For the first day of the Leopoldina Collegium, the Helmholtz Institute for Metabolic, Obesity, and Vascular Research (HI-MAG) in Leipzig opened its doors and offered participants a direct insight into current obesity research. Through expert presentations and guided tours, HI-MAG showcased its bench-to-bedside research approach. In addition to basic laboratory research, HI-MAG conducts numerous clinical trials at its clinical trial unit to better understand metabolic diseases, develop new treatment approaches, and identify preventive measures.

The Leopoldina Collegium 2026 opened with welcoming remarks and a round of introductions by Prof. Dr. Antje Körner, head of the “Childhood Obesity and Metabolic Research” group at HI-MAG and Professor of Metabolic Research at Leipzig University, and Sonja Kastilan, head of the Science Communication Department at the German National Academy of Sciences Leopoldina. Prof. Dr. Antje Körner then briefed the interested journalists on current research on treatment and prevention of childhood obesity. Among other things, she presented the LIFE Child clinical trial program, which investigates healthy child development and explores questions regarding the origins and prevention of non-communicable diseases. She emphasized that prevention is a key component in the fight against obesity and stressed that the window of opportunity for preventive measures begins early in childhood. She was joined by PD Dr. Dr. John Heiker, group leader of “MORe – Molecular Obesity Research” at HI-MAG, who provided insights into translational research on adipose tissue.

During a subsequent tour through the clinical trial units of HI-MAG and LIFE Child, the journalists gained firsthand insight into how clinical questions are addressed. In addition to visiting HI-MAG's state-of-the-art metabolic chambers, the journalists were introduced to various methods for measuring body composition and learned how examinations of study participants are conducted at the LIFE Child clinical trial unit. In addition to speaking with specialists such as Sarah Frenzel, coordinator of the HI-MAG clinical trials unit, and Nico Grafe, head of the LIFE Child clinical trials unit, the journalists also had the opportunity to speak with a patient from the Obesity Outpatient Clinic at University of Leipzig Medical Center. She shared her own treatment experiences.

The informative portion of the first day concluded with a moderated discussion on the topic “Understanding Obesity as a Chronic, Recurrent Disease,” with Prof. Dr. Körner, PD Dr. Dr. Heiker, and the patient from the obesity outpatient clinic as well as Prof. Dr. Lars Selig, Head of the Nutritional Medicine/Nutrition Outpatient Clinic at University of Leipzig Medical Center and Professor of Medical Education, SRH University of Applied Sciences Heidelberg/Campus Gera. He answered questions about the treatment of patients with obesity at the University of Leipzig Medical Center. All panelists agreed that, in addition to society’s recognition of obesity as a chronic disease, it is particularly important for patients to research new treatment options to accommodate the individual course of the disease.

Prevention and Treatment Strategies in Focus

The second day of the Leopoldina Collegium took place at the German National Academy of Sciences Leopoldina in Halle (Saale). Here, the topic of prevention was explored through presentations on experiences with the sugar tax by Prof. Dr. Michael Laxy, Professor of Public Health and Prevention at the TUM School of Medicine and Health at the Technical University of Munich (TUM), as well as on the question of how to motivate people to change their lifestyles, by Prof. Dr. Iris Pigeot, Director of the Leibniz Institute for Prevention Research and Epidemiology – BIPS in Bremen.

During the concluding panel discussion, the complexity of obesity as a chronic disease was further explored with expert insights from Prof. Dr. Andreas Birkenfeld, Medical Director of the Department of Diabetology, Endocrinology, and Nephrology at the University Hospital of Tübingen and Director of the Institute for Diabetes Research and Metabolic Diseases (IDM) at Helmholtz Munich, Prof. Dr. Susanna Hofmann, Professor of Lipid Metabolism and Metabolic Diseases at Ludwig Maximilians University Munich (LMU) and Head of the Independent Research Group “Women and Diabetes” at Helmholtz Munich, and Prof. Dr. Oliver Mann, Deputy Director of the Department of General, Visceral, and Thoracic Surgery at the University Medical Center Hamburg-Eppendorf.

The Leopoldina Collegium has been held 35 times since 2012 and focuses on current sociopolitical issues. The program’s goal is to bring together media representatives and researchers and to facilitate discussion on current research topics.

The conference was hosted by Prof. Stephan Herzig, Research Director at Helmholtz Munich and Director of the Helmholtz Diabetes Center. It was co-organized by Prof. Antje Körner, Head of the Childhood Obesity and Metabolic Research Division at the Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG) of Helmholtz Munich at Leipzig University, and Dr. Raffaele Teperino, Head of the Environmental Epigenetics Group at the Institute of Experimental Genetics at Helmholtz Munich.

The three-day scientific program looked at metabolic health from early development and pregnancy to adulthood and healthy aging. It combined presentations by internationally renowned Plenary Speakers with contributions from emerging scientists, including the nominees for the Helmholtz Young Investigator in Diabetes (HeIDi) Award, Flash Talks and poster presentations. The sessions covered a broad spectrum of current diabetes and metabolism research, including brain health and diabetes prevention, metabolic complications, obesity and molecular health risks, adipose tissue biology, maternal and child health, genetics and aging.

Two scientific highlights were the keynote lecture by Prof. Daniel J. Drucker (University of Toronto) on "GLP-1 Medicines – Ongoing Mechanisms and Mysteries." and the Helmholtz Diabetes Lecture, delivered by Prof. Juleen R. Zierath (Karolinska Institutet) on "Redefining Exercise as Medicine: Personalized Molecular Pathways From Insulin Resistance to Lifelong Metabolic Health." 

The Helmholtz Diabetes Lecture Award recognizes outstanding lifetime achievements in diabetes research and is sponsored by the German Center for Diabetes Research (DZD).

Recognizing Scientific Excellence 

Supporting and highlighting the next generation of diabetes researchers was an important part of the conference. The HeIDi Award recognizes outstanding early-career scientists whose innovative research advances the diabetes field. 

From this year's nominees, Prof. Katrin J. Svensson (Stanford University) and Dr. Sarah Xinwei Luo (A*STAR Institute of Molecular and Cell Biology) were selected as the 2026 HeIDi Award winners by an independent jury of Plenary Speakers. The HeIDi Awards were sponsored by Madrigal Pharmaceuticals. The conference format deliberately placed HeIDi nominees alongside established international researchers, giving emerging scientists a prominent platform within the scientific program.

Scientific contributions from the wider community were also recognized. Osvaldo Pereira (Helmholtz Munich) and Dr. Eleanor Raffan (University of Cambridge) received the Flash Talk Awards, sponsored by Sable Systems International, while Cristina Mencías (Helmholtz Munich) received the Poster Award, sponsored by EMBO. The Flash Talk and Poster Award winners were selected by the conference audience via QR-code voting, actively involving participants in recognizing outstanding presentations.

Scientific Exchange Beyond the Lecture Hall 

Exchange and networking were an integral part of all three conference days. The dedicated Posters & Sponsor Exhibition brought scientific posters and industry partners together in one central space. Coffee and lunch breaks were deliberately integrated into this area, creating regular opportunities for participants, speakers, early-career researchers and sponsors to meet and continue scientific discussions outside the formal sessions.

On the second evening, participants continued their discussions during a Networking Reception at the Helmholtz Munich Conference Center, directly following the scientific program.

Over three days, the conference connected different disciplines, career stages and perspectives around one common question: how can a better understanding of metabolism across the entire lifespan help advance the prevention and treatment of diabetes? The combination of established international experts, emerging researchers, interactive presentation formats and extensive opportunities for personal exchange made the conference a platform not only for presenting new findings, but also for developing new scientific connections and ideas.

Alongside Müller, Lora K. Heisler from the University of Aberdeen, Randy J. Seeley from the University of Michigan, and Brian Finan from Eli Lilly and Company were honored with the 2026 Gill Transformative Investigator Award.  

New Therapeutic Approaches for Obesity and Diabetes

Müller’s research has made an important contribution to improving our understanding of the biological mechanisms underlying obesity and diabetes. His work has provided key insights into GIP receptor biology in the central nervous system and contributed to the development of a new generation of incretin-based polyagonists.

These compounds activate several receptors simultaneously and can therefore influence different metabolic processes, including the regulation of blood glucose, appetite and body weight. The concept of polyagonists was originally developed by Matthias Tschöp and Richard DiMarchi and was subsequently further advanced, among others, by Müller and his team at Helmholtz Munich from a biological and mechanistic perspective.

More recent work by Müller and his team takes this concept one step further. They are investigating how incretin-based molecules can not only combine several metabolic signals, but also selectively deliver additional therapeutic components to specific cells. The aim is to develop new and even more precise approaches for the treatment of obesity and type 2 diabetes.

At the Gill Symposium, Müller presented his research in a talk entitled “From Novel Insights into Energy Metabolism Control by GIPR Agonism to New Therapies for Obesity and Diabetes”.

A Special Connection to Munich

Müller’s award also continues a special connection between metabolic research in Munich and the Gill Awards. Following Matthias Tschöp, Müller is the second scientist from a German research institution to receive a Gill distinction. Tschöp received the Gill Distinguished Scientist Award in 2014 while affiliated with the Technical University of Munich. He later served as Scientific Managing Director of Helmholtz Munich.

The Gill Transformative Investigator Award thus recognizes Müller’s long-standing contribution to a field of research that has fundamentally expanded the possibilities for treating obesity and type 2 diabetes in recent years.

Early detection can offer significant benefits. When children with early-stage type 1 diabetes are identified and monitored regularly, the risk of diabetic ketoacidosis (DKA) at clinical onset can be substantially reduced. The onset of diabetes may then be less severe, and insulin treatment can be started promptly, often on an outpatient basis. Early diagnosis also gives families time to prepare for living with the condition and its treatment.

In addition, identifying type 1 diabetes before symptoms appear creates an opportunity to consider disease-modifying therapies at an appropriate stage and potentially delay the clinical onset of the disease.

The Majority of Children Who Develop Type 1 Diabetes Have No Family History

Screening people from families already known to be at high risk is not enough: more than 85 per cent of people newly diagnosed with type 1 diabetes have no family history of the condition. Moreover, once islet autoantibodies have been confirmed, the disease progresses at a similar rate regardless of family history.

The consensus recommends an initial screening between the ages of two and four years. If no islet autoantibodies are detected, further screening should take place between the ages of six and eight and again between the ages of 10 and 15. Studies show that islet autoantibodies first appear particularly frequently during these stages of childhood.

Within these age ranges, the timing of screening can be adapted to existing national or regional screening programmes. The recommendations also allow for a phased introduction: depending on local circumstances, programmes could initially focus on children at increased risk before being expanded to the wider population.

“With this international consensus, we have established a common framework for how population-wide screening for type 1 diabetes can be implemented in practice,” says Prof. Anette-Gabriele Ziegler, Director of the Institute for Diabetes Research at Helmholtz Munich and lead author of the consensus paper. “The diagnosis of early-stage diabetes is a step-by-step process: it begins with a sensitive screening test and is confirmed by highly specific second-line tests and a second blood sample. The specific design of the screening programme should be adapted to the respective healthcare system and, where possible, linked to existing screening programmes.”

Clear Communication and Support Are Essential

A confirmed diagnosis should be communicated to families in person and in a clear and empathetic manner. Psychosocial support should also be available when needed.

Separate international consensus recommendations already provide guidance on the regular monitoring of people diagnosed with early-stage type 1 diabetes.

The new recommendations have received broad international support. A total of 20 professional and patient organisations endorse the consensus paper, including the European Association for the Study of Diabetes (EASD), the International Society for Paediatric and Adolescent Diabetes (ISPAD) and the International Diabetes Federation Europe (IDF Europe).

Original Publication

Ziegler et al., 2026: International consensus guidance for general population screening for islet autoantibodies to diagnose early‑stage type 1 diabetes: a nominal group technique process, Diabetologia. DOI: 10.1007/s00125-026-06841-z

The visit began with an introduction to Helmholtz Munich and its scientific mission by Dr. Michael Frieser. Administrative Managing Director, followed by an overview of HI-MAG’s research activities presented by institute director Prof. Matthias Blüher.

HI-MAG is a joint initiative of Helmholtz Munich, Leipzig University and University of Leipzig Medical Center. Its research focuses on understanding how adipose tissue dysfunction leads to metabolic and vascular diseases. Through its translational bench-to-bedside approach, HI-MAG combines fundamental research with clinical studies across all stages of life. The institute’s goal is not only to develop new therapeutic concepts for people living with obesity but also to identify opportunities for prevention early in life.

“HI-MAG demonstrates the great value of strong scientific partnerships. Together with Leipzig University and University of Leipzig Medical Center, we are able to advance outstanding research that addresses major health challenges and creates new opportunities for prevention and treatment,” said Dr. Michael Frieser.

A key highlight of the program was a presentation by Prof. Antje Körner, Head of Childhood Obesity and Metabolic Research at HI-MAG. She shared recent findings on metabolic complications in children with obesity and emphasized the importance of early intervention.

“We need to consider and address the origins of diseases such as obesity already in childhood. Understanding metabolic changes in childhood is essential if we want to reduce the burden of obesity-related diseases later in life,” said Prof. Körner.

Further presentations showcased HI-MAG’s vascular research and ongoing clinical studies investigating preventive approaches that could reduce the risk of metabolic diseases in children and adolescents. The presentations also highlighted the importance of longitudinal cohorts.

“Addressing complex questions in obesity and metabolic research requires access to well-characterized cohorts across the entire lifespan such as LIFE Child,” said Dr. Babett Gläser. “Long-term cohort studies provide an invaluable foundation for understanding disease development and identifying risk factors at an early stage.” The delegation also toured through the Clinical Trial Unit to learn more about the different clinical projects and visited HI-MAG’s metabolic chambers, a unique research facility that allows scientists to precisely study energy metabolism in both adults and children.

“The research presented at HI-MAG demonstrates how scientific excellence can contribute to addressing one of the most significant public health challenges of our time. What impressed me most is the institute’s long-term perspective: understanding disease mechanisms early, identifying individuals at risk, and developing concepts that enable prevention before illness occurs.” – Dr. Ulrike Poller

Prof. Matthias Blüher emphasized: “Our vision should be to prevent disease rather than treat its consequences. By identifying risk factors early and intervening at the right time, we have the opportunity to improve long-term health outcomes for future generations.”

The visit highlighted the importance of close exchange between science and policymakers to translate scientific discoveries into effective prevention strategies. Research at HI-MAG can help to pave the way toward a future in which prevention begins earlier, is more targeted, and ultimately more effective.

Elevated ADAMTSL4 Levels in Cachectic Patients with Colorectal and Lung Cancer

“We wanted to better understand which signals from the tumor trigger the breakdown of muscle and fat tissue,” says Dr. Mauricio Berriel Diaz, last author of the study and research group leader at the Institute for Diabetes and Cancer (IDC) at Helmholtz Munich. 

The team focused on ADAMTSL4, a protein released by tumor cells. In several mouse models of cancer cachexia, the researchers found elevated ADAMTSL4 levels in the blood. Higher ADAMTSL4 levels were also associated with greater weight loss and more pronounced cachexia in patients with colorectal and lung cancer.

To test whether ADAMTSL4 is indeed involved in the development of cachexia, the team specifically altered the amount of the protein in mouse tumor cells. When they switched off ADAMTSL4 production in tumor cells that normally induce cachexia, the animals lost significantly less muscle and fat mass. Conversely, when the researchers increased ADAMTSL4 production in tumor cells that otherwise do not cause cachexia, these cells formed cachexia-inducing tumors. 

“This allowed us to show that ADAMTSL4 is not merely associated with cachexia, but can actively drive the process,” says Dr. Juliano Machado, first author of the study and postdoc at the IDC.

ADAMTSL4 Locally Activates the TGF-β Signaling Pathway

In the next step, the team investigated how ADAMTSL4 exerts this effect. They found that the protein does not directly activate the breakdown of muscle and fat tissue, but rather acts through a known signaling pathway. On the surface of muscle cells, TGF-β1 – an important messenger for cell and tissue remodeling – is initially present in an inactive form. DAMTSL4 binds to a component of this dormant complex and thereby releases active TGF-β1. This then activates signaling pathways that promote protein breakdown in muscle cells and enhance fat breakdown in adipocytes.

This mechanism is particularly interesting for the development of potential therapies because directly blocking TGF-β is therapeutically challenging. The signaling pathway fulfills many important functions in the body; systemic inhibition could therefore be associated with considerable side effects. ADAMTSL4 may offer a way out of this dilemma: The protein is secreted by tumors, is elevated in cachexia, and appears to activate TGF-β locally in the affected tissues. 

“Instead of systemically blocking TGF-β itself, we could in the future try to specifically inhibit an upstream tumor factor – ADAMTSL4,” says Prof. Stephan Herzig, Director of the IDC. “This makes ADAMTSL4 a promising target for the development of new anti-cachectic therapies.”

Further Investigation of ADAMTSL4 as a Potential Therapeutic Target

At the same time, Berriel Diaz emphasizes that cancer cachexia is not a uniform process: “ADAMTSL4 levels are unlikely to be equally elevated in all patients; appetite regulation, inflammatory processes, and other tumor factors may also play a role.”

 The findings therefore also point toward personalized therapeutic strategies: In the future, it may be possible to identify patients with elevated ADAMTSL4 levels for whom targeted blockade of this signaling pathway could be particularly useful. 

“The results provide a basis for further investigating ADAMTSL4 as a therapeutic target,” Berriel Diaz concludes. “Looking ahead, it will be important to determine whether targeted inhibition of this factor can slow the loss of muscle and fat tissue in cancer cachexia.”

"M1 Cachexia Center" to Unite Munich's Cancer Cachexia Research

With the "M1 Munich Medicine Alliance", a new consortium is being established to bring together top-tier biomedical research in Munich. In its inaugural "Innovations for Patients" funding round, researchers at Helmholtz Munich – together with clinical partners at the Technical University of Munich (TUM) and Ludwig Maximilian University Munich (LMU) – secured substantial funding to establish the "M1 Cachexia Center". The center provides an important framework for developing new therapeutic approaches to cancer cachexia, an endeavor to which the present study will contribute.

Original Publication

Machado et al., 2026: Tumor-secreted ADAMTSL4 activates latent TGF-β1 to drive cancer cachexia. Cancer Discovery. DOI: 10.1158/2159-8290.CD-26-0045

The trials target different stages of this autoimmune disease – from a high risk of developing the condition to a recent diagnosis – and share a common goal: to slow the loss of insulin-producing beta cells.

In doing so, they bring findings from diabetes research directly into clinical application in patients. That this path can lead from research all the way to an approved therapy is illustrated by teplizumab, an agent that has been approved in Germany since January 2026.

The rationale behind all four trials is the same: large studies have shown that protecting and preserving beta-cell function is one of the most important immunomodulatory therapeutic targets in type 1 diabetes.

The clinical trials translate this insight into concrete treatment approaches – and, for the different disease stages, test which intervention can take effect at the right point in time.

Baricitinib – Protecting the Beta Cells

BARICADE DELAY and BARICADE PRESERVE are evaluating baricitinib, a Janus kinase (JAK) inhibitor already used in a range of autoimmune diseases. An earlier study showed that, following the onset of type 1 diabetes, baricitinib can preserve the function of insulin-producing beta cells for longer. These findings are now being advanced toward clinical application in two Phase 3 trials.
The two trials investigate whether the onset or progression of type 1 diabetes can be slowed with baricitinib:

• BARICADE DELAY examines whether, in individuals at high risk of type 1 diabetes (stage 1b or stage 2), baricitinib can delay or prevent the onset of clinical type 1 diabetes. This is a Phase 3 clinical trial.
• BARICADE PRESERVE investigates whether, in people with newly diagnosed type 1 diabetes, baricitinib can slow the progressive destruction of beta-cell function. This trial is likewise in Phase 3.

Further Immunomodulatory Approaches in Clinical Testing

As part of the INNODIA network, the study center is additionally involved in two new immunomodulatory trials, the SAFEGUARD and βETA PRESERVE trials. Both evaluate different agents with the aim of preserving beta-cell function for as long as possible after a diagnosis of type 1 diabetes, thereby enabling more favorable treatment – here, too, the focus is on translating promising approaches into clinical application.

• The SAFEGUARD trial investigates whether the drug SAB-142 can slow the loss of insulin-producing cells in the pancreas. This trial is in Phase 2b.
• The βETA PRESERVE trial examines whether the agent teplizumab leads to improved glycemic control and whether it enables people with type 1 diabetes to require less insulin. Teplizumab has been approved since January 2026 and may help preserve the body’s own insulin production for longer. This is a Phase 3 clinical trial.

Who Can Take Part in the Trials?

Families and other interested individuals can find detailed information on inclusion and exclusion criteria on the respective trial websites. Some key points:

• BARICADE DELAY: individuals aged 2–35 at high risk of type 1 diabetes. More info here.
• BARICADE PRESERVE: individuals aged 2–35 diagnosed with type 1 diabetes within the past 3 months. More info here.
• βETA PRESERVE: individuals aged 1–25 diagnosed with type 1 diabetes within the past 2 months. More info here.
• SAFEGUARD: individuals aged 12–40 diagnosed with type 1 diabetes within the past 100 days. More info here.

Further clinical trials on type 1 diabetes can be found at diabinfo.de.

BARICADE DELAY and BARICADE PRESERVE are conducted by Eli Lilly and Company, the βETA PRESERVE trial by Sanofi, and the SAFEGUARD trial by SAB Biotherapeutics.

Clinical Trials: The Path from Research to Therapy

Learn more about how Helmholtz Munich, together with clinical partners, deliberately translates research findings into new therapies:

 Translation: Where Medical Research Reaches People.
 

With the successful acquisition of these two MSCA Postdoctoral Fellowships, Helmholtz Munich further reinforces its international research environment and its commitment to supporting early career researchers through competitive European funding programs.

Both fellowships run for a duration of two years and strengthen Helmholtz Munich’s research activities in functional genomics, neuroscience, and metabolic disease.

EvoNeuHance: Gene Regulation in Early Brain Development

Frömel, a researcher in the Brain Epigenomics Research Unit at the Stem Cell Center, conducts his MSCA project EvoNeuHance under the supervision of Dr. Boyan Bonev (Brain Epigenomics, BEG). The project focuses on regulatory DNA elements known as enhancers, which play a central role in controlling gene activity during brain development.

EvoNeuHance investigates how changes in enhancer sequences across different primate species, together with cell specific regulatory factors, shape gene regulation during early neurogenesis. By systematically comparing enhancer activity across species and cell types, the project aims to uncover fundamental principles of cis  and trans regulatory interactions that contribute to the evolution of the primate brain.

The findings are expected to advance the understanding of gene regulatory mechanisms underlying brain development and evolutionary change.

BetaSpReg: RNA Processing in Pancreatic Beta Cells and Diabetes

Montaser carries out his MSCA fellowship project BetaSpReg at the Institute for Diabetes and Organoid Technology (IDOT) of the Helmholtz Diabetes Center, supervised by Prof. Matthias Hebrok. The project addresses diabetes mellitus, a disease characterized by the progressive loss of functional insulin producing beta cells.

BetaSpReg focuses on alternative splicing, a key mechanism of gene regulation that generates transcript and protein diversity. The project investigates how RNA binding proteins regulate splicing in human beta cells and how disruptions in these processes may contribute to beta cell dysfunction under diabetogenic stress.

By combining genome editing, transcriptomic analyses, and functional assays in human stem cell derived and primary islet models, the project aims to identify regulatory networks essential for maintaining beta cell function. In the long term, the results may open new avenues for RNA based therapeutic strategies in diabetes.

About MSCA Postdoctoral Fellowships

The MSCA Postdoctoral Fellowships are among the European Union’s flagship funding instruments for postdoctoral researchers, combining independent research projects with structured training and career development measures.
The program aims to support the career development of outstanding researchers, foster international mobility, and enhance scientific excellence across Europe. The fellowships are awarded through a highly competitive Europe-wide selection process.

The Receptor “Inceptor” as the Starting Point for a New Therapy

The number of people with diabetes is rising worldwide. As diabetes progresses, the insulin-producing cells of the pancreas gradually lose their function, stop responding to insulin, and eventually die.

Current medications cannot halt the progression of the disease; they can only treat its symptoms. This is exactly where Lickert's BetaProtect project comes in: it builds on the discovery of the insulin-inhibitory receptor "Inceptor" by Lickert and his team.

Next Step Toward Clinical Application

Building on promising results in mouse models, the team aims to develop a novel therapy for type 2 diabetes that could, ideally, even reverse the course of the disease. When the researchers blocked the receptor in mice, the cells responded better to insulin, remained functional longer, and even regenerated. 

With the support of the ERC Proof of Concept Grant, the spin-off company Viacure aims to leverage these basic research findings for the preclinical and clinical development of a therapy.

“This award is a tremendous honor and a recognition of the work of my entire team. It highlights the importance of long-term, interdisciplinary research to better understand the causes and consequences of obesity and to sustainably improve care for affected children and their families,” says Prof. Körner. “Every child deserves the opportunity to live a healthy life. Research helps us identify risks at an early stage, prevent complications, and create new perspectives for affected families.”

Körner’s research has been instrumental in identifying early childhood as a critical window for the development and manifestation of obesity. Her work focuses on understanding the biological changes in adipose tissue that are linked to metabolic complications. In addition, her team has developed novel approaches to more accurately predict the risk of severe obesity-related diseases, including type 2 diabetes.

Among her landmark achievements is the discovery of a previously unknown genetic cause of obesity. Körner has published more than 250 original scientific papers and has received numerous national and international awards. She has secured more than €11 million in competitive research funding, including grants from the European Union, the German Research Foundation (DFG), and the German Federal Ministry of Education and Research (BMBF).

A defining feature of her work is its integrative and translational approach. Körner combines experimental basic research with clinical, epidemiological, and genetic studies, enabling scientific discoveries to be translated into improved patient care. This approach is supported by strong research networks and unique infrastructures in Leipzig, many of which she helped establish.

Regional and national initiatives such as the Leipzig Center of Metabolism (LeiCeM) Cluster of Excellence, the German Center for Child and Adolescent Health (DZKJ), the LIFE Child cohort, and HI-MAG provide an outstanding scientific environment for investigating the origins and progression of obesity across the entire lifespan.

Awards and Honors

Sächsische Akademie der Wissenschaften, Leipziger Wissenschaftspreis, EASO-Novo Nordisk Foundation Obesity Prize for Excellence 2024 
 

“Until now, FGF21 has primarily been viewed as a hormone of energy metabolism,” says Prof. Timo D. Müller, Director of the Institute for Diabetes and Obesity (IDO) at Helmholtz Munich and senior author of the study. “Our results now show that FGF21 can also amplify the cellular response to protein folding stress.”

To investigate the mechanism in more detail, Müller’s team analyzed the molecular environment of the FGF21 receptor β-klotho. This revealed that FGF21 is linked to protein folding, the ER stress response, and sulfide signaling. Particularly striking was its proximity to enzymes involved in generating sulfide signals. Further experiments showed that FGF21 induces enzymatic sulfide production and thereby supports both the UPR and the ISR.

A key point is that FGF21 does not trigger this stress response itself. Instead, it amplifies the response under conditions of cellular stress. When the enzymatic production of sulfide signals is inhibited, FGF21 largely loses its effect; conversely, its action can be partially mimicked by a compound that releases hydrogen sulfide.

“Our data point to a new signaling pathway through which FGF21 supports the cellular stress response,” says Dr. Gerald Grandl, first author and co-corresponding author of the publication. “The study shows not only that FGF21 is linked to cellular stress, but above all by which mechanism this occurs. This gives us a better understanding of how metabolic regulation and cellular protective programs interact.”

The team observed these effects in cell cultures, liver tissue, and mouse models. At the same time, the researchers found that FGF21 depends on the receptor β-klotho for its action. Without this receptor, its influence on the stress response was lost. Overall, the study expands our understanding of FGF21: not only as a metabolic hormone, but also as a modulator of cellular stress adaptation.

“Our study is basic and preclinical research,” Müller emphasizes. “It does not provide direct clinical evidence for new therapies. However, FGF21 has long been regarded as an interesting target in metabolic research, including in the context of metabolic liver disease. Our new findings provide additional mechanistic support and may help guide translational approaches more precisely in the future.”

Original Publication

Grandl et al., 2026: FGF21 reduces ER-stress by enhancing the Unfolded Protein- and Integrated Stress Response through increased Sulfide Signaling. Cell Metabolism. https://doi.org/10.1016/j.cmet.2026.05.011

For the screening, a small blood sample is taken at participating pediatric practices and analyzed in the laboratory for islet autoantibodies. The researchers define an early stage as the confirmed presence of at least two different islet autoantibodies in two consecutive blood samples. In stage 1, blood glucose levels are still normal; in stage 2, the first signs of impaired glucose metabolism appear. Only stage 3 corresponds to clinical type 1 diabetes where insulin is required.

Most Children With Early-Stage Type 1 Diabetes Do Not Have a Family History of the Disease 

At the first screening, 590 children were found to have early-stage type 1 diabetes – corresponding to around 0.3 percent of the children screened. During follow-up, 212 of these children progressed to stage 3 type 1 diabetes. This represents 81 percent of the children who went on to develop clinical type 1 diabetes. After five years, the probability of progressing from an early stage to clinical type 1 diabetes was 36.2 percent. The research showed that while children with a first-degree relative with type 1 diabetes have a higher risk of developing type 1 diabetes, most of the children who develop stage 3 type 1 diabetes have no family history of the disease. Therefore, screening should not be limited to children with a family history of type 1 diabetes. Additionally, once an early stage has been diagnosed, the researchers observed no differences in disease progression in children with and without a family history. 

“These data show that screening in the general population makes sense,” says Dr. Christiane Winkler, who leads the Fr1da team at Helmholtz Munich and is first author of the study. “If we only test children with a family history of type 1 diabetes, we miss the majority of children who later develop stage 3 type 1 diabetes.”

A new finding is that the disease progresses at a similar rate across stages. The progression to advanced stages was around 20 percent every year in children who had stage 1 or stage 2 disease. 

“This is the first real evidence indicating that the disease process in the pancreas is happening from the outset of autoimmunity and potentially transforms our approach to the timing of therapies.” says Prof. Anette-Gabriele Ziegler, Director of the Institute of Diabetes Research at Helmholtz Munich and principal investigator of the study.

A second screening also proved important. Children were initially screened at an average age of 3 years. In more than 11,700 children who initially tested negative, the test was repeated around 3 years later. This identified 29 additional children with early-stage type 1 diabetes. Hence, rescreening identified new early-stage cases almost as frequently as at first screening. 

“Some children develop islet autoantibodies a little later in childhood,” says Winkler. “That is why we recommend a second test after a few years.” 

Diabetes Screening Is Feasible for All Children

For families, a positive screening result does not mean that the child already has diabetes symptoms or needs insulin immediately. Families receive information, education, and access to specialized diabetes centers. There, an oral glucose tolerance test is used to assess how stable the child’s metabolism still is. Regular follow-up examinations then take place. The goal is to detect the transition to stage 3 type 1 diabetes early and to prevent diabetic ketoacidosis whenever possible. 

“The Fr1da study has been instrumental in investigating general population type 1 diabetes screening,” says Anne Koralova, Program Officer at the Helmsley Charitable Trust. “At Helmsley, we support Fr1da because identifying type 1 diabetes early improves long-term health outcomes.”

The Fr1da data are also relevant for new prevention strategies. Disease-modifying therapies – treatments that can influence the course of the disease and delay the onset of stage 3 type 1 diabetes – require an early diagnosis. At the same time, the data show how quickly children progress from one stage to the next, providing an important basis for future studies. In the long term, Fr1da aims to help bring early detection into routine care. 

“The study shows that the disease process is the same in children with and without a family history of type 1 diabetes. This not only means that screening is implementable in the general population, but that therapies shown to be effective in one group will be effective in the other,” says Ziegler. “Our goal is for such screening to be offered to all children in the future, not only to individual risk groups”. 

“The ability to detect type 1 diabetes early through screening and monitoring is a significant breakthrough with vast potential to reach a broad population and change the course of the disease for those who will develop it. It is a cornerstone of Breakthrough T1D’s efforts to accelerate cures for type 1 diabetes,” said Esther Latres, Ph.D. Senior Vice President of Research at Breakthrough T1D. “The Fr1da study has advanced our understanding of disease progression in children and demonstrates the value and practicality of early detection as part of routine clinical care, advancing clinical trials, and enabling access to emerging disease-modifying therapies.”

Original Publication

Winkler et al., 2026: Screening Children for Early-Stage Type 1 Diabetes. JAMA. DOI: 10.1001/jama.2026.6085

Funding

The Fr1da study was supported by Breakthrough T1D, LifeScience Stiftung, the Leona M. an Harry B. Helmsley Charitable Trust, the Deutsche Diabetiker Bund e.V., the Bavarian Ministry of Economic Affairs, Energy, and Technology, the EASD-Novo Nordisk Foundation Diabetes Prize for Excellence and the German Center for Diabetes Research (DZD e. V.).
 

A team led by Prof. Ali Ertürk, Director of the Institute for Biological Intelligence (iBIO) at Helmholtz Munich and Professor at the LMU, has now developed MouseMapper, a suite of foundation-model-based deep-learning algorithms designed to analyze whole-body biological imaging data. The framework automatically segments 31 organs and tissue types while quantitatively mapping nerves and immune cells throughout the body, enabling comprehensive multi-system analysis in intact mice.

“MouseMapper is built on a foundation model, which means it generalizes far beyond the data it was originally trained on,” says Ying Chen, co-first author of the study. 

Looking Inside an Entire Transparent Mouse

To create whole-body maps, the researchers labeled nerves and immune cells in mice with fluorescent markers visible under the microscope. They then used tissue-clearing techniques to render the animals transparent while preserving the fluorescent signals, allowing imaging deep inside intact bodies.

Using specialized light-sheet microscopy, the team captured detailed three-dimensional images of entire mice, producing datasets containing tens of millions of cellular structures across organs and tissues. MouseMapper then analyzed these data automatically, identifying nerves, immune-cell clusters, and anatomical regions throughout the body.

This allowed the researchers to determine precisely where inflammation and structural damage occur across different tissues – including fat, muscle, liver, and peripheral nerves – without requiring researchers to preselect specific regions of interest.

New Insights Into Obesity, From Mouse to Human

To investigate how obesity reshapes the body, the researchers fed mice a high-fat diet that induced obesity and metabolic dysfunction similar to that observed in humans. Applying MouseMapper revealed widespread changes in both immune-cell organization and nerve architecture across the body. 

One of the most striking findings was a structural change to part of the trigeminal nerve, a major facial nerve that is responsible for facial sensation and motor functions. In obese mice, these sensory nerves had far fewer endings and branches, suggesting a loss of normal nerve function. Behavioral experiments further showed that the animals responded less to sensory stimulation than lean mice, linking the structural damage to impaired sensory function.

The researchers next examined the trigeminal ganglion, the structure containing the cell bodies of facial sensory neurons. Using spatial proteomics, they identified molecular alterations associated with nerve remodeling and inflammation. Remarkably, many of the same molecular signatures were also detected in trigeminal tissue from people with obesity, suggesting that the obesity-associated nerve alterations observed in mice also occur in humans.

“We revealed previously unknown structural and molecular changes in the trigeminal ganglion and its facial branches, and the same molecular signature was conserved in human tissue. This kind of finding simply cannot emerge from studying one organ at a time,” says Dr. Doris Kaltenecker, senior scientist at the Institute for Diabetes and Cancer (IDC) at Helmholtz Munich and first author of the study.

A Platform for Studying Systemic Disease

Beyond obesity, the researchers believe MouseMapper could transform the study of complex diseases that affect multiple organs systems simultaneously, including diabetes, cancer, neurodegeneration and autoimmune disorders. Unlike earlier methods focused on selected organs or tissues, MouseMapper provides an integrated whole-body analysis platform capable of identifying disease “hotspots” throughout the organism.

The team has made whole-body datasets publicly available online, allowing scientists worldwide to explore obesity-associated changes across tissues and organ systems.

“Our goal is to create a comprehensive framework for understanding how diseases affect the body as an interconnected system,” says Ali Ertürk. “Our long-term vision is to build truly realistic digital twins of mice in health and disease: cell-level atlases that we can query, perturb and screen in silico computationally. That would let us pinpoint the earliest changes a disease causes, design interventions to prevent them, and accelerate the discovery of new treatments while reducing the number of physical experiments we need to run.”

Original publication

Kaltenecker et al., 2026: A deep-learning framework reveals whole-body perturbations at cell level. Nature. DOI: 10.1038/s41586-026-10535-2 

Four Funded Projects with Helmholtz Munich Participation

• Among the selected projects are four initiatives with significant involvement from Helmholtz Munich:
• Neuronal Repair in Cerebrovascular Disease (Principal Investigator: Prof. Magdalena Götz) 
• M1 Cachexia Center (M1CC) (Principal Investigator: Prof. Stephan Herzig) 
• VISTA – Vision Restoration via Synthetic Enhancers and Targeted AAVs (Principal Investigator: Dr. Boyan Bonev) 
• MIRAGE – Multimodal Imaging Resource Platform for Accelerated Gene Therapy Evaluation (Co-Principal Investigator: Prof. Ali Ertürk, Dr. Christoph Gruber) 

The projects address diseases of major medical and societal importance, including cancer, cardiovascular diseases, metabolic disorders, neurodegenerative diseases, and vision loss. At the same time, they reflect the breadth of Munich’s biomedical research landscape, spanning innovative therapeutic strategies, advanced imaging technologies, and novel diagnostic approaches.

„As a research center, our task is to further strengthen the bridge between the laboratory and the clinic. Only then can personalized medicine realize its full potential and lead to tangible improvements for patients. The M1 Munich Medicine Alliance is an outstanding example of the successful collaboration between leading institutions in Munich. I am therefore particularly pleased that the funded projects have been announced and that the implementation of concrete innovations is now being advanced,” says Prof. Martin Hrabě de Angelis, member and spokesperson of the executive board (acting) at Helmholtz Munich, member of the board of the German Center for Diabetes Research (DZD), and founding member of the M1 Munich Medicine Alliance.

Driving Translation

The “Innovations for Patients” funding line combines two complementary funding formats: Flagship Projects, which support highly ambitious research initiatives with strong innovation potential, and Translational Groups, which advance patient-oriented research towards clinical application. In this way, the program supports both established investigators and researchers at early and mid-career stages.

In addition, the alliance is investing in new research infrastructures, including a Munich Clinical Studies Center and a Munich Medical Data Center. These initiatives aim to further strengthen the integration of research and clinical practice and enhance Munich’s position as a leading biomedical research hub. With the first funding period, the alliance is also laying the foundation for a long-term translational research structure that will further strengthen Munich’s position as an internationally recognized medical hub.

Further Information

• M1 Munich Medicine Alliance: https://m1.bayern/ 
• Photo gallery: https://www.stmwk.bayern.de/ministerium/bilder.html 

About the Friedrich Arnold Gries Award

The Friedrich Arnold Gries Award is presented to actively conducting medical researchers and scientists for outstanding, therapeutically relevant achievements in the field of microvascular and macrovascular complications of diabetes, as well as closely related diseases such as fatty liver disease. The award honors several outstanding publications or a coherent body of scientific work that has contributed to advances in the prevention, prognosis, and organ protection of diabetes.

Further information

• Institute for Diabetes and Cancer

• Division Diabetes Complications - Herzig Lab

• Focus Topic: Diabetes Research at Helmholtz Munich

This is where the work of Michele Solimena, Director of the Institute for Pancreatic Islet Research (IPI) at Helmholtz Munich, Speaker Paul Langerhans Institute Dresden of the German Center for Diabetes Research (PLID-DZD) and Professor of Molecular Diabetology at TU Dresden, begins. For decades, the cell biologist has been investigating the fundamental mechanisms of insulin production, storage, and secretion. His goal: to understand the biological processes in beta cells so precisely that new approaches for prevention and therapy become possible.

Pioneering work at the smallest units of insulin production

At the center of Solimena’s research are the insulin-secretory granules – tiny cellular structures in which insulin is stored and released when needed. His work has made a decisive contribution to deciphering their function.

He was able to show how beta cells dynamically adapt their insulin production by regulating the formation of new granules. In addition, he identified molecules that control the stability and translation of messenger RNAs for insulin and other important proteins.

Further fundamental findings concern the aging of these granules as well as their transport within the cell – processes that significantly influence how efficiently insulin is secreted.

Using state-of-the-art imaging techniques, his team was also able to map the microtubule network of the beta cell, which is considered a milestone in understanding cellular transport processes.

Bridge between basic research and clinical practice

Another focus of Solimena’s work lies in linking molecular basic research with clinical questions. By studying islet cells from living donors, his team was able to track in detail how beta cells change along the progression from normoglycemia to type 2 diabetes.

These findings provide important starting points for new diagnostic and therapeutic strategies, for example for the early detection of disease processes or for the targeted restoration of beta cell function.

While still a postdoc in the De Camilli’s lab, Solimena discovered the occurrence of autoantibodies against glutamic acid decarboxylase 65 (GAD65) in subjects affected by type 1 diabetes and in stiff-person syndrome, a rare neurological disorder affecting GABAergic neurons in the central nervous system. Today anti-GAD65 autoantibodies are the single most widely used autoantibody biomarker for diabetes classification.

Science with a clear vision

His research approach is shaped by a simple but decisive conviction: 

“We must understand how beta cells work, because their failure is the ultimate cause of all forms of diabetes,” says Solimena. 

This mindset has shaped his scientific work for decades – and has enabled numerous groundbreaking discoveries.

Recognition of an outstanding lifetime achievement

“With the awarding of the Paul Langerhans Medal, the German Diabetes Society honors a scientist who has decisively shaped our understanding of beta cell biology,” said Prof. Martin Hrabě de Angelis, member and spokesperson of the executive board (acting) at Helmholtz Munich and member of the board of the German Center for Diabetes Research (DZD). “His work has laid the foundation for new strategies for the prevention and treatment of diabetes – and has had an impact far beyond research.”

To the Original Press Release from the DZD

Press Releases 2026 | DZD - Deutsches Zentrum für Diabetesforschung

Further information

https://www.helmholtz-munich.de/diabetes-center/ipi/michele-solimena 
https://www.helmholtz-munich.de/ipi/research-groups/solimena-lab 

New Perspectives Through Multi-Organ and Multi-Omics Analyses

The incidence of T1D is rising worldwide, with more than half of new diagnoses occurring in adulthood. While most research focuses on the development of the autoimmune disease in children, disease progression in adults remains less understood. In addition, organs functionally connected to the pancreas such as the intestine may also be involved in the autoimmune process, which remains to be explored. 

Teresa Rodriguez-Calvo’s team is investigating which immune cells, inflammatory processes, and molecular signaling pathways are active in the pancreas and duodenum in T1D. The aim is to identify disease signatures that distinguish childhood- and adult-onset T1D and may reveal new targets for personalized immunomodulatory therapies. Spatially resolved analyses will further show how relevant cell types are distributed and interact along the gut–pancreas axis.

Granins – Key Proteins for Early Detection and Monitoring of T1D

The second funded project focuses directly on beta cells. Essential for their insulin production are granins (chromogranins and secretogranins), a cellular component supporting insulin granule formation, maturation and secretion. The researchers will examine how granins differ in pancreases without T1D, those that are autoantibody positive, and those that have been clinically diagnosed with T1D, how beta and alpha cells respond under cellular stress, and whether these changes can be detected in the blood as early biomarkers. 

“These projects let us explore type 1 diabetes from multiple angles, spanning the insulin-producing beta cell to inter-organ communication, to uncover patterns that could lead to improved diagnostics and more personalized treatments in the future,” says Teresa Rodriguez-Calvo.

Fewer Cases of Diabetic Ketoacidosist

Since 2015, pediatric practices in the participating federal states have tested more than 240,000 children as part of the Fr1da study. Researchers identified an early stage of type 1 diabetes in more than 730 children. A recent analysis shows that early diagnosis can be clinically relevant: Only 2.5 percent of the children identified through Fr1da developed diabetic ketoacidosis at the onset of the disease, a dangerous metabolic complication caused by severe insulin deficiency. Without early diagnosis, this rate has been above 20 percent in Germany for years.

If Fr1da detects an early stage of type 1 diabetes in a child, the team invites the family for further examinations at a pediatric diabetes clinic. There, physicians determine which disease stage the child is in: still normal glucose metabolism, first metabolic changes, or already manifest type 1 diabetes. Based on this, they establish a prevention plan with follow-up appointments; children with manifest type 1 diabetes are then referred to standard care.

Fr1da Creates Time for Education, Prevention, and Treatment

“With Fr1da, we do not first see type 1 diabetes when children become acutely ill, but much earlier,” says Prof. Anette-Gabriele Ziegler, Director of the Institute of Diabetes Research at Helmholtz Munich and scientific lead of the Fr1da study. “This creates time for education, prevention, and, where appropriate, medical intervention, while also helping us better understand the causes and course of the disease.”

To do this, Fr1da relies on a network of pediatric practices, laboratories, and pediatric diabetes centers built up over many years. “Our experience over the past several years shows that Fr1da screening can be well integrated into the daily routine of pediatric practices and is very well accepted by families. I very much hope that we will succeed in transitioning Fr1da into selective care or even into standard care,” says Dr. Michael Hubmann, President of the Berufsverband der Kinder- und Jugendärzt*innen e.V., German Association of Paediatric and Adolescent Care Specialists (BVKJ).

One in 250 Children Develops Type 1 Diabetes

Type 1 diabetes is not a rare disease: in Germany, around one in 250 children develops it. With the expansion to 12 federal states, Fr1da will now reach a large proportion of the population, as Ziegler emphasizes: “Far more children now have the opportunity to take part in Fr1da.” At the same time, this step shows that early detection is becoming increasingly important not only scientifically, but also from a health policy perspective: in the long term, access to it should not depend on where a child lives.

To support the expanded Fr1da program, the team has established a second central laboratory in Dresden alongside the central laboratory in Munich. Families and practices are also supported by three regional coordination centers in Munich, Dresden, and Hanover. Further information is available at www.fr1da.de. Questions can also be directed to the Fr1da hotline at 0800 464 88 35 or by email at diabetes.frueherkennungspam prevention@helmholtz-munich.de

The new video series is aimed at individuals who want to take preventive action for their health as well as people with type 2 diabetes. It combines medically sound information with exercises that are easy to do at home, in the office, or on the go.

The series begins with two explanatory videos featuring Prof. Christine Joisten, a specialist in general medicine with a focus on sports medicine at the German Sport University Cologne. In the videos, she explains why exercise is so important for health and how even small changes can have a positive impact.

Scientific studies show that even a small amount of additional exercise in everyday life can produce measurable effects. Just a moderate increase in daily activity can help to improve health—especially in people who have previously been less active.

First Exercise Videos: An Easy Way to Get Started at Home

In addition to the explanatory videos, the first exercise videos are available to follow along with. The exercises are specifically designed for everyday use and can be performed without special equipment or prior knowledge.

The 5–10-minute videos include, among other things:

• Mobilizing exercises in a seated position to promote mobility and activation after long periods of sitting 
• Simple standing exercises to activate the whole body and improve coordination and circulation 

The exercises can be customized and performed at your own pace. The aim is to incorporate low-threshold exercise into everyday life—regardless of fitness level.

More Content to Follow

The newly released videos are the first in a multi-part series. In the coming months, further exercise videos will be added, focusing on different areas such as flexibility, strength, and endurance.

A Collaborative Project With a Scientific Basis

The video series is published by diabinfo.de, a joint service of Helmholtz Munich, the German Diabetes Center (DDZ), and the German Center for Diabetes Research (DZD).

The videos were developed and produced in close cooperation with the German Sport University Cologne. Under the expert guidance of Prof. Christine Joisten, the latest scientific findings from physical activity and health research are incorporated into the content.

Watch Now and Follow Along

The first explanatory videos and exercise videos are now available on diabinfo.de and the diabinfo YouTube channel.

Further information on the video series and the topic of exercise can be found at www.diabinfo.de.

Müller’s team therefore pursued the idea of an “address label with cargo”: the researchers chemically linked a well-established incretin active component to a second pharmacological component – the drug lanifibranor, a so-called pan-PPAR agonist. The incretin part binds to GLP-1 or GIP receptors on the cell surface and ensures that the hybrid molecule is taken up into the cell. Inside the cell, the second component binds to PPARs – “switches” in the cell nucleus that regulate genes involved in fat and sugar metabolism. The aim is for this additional metabolic effect to arise specifically in GLP-1R/GIPR- expressing cells, rather than throughout the body.

Low Dose via a “Trojan Horse”

Functionally, the hybrid molecule combines five drug targets in one: it activates two receptors on the cell surface (GLP-1R and GIPR) and additionally engages three PPAR “switches” inside the cell. Müller describes the principle as a “Trojan horse”: the incretin part opens the door; the “cargo” acts only once it is inside the target cell. “A major advantage is the amount,” says Müller. “Because the second component is not administered separately and systemically, but ‘travels along’ with the incretin part, it can be used at a dose that is orders of magnitude lower.” In this way, the drug gains efficacy without amplifying side effects through broad distribution across the body.

In laboratory mice with diet-induced obesity, the approach showed clear effects: “The animals ate less and lost more weight than under a GLP-1/GIP co-agonist without cargo,” says Dr Daniela Liskiewicz, group leader at IDO and co-first author together with Dr. Aaron Novikoff. “In the head-to-head comparisons shown, the effect was in part even stronger than with a GLP-1-only drug.” The study therefore suggests that the coupling is not merely “more of the same”, but measurably strengthens incretin activity – at least in mice.

Additional Metabolic Readouts Improve

It was not only body weight that changed: in the experiments, blood-glucose values improved and there were indications of better insulin action in the body. Put simply, insulin was better able to “channel” glucose from the blood into tissues, and the liver released less glucose into the bloodstream. At the same time, the researchers report that typical gastrointestinal side effects were comparable in their assessment to those of existing incretin therapies – and that, in the parameters examined, they found no indications of two feared issues associated with the coupled component, namely fluid retention and anaemia.

Beyond glucose metabolism, the mouse data also provided indications of additional, potentially favourable effects on the heart and liver. It is important to note that this is a preclinical study: whether the results will translate to humans remains open – also because the GIP receptor differs between mice and humans. “We see a principle with strong effects in the animal model – now the task is to optimise the approach for humans and move it towards the clinic,” says Müller. For that development, strong industry partners will be needed, he adds.

Original Publication

Liskiewicz et al., 2026: GLP-1R–GIPR–PPARα/γ/δ quintuple agonism corrects obesity and diabetes in mice. Nature. DOI: 10.1038/s41586-026-10427-5

“I am deeply honored to receive this award,” says Anette-Gabriele Ziegler. “This recognition reflects the collective efforts of many colleagues and collaborators working toward a future without type 1 diabetes.”

The award includes a monetary prize sponsored by Sanofi. Ziegler will also deliver the 58th Claude Bernard Lecture at the upcoming EASD Annual Meeting in Milan on Tuesday, 28 September 2026 at 9:00 AM, where she will present her most important scientific achievements.
 

Type 1 diabetes is a chronic autoimmune disease characterized by the immune-mediated destruction of insulin-producing beta cells. Although traditionally regarded as a childhood-onset condition, it is now increasingly recognized that type 1 diabetes can also manifest during adolescence and adulthood. Helmholtz Munich researchers have investigated the prevalence of early-stage type 1 diabetes in young adults, addressing an underexplored phase of the disease. The study was conducted through close collaboration between the Institute of Epidemiology (EPI) and the Institute of Diabetes Research (IDF), combining expertise in population-based epidemiology and the pathophysiology of diabetes.

The analysis included 1,377 participants from the long-running LISA and GINIplus birth cohorts, which follow individuals prospectively from birth into young adulthood, with assessments conducted up to 25 years of age. Blood samples were screened for islet autoantibodies using the methodology established in the Fr1da Study, including confirmatory testing to ensure high analytical specificity. 

Islet Autoantibodies Can Develop During Adolescence and Early Adulthood

The results show that approximately 1.2 percent of previously undiagnosed young adults tested positive for islet autoantibodies, including 0.2 percent of participants who met the criteria for early-stage type 1 diabetes – prevalence rates comparable to those observed in children – and an additional 1.0 percent who had a single autoantibody. Longitudinal analyses indicated that, while the majority  of the autoantibody-positive individuals had these markers by age 15 years, new development of islet autoantibodies occurred after this age. This underscores that early immunological signs of type 1 diabetes can emerge during adolescence and young adulthood.

The findings provide new evidence that early-stage type 1 diabetes occurs in the general adult population, highlighting the potential value of extending screening strategies currently focusing on children to include young adults, particularly in those who have not been previously tested in adolescence.

Original Publication

Standl et al., Prevalence of early-stage type 1 diabetes in young adults: a population-based cohort study. The Lancet Diabetes & Endocrinology. DOI: 10.1016/ S2213-8587(26)00034-3

Two examples highlighted the potential of translational research: 

• Prof. Björn Eskofier, Principal Investigator for Translational Digital Health Group at AI for Health at Helmholtz Munich and Director of the Institute for Artificial Intelligence in Medicine at LMU University Hospital Munich, demonstrated how artificial intelligence can make large volumes of health data usable – improving the understanding of disease mechanisms and enabling personalized prevention and treatment strategies.  
• Prof. Heiko Lickert, Director of the Institute of Diabetes and Regeneration Research (IDR) at Helmholtz Munich and Professor at the Technical University of Munich (TUM), illustrated how new findings in diabetes research are gradually translated into innovative therapeutic approaches – from molecular insights to clinical application.  

The presentations underscored that translation is not a single step but a continuous process that connects basic research, preclinical models, data-driven analysis, and clinical implementation. 

In the subsequent discussion, participants highlighted the importance of appropriate policy frameworks to accelerate the transfer of research findings into healthcare and enable patients to benefit from innovations sooner. 

With its Expert Hour, Helmholtz Munich provides a platform for direct exchange between science and politics – with the shared aim of making scientific breakthroughs impactful and bringing new solutions to the people who need them most. 

Type 1 diabetes is a chronic condition in which the immune system attacks the insulin-producing cells of the pancreas, leading to lifelong dependence on insulin therapy. The autoimmune process that ultimately results in the onset of the disease often begins early in life yet is typically detected only when symptoms appear. When diagnosis and treatment are delayed, this can escalate into a life-threatening medical emergency. A simple blood test can detect type 1 diabetes in its early stages, by identifying islet autoantibodies, thereby revealing the autoimmune activity associated with type 1 diabetes long before symptoms develop. Early detection offers a critical opportunity for monitoring, timely intervention, and improved patient outcomes.

In 2023, EDENT1FI was launched, with the aim of bringing type 1 diabetes screening and monitoring to Europe. Building on the foundation and success of the Fr1da study which pioneered early-stage type 1 diabetes screening in Bavaria, Germany, EDENT1FI has established screening programs in Czechia, Poland, and Portugal and has strengthened existing initiatives in Germany, Italy, the UK, Denmark and Sweden.

“Although it was initially uncertain whether the screening principles developed in Germany through the Fr1da study could be successfully applied in regions with entirely different healthcare systems, these programs have already proven highly successful. EDENT1FI’s success demonstrates that early-stage type 1 diabetes screening can be effectively implemented throughout Europe,” says Anette-Gabriele Ziegler, Co-Lead Coordinator of EDENT1FI, Work Package 1 (Screening) Lead, Investigator for Fr1da and Director of the Institute of Diabetes Research at Helmholtz Munich and Chair of Diabetes and Gestational Diabetes at the TUM University Hospital.

Screening settings varied across countries, with programs conducted in primary care, hospitals, schools, and homes. Despite these differences, EDENT1FI successfully harmonized islet autoantibody detection and standardized data collection and processing across countries. The initiative also introduced central laboratories and robust quality control processes throughout Europe, enabling the screening of more than 100,000 children and adolescents at a rate of approximately 6,500 participants per month.

“The expansion of screening programs to other European countries will protect more children against serious metabolic derailments associated with later diagnoses of diabetes,” says Prof. Peter Achenbach, Deputy Director of the Institute of Diabetes Research at Helmholtz Munich, Investigator for Fr1da and EDENT1FI in Germany.  

Supporting Children and Adolescents with Early-Stage Type 1 Diabetes

Participation in the EDENT1FI screening program requires only a few drops of blood. Families receive counseling and ongoing support throughout the process. Children and adolescents identified with early-stage type 1 diabetes are closely monitored and informed about opportunities for early intervention. By equipping families with knowledge and resources, EDENT1FI aims to reduce the burden of an unexpected onset of clinical diabetes and empower them to manage life with type 1 diabetes effectively. EDENT1FI’s goal is to screen 220,000 children and adolescents from the general population across Europe to identify those with presymptomatic type 1 diabetes.  

"Reaching 100,000 screened children is a major step for early-stage diagnosis of type 1 diabetes. With recently approved and future disease modifying therapies, diagnosing children earlier becomes even more meaningful. This milestone shows how collaboration is reshaping the future of type 1 diabetes care," explains Chantal Mathieu, Lead Coordinator of EDENT1FI and Professor at the Faculty of Medicine at KU Leuven.

New Therapy Highlights Importance of Early Detection 

In January 2026, the immunomodulatory drug teplizumab was approved in Europe for use in children aged eight years and older with presymptomatic type 1 diabetes (Stage 2). This approval underscores the importance of early detection programs like EDENT1FI. Through early detection, families and clinicians can consider interventions such as teplizumab to delay the onset of the disease. Additional therapies that may prevent or delay the onset of type 1 diabetes are currently being studied in clinical trials.

About EDENT1FI

EDENT1FI is a collaborative initiative involving 27 partners from academia, industry, and charitable organizations across 13 European countries. The project is funded by the Innovative Health Initiative (IHI) through Horizon Europe, with additional support from the Helmsley Charitable Trust, Breakthrough T1D, and other stakeholders. Launched in 2023, EDENT1FI focuses on detecting type 1 diabetes in children and adolescents before clinical symptoms appear, with the goal of improving early intervention, refining risk stratification, and enabling the development of innovative therapies.
www.edent1fi.eu 

“The ADA is pleased to recognize these individuals and the vital role they play in advancing our mission to prevent and cure diabetes and improve the lives of all people affected by diabetes. Their incredible contributions are moving us closer to a world free of diabetes and all its burdens,” said Charles “Chuck” Henderson, Chief Executive Officer of the ADA.

The award recipients will be honored during an awards ceremony at the ADA’s 2026 Scientific Sessions, taking place in June. The Scientific Sessions represent the world’s largest scientific meeting dedicated to diabetes research, prevention, and care.

About the American Diabetes Association

The American Diabetes Association (ADA) is a leading nonprofit health organization in the United States, focused on the prevention and treatment of diabetes as well as supporting people living with the condition.