipp, Kang, Li, Karaparambil, Rebin, Kazarian, Narine, Khosonthongkee, Khanchai, Korablev, Denis, Kouzakov, Konstantin, Krasnoperov, Alexey, Kruth, Andre, Kutovskiy, Nikolay, Kuusiniemi, Pasi, Lachenmaier, Tobias, Landini, Cecilia, Leblanc, Sébastien, Lebrin, Victor, Lefevre, Frederic, Lei, Ruiting, Leitner, Rupert, Leung, Jason, Li, Demin, Li, Fei, Li, Fule, Li, Haitao, Li, Huiling, Li, Jiaqi, Li, Mengzhao, Li, Min, Li, Nan, Li, Nan, Li, Qingjiang, Li, Ruhui, Li, Shanfeng, Li, Tao, Li, Weidong, Li, Weiguo, Li, Xiaomei, Li, Xiaonan, Li, Xinglong, Li, Yi, Li, Yufeng, Li, Zhaohan, Li, Zhibing, Li, Ziyuan, Liang, Hao, Liang, Hao, Liebau, Daniel, Limphirat, Ayut, Limpijumnong, Sukit, Lin, Guey-Lin, Lin, Shengxin, Lin, Tao, Ling, Jiajie, Lippi, Ivano, Liu, Fang, Liu, Haidong, Liu, Hongbang, Liu, Hongjuan, Liu, Hongtao, Liu, Hui, Liu, Jianglai, Liu, Jinchang, Liu, Min, Liu, Qian, Liu, Qin, Liu, Runxuan, Liu, Shuangyu, Liu, Shubin, Liu, Shulin, Liu, Xiaowei, Liu, Xiwen, Liu, Yan, Liu, Yunzhe, Lokhov, Alexey, Lombardi, Paolo, Lombardo, Claudio, Loo, Kai, Lu, Chuan, Lu, Haoqi, Lu, Jingbin, Lu, Junguang, Lu, Shuxiang, Lu, Xiaoxu, Lubsandorzhiev, Bayarto, Lubsandorzhiev, Sultim, Ludhova, Livia, Lukanov, Arslan, Luo, Fengjiao, Luo, Guang, Luo, Pengwei, Luo, Shu, Luo, Wuming, Lyashuk, Vladimir, Ma, Bangzheng, Ma, Qiumei, Ma, Si, Ma, Xiaoyan, Ma, Xubo, Maalmi, Jihane, Malyshkin, Yury, Mandujano, Roberto Carlos, Mantovani, Fabio, Manzali, Francesco, Mao, Xin, Mao, Yajun, Mari, Stefano M., Marini, Filippo, Marium, Sadia, Martellini, Cristina, Martin-Chassard, Gisele, Martini, Agnese, Mayer, Matthias, Mayilyan, Davit, Mednieks, Ints, Meng, Yue, Meregaglia, Anselmo, Meroni, Emanuela, Meyhöfer, David, Mezzetto, Mauro, Miller, Jonathan, Miramonti, Lino, Montini, Paolo, Montuschi, Michele, Müller, Axel, Nastasi, Massimiliano, Naumov, Dmitry V., Naumova, Elena, Navas-Nicolas, Diana, Nemchenok, Igor, Nguyen Thi, Minh Thuan, Ning, Feipeng, Ning, Zhe, Nunokawa, Hiroshi, Oberauer, Lothar, Ochoa-Ricoux, Juan Pedro, Olshevskiy, Alexander, Orestano, Domizia, Ortica, Fausto, Othegraven, Rainer, Pan, Hsiao-Ru, Paoloni, Alessandro, Parmeggiano, Sergio, Pei, Yatian, Pelliccia, Nicomede, Peng, Anguo, Peng, Haiping, Perrot, Frédéric, Petitjean, Pierre-Alexandre, Petrucci, Fabrizio, Pilarczyk, Oliver, Piñeres Rico, Luis Felipe, Popov, Artyom, Poussot, Pascal, Pratumwan, Wathan, Previtali, Ezio, Qi, Fazhi, Qi, Ming, Qian, Sen, Qian, Xiaohui, Qian, Zhen, Qiao, Hao, Qin, Zhonghua, Qiu, Shoukang, Rajput, Muhammad Usman, Ranucci, Gioacchino, Raper, Neill, Re, Alessandra, Rebber, Henning, Rebii, Abdel, Ren, Bin, Ren, Jie, Ricci, Barbara, Robens, Markus, Roche, Mathieu, Rodphai, Narongkiat, Romani, Aldo, Roskovec, Bedřich, Roth, Christian, Ruan, Xiangdong, Ruan, Xichao, Rujirawat, Saroj, Rybnikov, Arseniy, Sadovsky, Andrey, Saggese, Paolo, Sanfilippo, Simone, Sangka, Anut, Sanguansak, Nuanwan, Sawangwit, Utane, Sawatzki, Julia, Sawy, Fatma, Schever, Michaela, Schwab, Cédric, Schweizer, Konstantin, Selyunin, Alexandr, Serafini, Andrea, Settanta, Giulio, Settimo, Mariangela, Shao, Zhuang, Sharov, Vladislav, Shaydurova, Arina, Shi, Jingyan, Shi, Yanan, Shutov, Vitaly, Sidorenkov, Andrey, Šimkovic, Fedor, Sirignano, Chiara, Siripak, Jaruchit, Sisti, Monica, Slupecki, Maciej, Smirnov, Mikhail, Smirnov, Oleg, Sogo-Bezerra, Thiago, Sokolov, Sergey, Songwadhana, Julanan, Soonthornthum, Boonrucksar, Sotnikov, Albert, Šrámek, Ondřej, Sreethawong, Warintorn, Stahl, Achim, Stanco, Luca, Stankevich, Konstantin, Štefánik, Dušan, Steiger, Hans, Steinmann, Jochen, Sterr, Tobias, Stock, Matthias Raphael, Strati, Virginia, Studenikin, Alexander, Sun, Shifeng, Sun, Xilei, Sun, Yongjie, Sun, Yongzhao, Suwonjandee, Narumon, Szelezniak, Michal, Tang, Jian, Tang, Qiang, Tang, Quan, Tang, Xiao, Tietzsch, Alexander, Tkachev, Igor, Tmej, Tomas, Torri, Marco Danilo Claudio, Treskov, Konstantin, Triossi, Andrea, Troni, Giancarlo, Trzaska, Wladyslaw, Tuve, Cristina, Ushakov, Nikita, van den Boom, Johannes, van Waasen, Stefan, Vanroyen, Guillaume, Vedin, Vadim, Verde, Giuseppe, Vialkov, Maxim, Viaud, Benoit, Vollbrecht, Cornelius Moritz, Volpe, Cristina, Vorobel, Vit, Voronin, Dmitriy, Votano, Lucia, Walker, Pablo, Wang, Caishen, Wang, Chung-Hsiang, Wang, En, Wang, Guoli, Wang, Jian, Wang, Kunyu, Wang, Lu, Wang, Meifen, Wang, Meng, Wang, Meng, Wang, Ruiguang, Wang, Siguang, Wang, Wei, Wang, Wenshuai, Wang, Xi, Wang, Xiangyue, Wang, Yangfu, Wang, Yaoguang, Wang, Yi, Wang, Yi, Wang, Yifang, Wang, Yuanqing, Wang, Yuman, Wang, Zhe, Wang, Zheng, Wang, Zhimin, Wang, Zongyi, Waqas, Muhammad, Watcharangkool, Apimook, Wei, Lianghong, Wei, Wei, Wei, Wenlu, Wei, Yadong, Wen, Kaile, Wen, Liangjian, Wiebusch, Christopher, Wong, Steven Chan-Fai, Wonsak, Bjoern, Wu, Diru, Wu, Qun, Wu, Zhi, Wurm, Michael, Wurtz, Jacques, Wysotzki, Christian, Xi, Yufei, Xia, Dongmei, Xie, Xiaochuan, Xie, Yuguang, Xie, Zhangquan, Xing, Zhizhong, Xu, Benda, Xu, Cheng, Xu, Donglian, Xu, Fanrong, Xu, Hangkun, Xu, Jilei, Xu, Jing, Xu, Meihang, Xu, Yin, Xu, Yu, Yan, Baojun, Yan, Taylor, Yan, Wenqi, Yan, Xiongbo, Yan, Yupeng, Yang, Anbo, Yang, Changgen, Yang, Chengfeng, Yang, Huan, Yang, Jie, Yang, Lei, Yang, Xiaoyu, Yang, Yifan, Yang, Yifan, Yao, Haifeng, Yasin, Zafar, Ye, Jiaxuan, Ye, Mei, Ye, Ziping, Yegin, Ugur, Yermia, Frédéric, Yi, Peihuai, Yin, Na, Yin, Xiangwei, You, Zhengyun, Yu, Boxiang, Yu, Chiye, Yu, Chunxu, Yu, Hongzhao, Yu, Miao, Yu, Xianghui, Yu, Zeyuan, Yu, Zezhong, Yuan, Chengzhuo, Yuan, Ying, Yuan, Zhenxiong, Yuan, Ziyi, Yue, Baobiao, Zafar, Noman, Zambanini, Andre, Zavadskyi, Vitalii, Zeng, Shan, Zeng, Tingxuan, Zeng, Yuda, Zhan, Liang, Zhang, Aiqiang, Zhang, Feiyang, Zhang, Guoqing, Zhang, Haiqiong, Zhang, Honghao, Zhang, Jiawen, Zhang, Jie, Zhang, Jin, Zhang, Jingbo, Zhang, Jinnan, Zhang, Peng, Zhang, Qingmin, Zhang, Shiqi, Zhang, Shu, Zhang, Tao, Zhang, Xiaomei, Zhang, Xuantong, Zhang, Xueyao, Zhang, Yan, Zhang, Yinhong, Zhang, Yiyu, Zhang, Yongpeng, Zhang, Yuanyuan, Zhang, Yumei, Zhang, Zhenyu, Zhang, Zhijian, Zhao, Fengyi, Zhao, Jie, Zhao, Rong, Zhao, Shujun, Zhao, Tianchi, Zheng, Dongqin, Zheng, Hua, Zheng, Minshan, Zheng, Yangheng, Zhong, Weirong, Zhou, Jing, Zhou, Li, Zhou, Nan, Zhou, Shun, Zhou, Tong, Zhou, Xiang, Zhu, Jiang, Zhu, Kangfu, Zhu, Kejun, Zhu, Zhihang, Zhuang, Bo, Zhuang, Honglin, Zong, Liang, and Zou, Jiaheng

Published
2022
Full Text
View/download PDF

199. Postprandial Dynamics of Proglucagon Cleavage Products and Their Relation to Metabolic Health

Author

Robert Wagner, Sabine S. Eckstein, Louise Fritsche, Katsiaryna Prystupa, Sebastian Hörber, Hans-Ulrich Häring, Andreas L. Birkenfeld, Andreas Peter, Andreas Fritsche, and Martin Heni

Subjects
glucagon, Glucagen-like peptides, insulin, metabolism, glicentin, Diseases of the endocrine glands. Clinical endocrinology, RC648-665
Abstract

IntroductionWhile oral glucose ingestion typically leads to a decrease in circulating glucagon levels, a substantial number of persons display stable or rising glucagon concentrations when assessed by radioimmunoassay (RIA). However, these assays show cross-reactivity to other proglucagon cleavage products. Recently, more specific assays became available, therefore we systematically assessed glucagon and other proglucagon cleavage products and their relation to metabolic health.Research Design and MethodsWe used samples from 52 oral glucose tolerance tests (OGTT) that were randomly selected from persons with different categories of glucose tolerance in an extensively phenotyped study cohort.ResultsGlucagon concentrations quantified with RIA were non-suppressed at 2 hours of the OGTT in 36% of the samples. Non-suppressors showed lower fasting glucagon levels compared to suppressors (p=0.011). Similar to RIA measurements, ELISA-derived fasting glucagon was lower in non-suppressors (p

Published
2022
Full Text
View/download PDF

200. Obesity and Impaired Metabolic Health Increase Risk of COVID-19-Related Mortality in Young and Middle-Aged Adults to the Level Observed in Older People: The LEOSS Registry

Author

Norbert Stefan, Katrin Sippel, Martin Heni, Andreas Fritsche, Robert Wagner, Carolin E. M. Jakob, Hubert Preißl, Alexander von Werder, Yascha Khodamoradi, Stefan Borgmann, Maria Madeleine Rüthrich, Frank Hanses, Martina Haselberger, Christiane Piepel, Martin Hower, Jürgen vom Dahl, Kai Wille, Christoph Römmele, Janne Vehreschild, Melanie Stecher, Michele Solimena, Michael Roden, Annette Schürmann, Baptist Gallwitz, Martin Hrabe de Angelis, David S. Ludwig, Matthias B. Schulze, Bjoern Erik Ole Jensen, and Andreas L. Birkenfeld

Subjects
obesity, diabetes, hypertension, impaired metabolic health, mortality, COVID-19, Medicine (General), R5-920
Abstract

Advanced age, followed by male sex, by far poses the greatest risk for severe COVID-19. An unresolved question is the extent to which modifiable comorbidities increase the risk of COVID-19-related mortality among younger patients, in whom COVID-19-related hospitalization strongly increased in 2021. A total of 3,163 patients with SARS-COV-2 diagnosis in the Lean European Open Survey on SARS-CoV-2-Infected Patients (LEOSS) cohort were studied. LEOSS is a European non-interventional multi-center cohort study established in March 2020 to investigate the epidemiology and clinical course of SARS-CoV-2 infection. Data from hospitalized patients and those who received ambulatory care, with a positive SARS-CoV-2 test, were included in the study. An additive effect of obesity, diabetes and hypertension on the risk of mortality was observed, which was particularly strong in young and middle-aged patients. Compared to young and middle-aged (18–55 years) patients without obesity, diabetes and hypertension (non-obese and metabolically healthy; n = 593), young and middle-aged adult patients with all three risk parameters (obese and metabolically unhealthy; n = 31) had a similar adjusted increased risk of mortality [OR 7.42 (95% CI 1.55–27.3)] as older (56–75 years) non-obese and metabolically healthy patients [n = 339; OR 8.21 (95% CI 4.10–18.3)]. Furthermore, increased CRP levels explained part of the elevated risk of COVID-19-related mortality with age, specifically in the absence of obesity and impaired metabolic health. In conclusion, the modifiable risk factors obesity, diabetes and hypertension increase the risk of COVID-19-related mortality in young and middle-aged patients to the level of risk observed in advanced age.

Published
2022
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results