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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

Siegfried Ussar
Matthias Tunger Photodesign
Ussar Lab

Adipocytes and Metabolism

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

Astrocyte-Neuron Networks

Paul Pfluger Portrait Querformat
Matthias Tunger Photodesign
Pfluger Lab

(NBD) Neurobiology of Diabetes

Porträt Fabiana Perocchi
©Michael Haggenmueller
Perocchi Lab

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
Dr. Dominik Lutter

Computational Discovery Research

Portrait Timo Müller
Helmholtz Munich | Haggenmüller
Prof. Dr. Timo Müller, Institute Director

Animal Administration

Maryna Bondarava
Helmholtz Munich | © Michael Haggenmüller
Dr. Maryna Bondarava / Head of Research Management

IDO Management

View team

Our staff

Siegfried Ussar

Dr. Siegfried Ussar

Deputy Director (acting), Group Leader View profile
Porträt Cristina Garcia Caceres

Prof. Dr. Cristina García Cáceres

Deputy Director (acting), Group Leader 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

Verena Schöler

Scientist

Daniela Heine

Lab manager

Dr. Sabina Chubanava

Postdoc

Daniel Brandt

Technician

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

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

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

Lisa Ständer

PhD Student

Wenjie Lu

Technician

Sneha Prakash

PhD Student

Özum Sehnaz Caliskan

PhD Student
Porträt Carina Dürr

Carina Dürr

PhD Student

Nicole Klas

Technician

Felix Klingelhuber

PhD Student

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

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

Xenia Leonhardt

Technician
Porträt Xue Liu

Liu Xue

PhD Student
Porträt Xiaocheng Yan

Xiaocheng Yan

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 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

Recent Publication Highlights

See all

2023 Nature Metabolism

El K, Douros JD, Willard FS, Novikoff A, Sargsyan A, Perez-Tilve D, Wainscott DB, Yang B, Chen A, Wothe D, Coupland C, Tschöp MH, Finan B, D'Alessio DA, Sloop KW, Müller TD, Campbell JE.

The incretin co-agonist tirzepatide requires GIPR for hormone secretion from human islets

The incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) mediate insulin responses that are proportionate to nutrient intake to facilitate glucose tolerance1. The GLP-1 receptor (GLP-1R) is an established drug target for the treatment of diabetes and obesity2, whereas the therapeutic potential of the GIP receptor (GIPR) is a subject of debate. Tirzepatide is an agonist at both the GIPR and GLP-1R and is a highly effective treatment for type 2 diabetes and obesity3,4. However, although tirzepatide activates GIPR in cell lines and mouse models, it is not clear whether or how dual agonism contributes to its therapeutic benefit. Islet beta cells express both the GLP-1R and the GIPR, and insulin secretion is an established mechanism by which incretin agonists improve glycemic control5. Here, we show that in mouse islets, tirzepatide stimulates insulin secretion predominantly through the GLP-1R, owing to reduced potency at the mouse GIPR. However, in human islets, antagonizing GIPR activity consistently decreases the insulin response to tirzepatide. Moreover, tirzepatide enhances glucagon secretion and somatostatin secretion in human islets. These data demonstrate that tirzepatide stimulates islet hormone secretion from human islets through both incretin receptors.

2023 Mar Cell Metab.

González-García I, García-Clavé E, Cebrian-Serrano A, Le Thuc O, Contreras RE, Xu Y, Gruber T, Schriever SC, Legutko B, Lintelmann J, Adamski J, Wurst W, Müller TD, Woods SC, Pfluger PT, Tschöp MH, Fisette A, García-Cáceres C.

Estradiol regulates leptin sensitivity to control feeding via hypothalamic Cited1

Until menopause, women have a lower propensity to develop metabolic diseases than men, suggestive of a protective role for sex hormones. Although a functional synergy between central actions of estrogens and leptin has been demonstrated to protect against metabolic disturbances, the underlying cellular and molecular mechanisms mediating this crosstalk have remained elusive. By using a series of embryonic, adult-onset, and tissue/cell-specific loss-of-function mouse models, we document an unprecedented role of hypothalamic Cbp/P300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 1 (Cited1) in mediating estradiol (E2)-dependent leptin actions that control feeding specifically in pro-opiomelanocortin (Pomc) neurons. We reveal that within arcuate Pomc neurons, Cited1 drives leptin's anorectic effects by acting as a co-factor converging E2 and leptin signaling via direct Cited1-ERα-Stat3 interactions. Together, these results provide new insights on how melanocortin neurons integrate endocrine inputs from gonadal and adipose axes via Cited1, thereby contributing to the sexual dimorphism in diet-induced obesity.

2023 Feb Nat Commun.

Kulaj K, Harger A, Bauer M, Caliskan ÖS, Gupta TK, Chiang DM, Milbank E, Reber J, Karlas A, Kotzbeck P, Sailer DN, Volta F, Lutter D, Prakash S, Merl-Pham J, Ntziachristos V, Hauner H, Pfaffl MW, Tschöp MH, Müller TD, Hauck SM, Engel BD, Gerdes JM, Pfluger PT, Krahmer N, Stemmer K.

Adipocyte-derived extracellular vesicles increase insulin secretion through transport of insulinotropic protein cargo

Adipocyte-derived extracellular vesicles (AdEVs) are membranous nanoparticles that convey communication from adipose tissue to other organs. Here, to delineate their role as messengers with glucoregulatory nature, we paired fluorescence AdEV-tracing and SILAC-labeling with (phospho)proteomics, and revealed that AdEVs transfer functional insulinotropic protein cargo into pancreatic β-cells. Upon transfer, AdEV proteins were subjects for phosphorylation, augmented insulinotropic GPCR/cAMP/PKA signaling by increasing total protein abundances and phosphosite dynamics, and ultimately enhanced 1st-phase glucose-stimulated insulin secretion (GSIS) in murine islets. Notably, insulinotropic effects were restricted to AdEVs isolated from obese and insulin resistant, but not lean mice, which was consistent with differential protein loads and AdEV luminal morphologies. Likewise, in vivo pre-treatment with AdEVs from obese but not lean mice amplified insulin secretion and glucose tolerance in mice. This data suggests that secreted AdEVs can inform pancreatic β-cells about insulin resistance in adipose tissue in order to amplify GSIS in times of increased insulin demand.

2023 Diabetologia

Lutter D, Sachs S, Walter M, Kerege A, Perreault L, Kahn DE, Wolide AD, Kleinert M, Bergman BC, Hofmann SM.

Skeletal muscle and intermuscular adipose tissue gene expression profiling identifies new biomarkers with prognostic significance for insulin resistance progression and intervention response

Although insulin resistance often leads to type 2 diabetes mellitus, its early stages are often unrecognised, thus reducing the probability of successful prevention and intervention. Moreover, treatment efficacy is affected by the genetics of the individual. We used gene expression profiles from a cross-sectional study to identify potential candidate genes for the prediction of diabetes risk and intervention response.

Our Networks and Affiliations

Contact

Porträt Marion Konheiser

Marion Konheiser

Assistant to the Director

Building 3620, Room 242c