CBMR International PhD and Postdoc Program

While recent pharmacological advances have transformed obesity treatment, achieving sustained weight loss remains a major clinical challenge. Many individuals discontinue current therapies due to side effects or limited long-term effectiveness, and weight regain is common once treatment stops. This points to a critical unmet need: developing novel, durable interventions that support long-term metabolic health without continuous pharmacological intervention.

This project explores an innovative therapeutic strategy aimed at reprogramming the biological mechanisms that defend against sustained weight loss. Inspired by emerging insights into central pathways that regulate body weight stability, we aim to engage alternative molecular systems capable of inducing lasting changes in energy balance. Preclinical findings from our lab suggest that modulating these pathways can produce persistent weight-lowering effects, offering a promising direction beyond conventional gut hormone-based therapies.

To identify novel therapeutic agents, we will deploy a multidisciplinary discovery pipeline that integrates selection-based screening technologies and next-generation protein design tools. These efforts will focus on developing molecules that selectively target a receptor complex implicated in long-term energy homeostasis. Lead candidates will undergo in vitro and in vivo evaluation in well-established preclinical obesity models to assess efficacy, durability, and safety.

By targeting mechanisms distinct from those engaged by current treatments, this project seeks to lay the groundwork for a new class of obesity therapeutics. If successful, the approach has the potential to overcome the limitations of existing drugs and deliver more effective, sustainable solutions for individuals living with obesity and related metabolic diseases.

Apply here.

This postdoctoral research project aims to uncover the molecular mechanisms by which exercise improves insulin sensitivity in individuals with Type 2 diabetes. Despite the success of GLP-1 receptor agonists, they do not address skeletal muscle insulin resistance, the primary site of glucose disposal. Exercise, a potent physiological insulin sensitizer, induces beneficial metabolic adaptations through energetic stress. However, the molecular transducers mediating these effects remain largely unidentified.

The project will leverage state-of-the-art CRISPR technologies to decipher key molecular nodes of the insulin sensitizing effect of exercise. Using both in vitro and in vivo models, the study will investigate candidate regulators. Functional validation will involve gene silencing, overexpression, and metabolic assays to assess their roles in glucose uptake and insulin signaling.

The candidate will work within a multidisciplinary team at CBMR, collaborating with experts in metabolism, bioinformatics, and clinical physiology. Access to CBMR’s enabling biology platforms and large-scale genetic datasets will support the identification of novel therapeutic targets and biomarkers.

Ultimately, this research bridges exercise physiology and translational medicine, aiming to inform the development of exercise-mimetic therapies and personalized interventions for managing Type 2 diabetes.

Apply here.

How can our understanding of precision medicine be enriched through a humanities approach to individual experiences of health? More specifically, how can a public exhibition enable visitors fruitfully to engage with that understanding? This postdoc enquiry lies at the hinge between these questions. It will be part of the engagement project Let’s Get Personal: a curatorial initiative based on a major new gallery that will explore personalized medicine in historical, social and cultural contexts. It will be hosted at Medical Museion: a university museum that combines public programming with an interdisciplinary research group.

Built on scientific research, more precise medical treatments and supporting health infrastructures, medicine is currently being thoroughly personalized. These recent innovations have potentially ground-breaking implications for the future of health and medicine; but there is, and always has been, a tension between actual experiences of being sick and less personal attempts to understand and treat diseases scientifically. Let’s Get Personal is a form of ‘public enquiry’ that combines collaborative and humanities-oriented research with stakeholder workshops, live public events and a major exhibition.

The Postdoc will be integrated into three project stages: (a) development of themes and pilot initiatives; (b) curatorial production of a major new thematic gallery (late-2027 launch); and (c) the use of an exhibition as a platform for further public events, stakeholder workshops, podcasts, and visitor evaluation. Matching those stages, the Postdoc’s approach will evolve methodologically from literature reviews and companion enquiries through investigations around exhibition curation and finally on to observations and analysis of visitor/stakeholder engagement.

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The basic focus of the Schwartz Group has for many years been on GPCR structure, function, and dynamics originally based on peptide hormone and neuropeptide receptors but has over the last decade moved into GPCR sensing of nutrient, microbial and metabolic stress metabolites. However, in the present project we are moving back to our roots to study how gut and pancreatic peptide hormones signal from the periphery to the brain, and how the different peptide hormones and their receptors interact in the control of key populations of neurons in particular in the dorsal vagal complex of the brainstem. Here, afferent vagal neuronal signaling and hormonal sensing from the gut, liver, adipose etc. is integrated to control signaling to other CNS centers such as the hypothalamus as well as efferent vagal signaling to the periphery. Importantly, we have recently obtained novel insight into key receptor systems and their interactions, which appears to totally change our understanding of the function of the central vagal relay system.

The project aims at characterizing these novel mechanisms by use of a combination of genetic rodent models, proprietary pharmacological tools and e.g. immunoneutralization in an interdisciplinary close collaboration with the Gerhart-Hines, Clemmensen and Pers groups as well as the Computational Chemistry Unit, all at CBMR, and with the Martin Myers Neuroscience lab in Michigan. The project aims at establishing novel means to improve not only the efficacy but – importantly – also the tolerability of GLP-1 and amylin-based anti-obesity drugs.    

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Physical activity is a cornerstone of metabolic health, yet the molecular mechanisms through which exercise improve muscle function and insulin sensitivity remain incompletely understood. This PhD project aims to identify and functionally characterize novel proteins that mediate the beneficial effects of exercise on skeletal muscle health and whole-body metabolism.

Building on our recent work, where deep proteomic profiling of human skeletal muscle and plasma identified hundreds of proteins responsive to exercise training, the candidate will focus on determining the causal roles of selected proteins. Due to the large number of candidates and the limitations of mammalian models for high-throughput functional testing, the project will leverage Drosophila melanogaster as a genetically tractable in vivo model. The candidate will use a combination of bioinformatics, tissue-specific RNAi screening, and metabolic phenotyping to identify conserved regulators of muscle metabolism and insulin sensitivity.

The project is a collaboration between the Functional Proteomics in Metabolism Group at the Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR) and the Endocrinology and Metabolism Lab of Prof. Kim Rewitz at the Department of Biology, University of Copenhagen. The candidate will be part of an interdisciplinary environment that brings together expertise in proteomics, molecular biology, functional genomics, and computational biology.

The project offers an exciting opportunity to contribute to the discovery of novel molecular targets linking exercise to metabolic health, with implications for tackling insulin resistance and type 2 diabetes.

Apply here.

Adipose tissue is increasingly recognized as an interactive endocrine organ central to whole-body metabolic homeostasis. In obesity, expansion of white adipose tissue occurs through both an increase in cell size (hypertrophy) and number (hyperplasia). While this expansion is initially adaptive, prolonged hypertrophy leads to inflammation, fibrosis, and insulin resistance. One emerging concept is that the balance between adipocyte expansion and the supporting neurovascular network is crucial for maintaining healthy adipose tissue function.

This PhD project aims to explore how secreted peptides from adipocytes regulate neurovascular remodeling during adipose tissue expansion and how this contributes to metabolic health. Using a multi-omics approach, we have established a library of peptides released from human adipocytes, which are ranked and shortlisted for relevance in a neurovascular context using computational approaches. The project will combine high-content imaging, transcriptomics, and in vitro co-culture systems to assess the effects of top candidate peptides on angiogenesis and neurite outgrowth.

Building on these in vitro insights, in vivo CRISPR/Cas9 combined with AAV-mediated models will be used to modulate key peptides in adipose tissue, with comprehensive phenotyping to assess their impact on adipose remodeling, glucose metabolism, and inflammation. Advanced 3D imaging and whole tissue clearing will allow visualization of neurovascular architecture in response to these interventions.

This project offers an exciting opportunity to work at the interface of molecular biology, metabolism, and tissue engineering, with the goal of identifying novel therapeutic targets for improving adipose tissue function and cardiometabolic health in obesity.

Apply here.

AMP-activated protein kinase (AMPK) is a central regulator of cellular energy homeostasis, activated in response to energetic stress and coordinates metabolic pathways to maintain cellular energy balance. AMPK has long been considered a promising therapeutic target for cardiometabolic diseases due to its beneficial effects, including stimulation of insulin-independent glucose uptake, enhancement of fatty acid oxidation, and improved insulin sensitivity in skeletal muscle. However, despite intensive efforts, the development of pharmacological agents that activate AMPK without eliciting adverse effects associated with systemic AMPK activation remains a significant challenge.

The primary objective of this PhD project is to elucidate the molecular mechanisms by which AMPK regulates physiological processes in metabolic tissues through specific post-translational modifications (PTMs), such as reversible phosphorylation by kinases and phosphatases. The project aims to develop/employ novel strategies to manipulate or mimic these regulatory mechanisms applying the targeted PTM technologies (e.g., proteolysis-targeting chimeras) and/or small-molecule modulators in cellular and tissue/preclinical models. We adopt a collaborative and interdisciplinary approach, integrating in-depth biochemical analyses of AMPK and its mutants in vitro - in partnership with structural biologists and proteomics experts -with extensive cell culture experiments utilizing gene-edited cell lines for signaling studies. In addition, in vivo investigations using genetically modified and drug-treated mouse models will be conducted to explore the role of AMPK in glucose homeostasis and energy metabolism.

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The bidirectional communication between the adipose tissue and the central nervous system is crucial for sustaining metabolic homeostasis and health. We recently identified a novel secretory cell type in mouse and human adipose tissue that we believe to play a central role in this fat-brain signaling axis. In this project, we would like to interrogate the role of these cells in modulating systemic energy homeostasis. Additionally, we will functionally investigate what specific factors or signals these cells are releasing and explore the therapeutic potential of select secreted factors for mitigating metabolic disease. Given that we find this cell population to be linked to the control of energy-expenditure, this project holds the potential to identify therapeutic candidates that would ideally complement the current appetite-suppressing obesity drugs.

During the project, you will work with primary mouse and human adipocytes, leverage newly generated genetic mouse models, employ novel pharmacological and viral targeting strategies, and learn advanced metabolic phenotyping techniques. The project is co-supervised by Associate Professor Camilla Schéele, who is a world leader in human adipose physiology. You will also have the opportunity to work with an international team of collaborators both at CBMR (Assoc. Prof. Brice Emanuelli and Prof. Ruth Loos) and abroad (Prof. Patrick Seale, Prof. Henning Fenselau, and Assoc. Prof. Lawrence Kazak).

Apply here.