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Confocal microscopy image of a mouse brain
Helmholtz Munich | © Ismael Gonzalez-Garcia

Helmholtz Diabetes Center Institute for Diabetes and Obesity (IDO)

The IDO investigates the diseases of the metabolic syndrome by means of systems biological and translational approaches on the basis of cellular systems, genetically modified mouse models and clinical intervention studies.

The IDO investigates the diseases of the metabolic syndrome by means of systems biological and translational approaches on the basis of cellular systems, genetically modified mouse models and clinical intervention studies.

Our Research Groups

Portrait Timo Müller
Helmholtz Munich | Haggenmüller
Müller Lab

Molecular Pharmacology

Porträt Cristina Garcia Caceres
Helmholtz Munich | ©Michael Haggenmueller
García Cáceres Lab

Astrocyte-Neuron Networks

Porträt Fabiana Perocchi
©Michael Haggenmueller
Perocchi Lab/ Independent Research Group

Functional Genomics of Mitochondria

Porträt Natalie Krahmer
Helmholtz Munich | ©Michael Haggenmueller
Krahmer Lab

Cellular Proteomics and Metabolic Signaling

IDO_Cebrian Serrano, Alberto
Helmholtz Munich | © Michael Haggenmüller
Cebrian Serrano Lab

Genetics

Dominik Lutter 3
Matthias Tunger Photodesign
Lutter Lab

Computational Discovery Research

View Lab

Our Independent Research Units

Siegfried Ussar
Matthias Tunger Photodesign
Ussar Lab

Adipocytes and Metabolism

Paul Pfluger Portrait Querformat
Matthias Tunger Photodesign
Pfluger Lab

(NBD) Neurobiology of Diabetes

Our Administrational Units

Portrait Timo Müller
Helmholtz Munich | Haggenmüller
Prof. Dr. Timo Müller

Animal Administration

Maryna Bondarava
Helmholtz Munich | © Michael Haggenmüller

Our staff

Porträt Cristina Garcia Caceres

Prof. Dr. Cristina García Cáceres

Deputy Director (acting), Group Leader View profile
Siegfried Ussar

Dr. Siegfried Ussar

Director of Research Unit Adipocytes and Metabolism View profile
Porträt Fabiana Perocchi

Prof. Dr. Fabiana Perocchi

Group Leader (W3 Associate Professor)
IDO_Cebrian Serrano, Alberto

Dr. Alberto Cebrian Serrano

Group Leader View profile
Porträt Sonja Schriever

Dr. Sonja Schriever

Deputy Head
Portrait Philipp Melander

Philipp Melander

Koordinator Budget & Personal
Porträt Marion Konheiser

Marion Konheiser

Assistant to the Director
IMG_7203_Lena_profile_left 1

Lena Heisel

Team Assistant
Katharina Haas

Dr. Katharina Haas

Scientist

Daniela Heine

Lab manager
Porträt Sabina Chubanava

Dr. Sabina Chubanava

Postdoc

Daniel Brandt

Technician

Dr. Pâmela Kakimoto

Postdoc

Dr. Gandhari Maity Kumar

Postdoc

Dr. Khanh Vo

Postdoc (parental leave)
Porträt Lingru Kang

Lingru Kang

PhD Student
Porträt Chenxi Wang

Chenxi Wang

PhD Student

Guantong Hu

TA

Yingzi Shi

PhD

Robert Gutgesell

PhD Student

Peggy Dörfelt

Technician
deBernardis Murat Cahue

Dr. Cahuê De Bernardis Murat

Postdoc

Dr. Edward Milbank

Postdoc

Noémi Mallet

Technician
Porträt Cristina Mencias

Cristina Mencías

PhD Student

Berivan Sahin

PhD

Dr. Ekta Pathak

Postdoc
Daniel Haas

Daniel Haas

PhD Student
Porträt Irem Altun

Dr. Irem Altun

Postdoc

Dr. Beata Legutko

Senior Scientist

Marlene Kilian

Technician
Porträt Clarita Layritz

Clarita Layritz

Technician

Dr. Gerald Grandl

Postdoc

Wenjie Lu

Technician

Sneha Prakash

PhD Student

Özum Sehnaz Caliskan

PhD Student
Porträt Carina Dürr

Carina Dürr

PhD Student

Nicole Klas

Technician
Porträt Zamani Samira

Samira Zamani

PhD Student

Ahmed Khalil

Postdoc

Andreas Israel

Technician
Porträt Melanie Huber

Melanie Huber

PhD Student

Dr. Daniela Liśkiewicz

Postdoc

Anna Molenaar

PhD Student
Porträt Franziska Lechner

Franziska Lechner

PhD Student

Seun Akindehin

PhD Student (HDC School)

Callum Coupland

PhD Student

Russell Lorenzo Castelino

PhD Student

Dr. Meri De Angelis

Postdoc

Sara Ribičić Vilić

Research Scientist

Miriam Krekel

Technician

Inderjeet Singh

PhD student
Porträt Ophelia Le Thuc

Dr. Ophélia Le Thuc

Postdoc
Porträt Cassie Hollemann

Cassie Hollemann

Technician

Dr. Yanjun Xu

Postdoc
Porträt Margarita Chudenkova

Margarita Chudenkova

PhD Student
Michael Sheng Fu Feng

Michael Sheng-Fu Feng

PhD Student
Porträt Denis Vecellio

Dr. Denis Vecellio Reane

Postdoc

Safal Walia

PhD Student

Balma Carcia Colomer

Technician

Sophie Wilson

PhD Student

Zeynep Okutan

Master Student

Julio Ruiz Trave

Technicain

Xenia Leonhardt

Technician
Porträt Xue Liu

Liu Xue

PhD Student

Dr. Aaron Novikoff

Postdoc
Porträt Songül Sahin

Songül Sahin

Lab Assistant

Dr. Arkadiusz Liśkiewicz

Postdoc
Porträt Elena Garcia

Elena Garcia Clave

PhD Student (HDC)

Eva Maria Trautmann

PhD Student

Hilda Carolina Delgado De la Herrán

PhD Student

Natalia Prudente de Mello

PhD Student
Porträt Miriam Bernecker

Miriam Bernecker

PhD Student (HDC)

Dr. Yiming Cheng

Senior Bioinformatician/Scientist

Dr. Konstantinos Makris

Postdoc

Dr. Mariana Ponce-de-Leon

Postdoc

Sabrina Alexandra Liedtke

Master Student

Santhosh Kumar

Master Student

Laura Pernetta

Master Student

Recent Publication Highlights

See all

April 2024 Nature Metabolism

Felix Klingelhuber, Scott Frendo-Cumbo, Muhmmad Omar-Hmeadi, Lucas Massier, Pamela Kakimoto, Austin J. Taylor, Morgane Couchet, Sara Ribicic, Martin Wabitsch, Ana C. Messias, Arcangela Iuso, Timo D. Müller, Mikael Rydén, Niklas Mejhert & Natalie Krahmer

A spatiotemporal proteomic map of human adipogenesis

White adipocytes function as major energy reservoirs in humans by storing substantial amounts of triglycerides, and their dysfunction is associated with metabolic disorders; however, the mechanisms underlying cellular specialization during adipogenesis remain unknown. Here, we generate a spatiotemporal proteomic atlas of human adipogenesis, which elucidates cellular remodelling as well as the spatial reorganization of metabolic pathways to optimize cells for lipid accumulation and highlights the coordinated regulation of protein localization and abundance during adipocyte formation. We identify compartment-specific regulation of protein levels and localization changes of metabolic enzymes to reprogramme branched-chain amino acids and one-carbon metabolism to provide building blocks and reduction equivalents. Additionally, we identify C19orf12 as a differentiation-induced adipocyte lipid droplet protein that interacts with the translocase of the outer membrane complex of lipid droplet-associated mitochondria and regulates adipocyte lipid storage by determining the capacity of mitochondria to metabolize fatty acids. Overall, our study provides a comprehensive resource for understanding human adipogenesis and for future discoveries in the field.

February 2024 Nature Metabolism

Grandl G, Collden G, Feng J, Bhattacharya S, Klingelhuber F, Schomann L, Bilekova S, Ansarullah, Xu W, Far FF, Tost M, Gruber T, Bastidas-Ponce A, Zhang Q, Novikoff A, Liskiewicz A, Liskiewicz D, Garcia-Caceres C, Feuchtinger A, Tschöp MH, Krahmer N, Lickert H, Müller TD.

Global, neuronal or β cell-specific deletion of inceptor improves glucose homeostasis in male mice with diet-induced obesity

Insulin resistance is an early complication of diet-induced obesity (DIO)1, potentially leading to hyperglycaemia and hyperinsulinaemia, accompanied by adaptive β cell hypertrophy and development of type 2 diabetes2. Insulin not only signals via the insulin receptor (INSR), but also promotes β cell survival, growth and function via the insulin-like growth factor 1 receptor (IGF1R)3,4,5,6. We recently identified the insulin inhibitory receptor (inceptor) as the key mediator of IGF1R and INSR desensitization7. But, although β cell-specific loss of inceptor improves β cell function in lean mice7, it warrants clarification whether inceptor signal inhibition also improves glycaemia under conditions of obesity. We assessed the glucometabolic effects of targeted inceptor deletion in either the brain or the pancreatic β cells under conditions of DIO in male mice. In the present study, we show that global and neuronal deletion of inceptor, as well as its adult-onset deletion in the β cells, improves glucose homeostasis by enhancing β cell health and function. Moreover, we demonstrate that inceptor-mediated improvement in glucose control does not depend on inceptor function in agouti-related protein-expressing or pro-opiomelanocortin neurons. Our data demonstrate that inceptor inhibition improves glucose homeostasis in mice with DIO, hence corroborating that inceptor is a crucial regulator of INSR and IGF1R signalling.

Dezember 2023 Nature Metabolism

Liskiewicz A, Khalil A, Liskiewicz D, Novikoff A, Grandl G, Maity-Kumar G, Gutgesell RM, Bakhti M, Bastidas-Ponce A, Czarnecki O, Makris K, Lickert H, Feuchtinger A, Tost M, Coupland C, Ständer L, Akindehin S, Prakash S, Abrar F, Castelino RL, He Y, Knerr PJ, Yang B, Hogendorf WFJ, Zhang S, Hofmann SM, Finan B, DiMarchi RD, Tschöp MH, Douros JD, Müller TD.

Glucose-dependent insulinotropic polypeptide regulates body weight and food intake via GABAergic neurons in mice

The development of single-molecule co-agonists for the glucagon-like peptide-1 (GLP-1) receptor (GLP-1R) and glucose-dependent insulinotropic polypeptide (GIP) receptor (GIPR) is considered a breakthrough in the treatment of obesity and type 2 diabetes. But although GIPR–GLP-1R co-agonism decreases body weight with superior efficacy relative to GLP-1R agonism alone in preclinical1,2,3 and clinical studies4,5, the role of GIP in regulating energy metabolism remains enigmatic. Increasing evidence suggests that long-acting GIPR agonists act in the brain to decrease body weight through the inhibition of food intake3,6,7,8; however, the mechanisms and neuronal populations through which GIP affects metabolism remain to be identified. Here, we report that long-acting GIPR agonists and GIPR–GLP-1R co-agonists decrease body weight and food intake via inhibitory GABAergic neurons. We show that acyl-GIP decreases body weight and food intake in male diet-induced obese wild-type mice, but not in mice with deletion of Gipr in Vgat(also known as Slc32a1)-expressing GABAergic neurons (Vgat-Gipr knockout). Whereas the GIPR–GLP-1R co-agonist MAR709 leads, in male diet-induced obese wild-type mice, to greater weight loss and further inhibition of food intake relative to a pharmacokinetically matched acyl-GLP-1 control, this superiority over GLP-1 vanishes in Vgat-Gipr knockout mice. Our data demonstrate that long-acting GIPR agonists crucially depend on GIPR signaling in inhibitory GABAergic neurons to decrease body weight and food intake.

Our Networks and Affiliations

Contact

Porträt Marion Konheiser

Marion Konheiser

Assistant to the Director

Building 3620, Room 242c