Senior Scientist
Dr. Gencer Sancar
My long-term vision is to contribute fundamentally to our understanding of how adipose tissue dysfunction drives insulin resistance and type 2 diabetes, and to translate these mechanistic insights into novel therapeutic strategies. I aim to identify key molecular regulators that can be targeted to restore healthy adipose tissue function and systemic metabolic balance.
Academic Career and Research Areas
Dr. Gencer Sancar is a molecular metabolic researcher whose career has been driven by a deep interest in understanding how adipose tissue regulates systemic metabolism and contributes to the pathogenesis of type 2 diabetes (T2D). He currently leads an independent research group at the Institute for Diabetes Research and Metabolic Diseases (IDM) in Tübingen, part of Helmholtz Munich, where his team investigates the cellular and molecular mechanisms underlying adipose tissue dysfunction and insulin resistance.
Dr. Sancar earned his PhD in Biochemistry at Heidelberg University, where he studied the circadian control of metabolism in the model organism Neurospora crassa. He then continued as a postdoctoral fellow at Heidelberg University Biochemistry Center and subsequently joined the Salk Institute in San Diego, working in the laboratory of Prof. Ronald M. Evans. There, he made key contributions to understanding fibroblast growth factor 1 (FGF1) regulate lipolysis and indirectly regulate blood glucose levels via suppressing hepatic glucose production.
Since returning to Germany in 2022 to establish his own group at IDM/Helmholtz Munich, Dr. Sancar has focused on the role of adipose signaling pathways—particularly the FGF1/PDE4D axis—in regulating lipolysis, adipogenesis, and insulin action. His group combines advanced in vivo models, human primary adipocytes, and state-of-the-art biosensors to uncover how adipose tissue function shapes whole-body glucose and lipid homeostasis.
The goal of his research is to identify novel signaling nodes that could serve as therapeutic entry points to restore healthy adipose tissue function and prevent or reverse insulin resistance. His discoveries—such as the identification of p21-activated kinases (PAKs) as regulators of the FGF1/PDE4D antilipolytic pathway—highlight new mechanisms through which insulin resistance develops and may be therapeutically targeted.
Dr. Sancar's work has direct implications for the development of more effective treatments for T2D, particularly in patients where adipose dysfunction is a primary driver of metabolic deterioration. His collaborative research spans both basic and translational science, involving partners across Helmholtz Munich, the German Center for Diabetes Research (DZD), and international institutions. By linking molecular mechanisms to human pathophysiology, his research helps bridge the gap between laboratory discovery and clinical innovation.
Fields of Work and Expertise
Adipose tissue signaling Lipolysis Insulin resistance Type 2 Diabetes Lipid utilization
Professional Background
Group Leader at the for Diabetes Research and Metabolic Diseases
Postdoctoral Fellow, Salk Institute for Biological Studies, San Diego, CA, USA in the laboratory of Dr Ronald M Evans
Postdoctoral Fellow, Heidelberg University Biochemistry Center, Heidelberg, Germany in the laboratory of Dr Michael Brunner
M.Sc. and PhD thesis, Heidelberg University Biochemistry Center, Heidelberg, Germany in the laboratory of Dr Michael Brunner
Honors and Awards
- DFG (German Research Foundation) Individual Grant 2026
- DZD (Deutsches Zentrum für Diabetesforschung) Research Fellowship 2024-2026 & 2025-2027
- DDG (Deutsche Diabetes Gesellschaft) Research Fellowship 2023 & 2024
- DFG Research Fellowship for postdoctoral studies in US 2016-2019
Publications
Hinrichs, A. ; Pafili, K. ; Sancar, G. ; Laane, L. ; Zettler, S. ; Torgeman, M. ; Kessler, B. ; Nono, J.L. ; Kunz, S. ; Rathkolb, B. ; Barosa, C. ; Prehn, C. ; Cecil, A. ; Renner, S. ; Kemter, E. ; Kahl, S. ; Szendroedi, J. ; Bidlingmaier, M. ; Jones, J.G. ; Hrabě de Angelis, M. ; Roden, M. ; Wolf, E.
Corrigendum to "Transient juvenile hypoglycemia in GH insensitive Laron syndrome pigs is associated with insulin hypersensitivity" [Mol Metabol (2025) 102273].Hinrichs, A. ; Pafili, K. ; Sancar, G. ; Laane, L. ; Zettler, S. ; Torgeman, M. ; Kessler, B. ; Nono, J.L. ; Kunz, S. ; Rathkolb, B. ; Barosa, C. ; Prehn, C. ; Cecil, A. ; Renner, S. ; Kemter, E. ; Kahl, S. ; Szendroedi, J. ; Bidlingmaier, M. ; Jones, J.G. ; Hrabě de Angelis, M. ; Roden, M. ; Wolf, E.
Transient juvenile hypoglycemia in GH insensitive Laron syndrome pigs is associated with insulin hypersensitivity.Krier, J. ; Spähn, D. ; Lopez, D.A.J. ; Nono, J.L. ; Seigner, J. ; Ussar, S. ; Lukowski, R. ; Birkenfeld, A.L. ; Sancar, G.
PDE4D and PDE3B orchestrate distinct cAMP microdomains in 3T3-L1 adipocytes.Seigner, J. ; Krier, J. ; Spähn, D. ; Sandforth, L. ; Nono, J.L. ; Lukowski, R. ; Birkenfeld, A.L. ; Sancar, G.
p21-activated kinases (PAKs) regulate FGF1/PDE4D antilipolytic pathway and insulin resistance in adipocytes.Lorza-Gil, E. ; Strauss, O. ; Ziegler, E. ; Kansy, K. ; Katschke, M.-T. ; Rahimi, G. ; Neuscheler, D. ; Sandforth, L. ; Sandforth, A. ; Sancar, G. ; Kaufmann, B. ; Hartmann, D. ; Singer, S.R. ; Mihaljevic, A.L. ; Jumpertz von Schwartzenberg, R. ; Sbierski-Kind, J. ; Müller, T.D. ; Birkenfeld, A.L. ; Gerst, F.
Incretin-responsive human pancreatic adipose tissue organoids: A functional model for fatty pancreas research.Sancar, G. ; Birkenfeld, A.L.
The role of adipose tissue dysfunction in hepatic insulin resistance and T2D.Lorza-Gil, E. ; Ekim Üstünel, B. ; Sancar, G.
Editorial: Organ crosstalk in the pathophysiology and treatment of type-2 diabetes.Sandforth, L. ; Brachs, S. ; Reinke, J. ; Willmes, D. ; Sancar, G. ; Seigner, J. ; Juarez Lopez, D.A. ; Sandforth, A. ; McBride, J.D. ; Ma, J.X. ; Haufe, S. ; Jordan, J. ; Birkenfeld, A.L.
Role of human Kallistatin in glucose and energy homeostasis in mice.Sandforth, A. ; Jumpertz von Schwartzenberg, R. ; Arreola, E.V. ; Hanson, R.L. ; Sancar, G. ; Katzenstein, S. ; Lange, K. ; Preissl, H. ; Dreher, S. ; Weigert, C. ; Wagner, R. ; Kantartzis, K. ; Machann, J. ; Schick, F. ; Lehmann, R. ; Peter, A. ; Katsouli, N. ; Ntziachristos, V. ; Dannecker, C. ; Fritsche, L. ; Perakakis, N. ; Heni, M. ; Nawroth, P.P. ; Kopf, S. ; Pfeiffer, A.F.H. ; Kabisch, S. ; Stumvoll, M. ; Schwarz, P.E.H. ; Hauner, H ; Lechner, A. ; Seissler, J. ; Yurchenko, I. ; Icks, A. ; Solimena, M. ; Häring, H.-U. ; Szendroedi, J. ; Schürmann, A. ; Hrabě de Angelis, M. ; Blüher, M. ; Roden, M. ; Bornstein, S. ; Stefan, N. ; Fritsche, A. ; Birkenfeld, A.L.
Mechanisms of weight loss-induced remission in people with prediabetes: A post-hoc analysis of the randomised, controlled, multicentre Prediabetes Lifestyle Intervention Study (PLIS).
