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.

Contact

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

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Nerve cells of the vagus nerve fulfil opposing tasks

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Researchers reveal the diversity of our neurons

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A newly discovered protein could serve as a target for drug therapy

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

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Fat activates nociceptin neurons in the hypothalamus of mice

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Eating with all senses

2020 Steculorum, Sophie

Behavioural Biology Medicine Neurosciences

Our understanding of how our brain governs food intake has recently been revolutionized by the discovery that key hunger neurons are switched off within a few seconds upon detection of food cues that signal to the brain food vicinity, like sight or smell. Following on these seminal discoveries and building upon the challenge of better characterizing the critical mechanism by which our brain orchestrates feeding behavior, our group is keen on elucidating the influence of our senses on brain circuits governing appetite and metabolism. 

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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.

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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.

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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.

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Genetic predisposition for obesity influences learning behaviour

2016 Tittgemeyer, Marc; Brüning, Jens

Neurosciences

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.

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