Marc Tittgemeyer

Survival under selective pressure is driven by the ability of our brain to use sensory information to our advantage to control physiological needs. In this context, neural circuits receive and integrate external environmental cues and internal metabolic signals to form learned sensory associations, which consequently motivate and adapt our behaviour. The dopaminergic midbrain plays a crucial role in learning adaptive behaviour and is particularly sensitive to peripheral metabolic mediators, including intestinal signal peptides like GLP-1, insulin or leptin.

Recently, the group has demonstrated that adaptive learning is reduced when metabolic sensing is impaired in obesity, leading to disrupted circuit mechanisms of integrating and interpreting sensory information; hence, there is an inadequate sensing of physiological need and dyscalibrated motivational drive. We have furthermore shown that not only metabolic mediators interact with sensory regulation and motivated behaviour but also nutrients directly. Food palatability may act on the dopaminergic reward system to modulate incentive motivation and override homeostatic control, and Western diets can directly affect neurobehavioural adaptations beyond food intake that may increase the risk for subsequent overeating and weight gain.

Building on these achievements, we further focus on the physiological mechanisms by which internal bodily signals are communicated to and sensed by the brain to adapt the organism´s behaviour to its metabolic state and physiological need, especially related to the role of diet-induced neuroinflammation and ageing processes.