Max Planck Institute for Metabolism Research

The brain releases the hormone corticosterone after short fasting that boosts autophagy

Possible target for drugs to combat the yo-yo effect

Why we can't keep our hands off chocolate bars and co.

Priorities change depending on hunger level

Nerve cells of the vagus nerve fulfil opposing tasks

The hypothalamus is an area in the brain that regulates metabolism. It consists of neuronal groups, one of which is the Pro-opiomelanocortin- expressing group. POMC neurons drive satiety and use of stored energy in the body. Studying this neuronal group has led us to find different subgroups within a population that was thought to be uniform. We are studying in detail how they influence metabolism.

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. 

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 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 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.