About our research
Overweight and obesity are associated with a high risk for metabolic disease such as diabetes, cardiovascular diseases and certain types of cancers. Hormonal factors such as peptides, small molecules and other bioactive molecules control metabolic homeostasis by orchestrating the communication of several organs in the body. Malfunction at the level of their production or their actions at target cells leads to metabolic disease. Up to this date many endocrine factors involved in metabolic disease remain elusive. However, recent technological advances such as mutli-omics (genomics, proteomics, metabolomics) has allowed for the rapid identification of novel signaling molecules.
G-protein-coupled receptors (GPCRs) are the largest family of cell plasma membrane receptors with approximately 800 proteins in the human genome. GPCRs translate the effects of a wide range of peptide hormones and bioactive molecules (receptor ligands) into intracellular signaling events, providing a direct mechanism for cellular responses to endocrine signals. Furthermore, GPCR signaling is tunable, ligand and cell type specific, making them ideal drug candidates. Due to their important roles in the pathophysiology of many serious diseases GPCRs are targets of nearly half of today´s pharmaceuticals, however a very small portion targets metabolic diseases.
In the group of Endocrine Pharmacology we study novel ligand-receptor pairs, which control key adipocyte functions involved in adipocyte size, energy storage, energy expenditure, ageing dependent malfunction as well as the communication of the adipose tissue with other metabolic organs, such as liver and muscle. To that end we utilize multi-omics approaches and focus on the development of novel strategies for peptide identification and GPCR deorphanization. Furthermore, combining a wide range of pharmacological tools, in vitro and in vivo models we aim to understand these newly identified signaling pathways in white and brown adipocytes. Eventually we seek to harness this information for the development of novel therapeutics against metabolic disease, particularly obesity and Type 2 diabetes.
Doctoral Researcher
Doctoral Researcher
Doctoral Researcher
Our Most Recent Publications
Köker, S.C. ; Tsokanos, F.-F. ; El-Merahbi, R. ; Jha, A.K. ; Cicatelli, K. ; Weber, P. ; Mhamane, A. ; Kaltenecker, D. ; Morigny, P. ; Loft, A. ; Klepac, K. ; Maida, A. ; Molocea, C.-E. ; Hass, D, ; Vogl, E.S. ; Alfaro, A.J. ; Sun, W. ; Zitzelsberger, H. ; Unger, K. ; Szendrödi, J. ; Li, Y. ; Diaz, M.B. ; Wolfrum, C. ; Bartelt, A. ; Herzig, S. ; Georgiadi, A.
The TBLR1/TBL1 co-factor complex acts as a transcriptional checkpoint in the brown adipose tissue response to prolonged cold exposure.Reinisch, I. ; Michenthaler, H. ; Sulaj, A. ; Moyschewitz, E. ; Krstic, J. ; Galhuber, M. ; Xu, R. ; Riahi, Z. ; Wang, T. ; Vujić, N. ; Amor, M. ; Zenezini Chiozzi, R. ; Wabitsch, M. ; Kolb, D. ; Georgiadi, A. ; Glawitsch, L. ; Heitzer, E. ; Schulz, T.J. ; Schupp, M. ; Sun, W. ; Dong, H. ; Ghosh, A. ; Hoffmann, A. ; Kratky, D. ; Hinte, L.C. ; von Meyenn, F. ; Heck, A.J.R. ; Blüher, M. ; Herzig, S. ; Wolfrum, C. ; Prokesch, A.
Adipocyte p53 coordinates the response to intermittent fasting by regulating adipose tissue immune cell landscape.Alfaro, A.J. ; Dittner, C. ; Becker, J. ; Loft, A. ; Mhamane, A. ; Maida, A. ; Georgiadi, A. ; Tsokanos, F.-F. ; Klepac, K. ; Molocea, C.-E. ; El-Merahbi, R. ; Motzler, K. ; Geppert, J. ; Karikari, R.A. ; Szendrödi, J. ; Feuchtinger, A. ; Hofmann, S.M. ; Karaca, S. ; Urlaub, H. ; Berriel Diaz, M. ; Melchior, F. ; Herzig, S.
Fasting-sensitive SUMO-switch on Prox1 controls hepatic cholesterol metabolism.Contact Us