Professor for "Basic Principles of Metabolic Diseases" at ECAS, interested in membrane trafficking and metabolism. #liver #diabetes #NAFLD

Mannheim, Baden-Württemberg
Joined April 2019
BTW, we are hiring :-)!
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Happy to share that I have joined the Medical Faculty of Mannheim at Heidelberg University as full professor starting this month. Looking forward to new challenges and interactions. Thanks to everybody, especially my group, friends and colleagues! @helmholtz_diabc @ZeigererLab
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Great fun at the mitochondria and bioenergetics workshop in Brazil together with my dear colleagues from the Rohm lab @RohmMaria from @helmholtz_diabc. Thanks for having us @luiz_leiria!
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Super proud of my PhD student @kmotzler presenting at the Glucagon Conference our story about the spatial regulation of #glucagon signaling by the #endosomal protein Vps37a. With @RevathiSekar14 @helmholtz_diabc @ZeigererLab @HelmholtzMunich @Cell_Metabolism
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Thanks to all coauthors for their important contributions! Very happy to see this work out now. With @TimoMueller_IDO, @NatalieKrahmer, Oliver Plettenburg, Marta Miaczynska, Christian Behrends, Michael Roden, Matthias Blüher, Jürgen Okun, Stephan Herzig & the entire @ZeigererLab
Can we alter glucagon receptor signaling outcomes by changing it’s localization within the cell? Yes, we can! Let me explain how (and why that matters). (1/7) @RevathiSekar14 @kmotzler @helmholtz_diabc @HelmholtzMunich @Cell_Metabolism @CellPressNews tinyurl.com/y5fbu2bc
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Therefore, Vps37a KD appears to uncouple the two Gcgr signaling arms and allows to alter it’s effects on glucose #metabolism individually. We show that it does so by accumulating Gcgr at #endosomes, where it only signals to cAMP/PKA/p-Creb. But why is that important? (5/7)
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As #glucagon signaling is normally affecting both, hepatic glucose and lipid utilization, we were wondering how lipid metabolism is affected by Vps37a KD. Strikingly, lipid content and usage were completely unchanged under Vps37a KD in diabetes models. (4/7)
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The increased glucose production is linked to overactivated glucagon signaling to PKA/p-Creb in livers lacking Vps37a. Remarkably, this overactivation wanes when depleting Vps37a from livers that lack #Gcgr. Thus, the effects of Vps37a on blood glucose are Gcgr-dependent. (3/7)
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Patients with #T2D or #NAFLD have reduced levels of Vps37a in their livers. Interestingly, depletion of Vps37a from livers results in increased hepatic glucose production. In our most recent publication, we studied the function of #ESCRT-I subunit Vps37a in liver. (2/7)
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Wanna join a fun team working on the cell biology of metabolism @ZeigererLab in beautiful Munich? We are looking for a postdoc with a 3-year @dfg_public funded position. Please RT! @HelmholtzMunich @helmholtz_diabc