Max Planck Institute for Metabolism Research

Max Planck Institute for Metabolism Research

The human brain analyses nutrient-related and hormonal signals of the body periphery and controls by hunger and saturation induction the energy homeostasis. This central nervous control is complex and until now not fully understood. Research at the Max Planck Institute for Metabolism Research (formerly: Max Planck Institute for Neurological Research) is dedicated to deciphering these most intricate neuro-circuits. The researchers use multimodal and molecular imaging to describe intact but also abnormal metabolic regulation. Once neuronal signaling pathways of the metabolism are completely understood both in healthy people and patients, new molecular therapies for diseases such as type 2 diabetes and obesity may be developed in the long run.


Gleueler Str. 50
50931 Köln
Phone: +49 221 4726-0
Fax: +49 221 4726-298

PhD opportunities

This institute has an International Max Planck Research School (IMPRS):

IMPRS on Ageing

In addition, there is the possibility of individual doctoral research. Please contact the directors or research group leaders at the Institute.

Department Neuronal Control of Metabolism

Award for excellence in Alzheimer research

Researchers honoured for their findings on brain cleansing and its importance in dementia

Specialised nerve cells increase the appetite for high-fat foods

Fat activates nociceptin neurons in the hypothalamus of mice

Award for therapy for muscle weakness

Adrian Krainer and Richard Finkel receive the K. J. Zülch Prize for their development and testing of a drug for spinal muscular atrophy

Improved diabetes in spite of obesity

Intervention in fat metabolism improves fatty liver disease and glucose metabolism of obese mice

Insulin protects against colorectal cancer

Signaling pathway strengthens the intestinal barrier

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The role of neurotransmitters in mediating hunger and satiety

2019 Fenselau, Henning

Medicine Neurosciences

The hypothalamus works as a key regulatory center of food intake. Since many different neurons are involved in this regulation, it has so far been virtually impossible to understand the underlying neural circuits of this brain area and their connections. Using cell-type-specific genetic, electrophysiological and optical approaches, we identified previously unknown „satiety neurons“ and uncovered which neurotransmitter mediates the communication of hunger neurons.


Obesity promotes the development of colorectal cancer

2018 Wunderlich, Thomas

Immunobiology Medicine

Obesity represents a major risk factor for colorectal cancer (CRC). Mouse studies demonstrate that the chronic low grade inflammation associated with obesity impairs intestinal insulin sensitivity and modulates the colorectal tumor microenvironment (TME), thus compromising the gut barrier and promoting CRC. These studies assign obesity-induced inflammation a critical role in the progression of CRC.


Coordination of food intake, locomotion and sleep by the lateral hypothalamus

2017 Korotkova, Tatiana

Immunobiology Infection Biology Medicine Neurosciences

Coordination of food intake, locomotion and sleep is crucial for survival, its impairment is a symptom of multiple sleep and eating disorders. We found that optogenetic activation of GABA cells in the lateral hypothalamus leads to awakening from non-REM sleep and increases food intake. Further we characterized the neuronal circuit, which connects the prefrontal cortex and the lateral hypothalamus and utilizes gamma oscillations to organize function-selective firing of neurons and to promote food-seeking.


Genetic predisposition for obesity influences learning behaviour

2016 Tittgemeyer, Marc; Brüning, Jens


Variations in the fat mass and obesity-associated (FTO) gene are associated with obesity. The same variants of FTO affect dopamine-dependent midbrain responses and learning from negative outcomes in humans. They furthermore modulate the connectivity in a basic reward circuit of meso-striato-prefrontal regions and facilitate neural responses elicited by food cues. These findings provide evidence for FTO-specific differences in both brain structure and function in individuals, thereby contributing to a mechanistic understanding of why FTO is a predisposing factor for obesity.


Regulatory mechanisms of neuronal glucose uptake

2015 Jais, Alexander; Brüning, Jens C.

Medicine Neurosciences

This study demonstrates the complex regulatory mechanisms for the maintenance of physiological glucose transport and identifies vascular endothelial growth factor (VEGF) as critical regulator of glucose transport across the blood-brain barrier. These experiments reveal that transient, high-fat diet-elicited reduction of brain glucose uptake initiates a compensatory increase of VEGF-production and assign obesity-associated macrophage activation a homeostatic role to restore cerebral glucose metabolism, preserve cognitive function and limit neurodegeneration in obesity.

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