Molecular Metabolism in Adipose & Diabetes Lab (M²A Lab)
Our goal is to uncover new molecular mechanisms underlying adipose tissue dysfunction and insulin resistance, which are central contributors to the development of type 2 diabetes. By dissecting the molecular basis of impaired adipose tissue function, we aim to identify novel therapeutic targets and strategies for preventing and treating type 2 diabetes.
The research in our group focuses on identifying novel regulators of insulin signaling and lipolysis in adipocytes—two interconnected processes that are often impaired in insulin-resistant states. By leveraging advanced molecular biology approaches, such as the development of genetically encoded biosensors, high-content functional screens, and viral-based gene delivery systems, we aim to dissect the signaling networks and metabolic alterations that accompany insulin resistance. Through this mechanistic understanding, we strive to pinpoint new druggable targets and facilitate the discovery of next-generation insulin sensitizers, ultimately advancing therapeutic options for individuals living with type 2 diabetes.
Our goal is to uncover new molecular mechanisms underlying adipose tissue dysfunction and insulin resistance, which are central contributors to the development of type 2 diabetes. By dissecting the molecular basis of impaired adipose tissue function, we aim to identify novel therapeutic targets and strategies for preventing and treating type 2 diabetes.
The research in our group focuses on identifying novel regulators of insulin signaling and lipolysis in adipocytes—two interconnected processes that are often impaired in insulin-resistant states. By leveraging advanced molecular biology approaches, such as the development of genetically encoded biosensors, high-content functional screens, and viral-based gene delivery systems, we aim to dissect the signaling networks and metabolic alterations that accompany insulin resistance. Through this mechanistic understanding, we strive to pinpoint new druggable targets and facilitate the discovery of next-generation insulin sensitizers, ultimately advancing therapeutic options for individuals living with type 2 diabetes.
TA
MTA
TA
Study Nurse
MD student
MD student
BSc Student
Recent 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).
Primary Investigator
