Neurocircuit Wiring and Function

The escalating burden of obesity and Type 2 Diabetes Mellitus triggers an urge to further delineate the exact mechanisms that govern fundamental behavioral and physiological processes such as feeding or maintenance of steady body weight and glycemia. To build upon this challenge, our group is keen to deepen our understanding of the fundamental principles of the central control of metabolism from embryo to adult. 

Our general interest is to decipher the exact neuronal networks controlling energy and glucose homeostasis by uncovering their precise functions and their developmental wiring.

Projects conducted in our group ultimately intent on furthering our understanding of the pathophysiology of obesity and Type 2 Diabetes Mellitus and to provide new insights regarding interventional approaches to tackle these metabolic diseases.

Research interests

Defining the exact neurocircuits controlling energy and glucose homeostasis 

We seek at further defining the architecture and the functional principles of neuronal-based circuits controlling energy and glucose homeostasis in adults. By doing so, we hope to better delineate how the brain controls metabolic processes and to identify the exact neurocircuits involved in these events. Our projects notably intend to understand how the organism senses and integrates its environment and adapt its behavior according to its physiological and nutritional needs. To answer these fundamental questions, we are employing state-of-the-art technologies in systems neuroscience such as optogenetics, chemogenetics, and in vivo calcium imaging in concert with a broad range of tests assessing metabolism and behavior.

Studying the developmental programming of obesity and metabolic diseases 

Metabolic disorders are increasingly diagnosed in childhood and have recognized roots in very early life. Indeed, compelling evidence from animals and epidemiological studies reveal that abnormal changes in the maternal, fetal, and neonatal environment substantially contribute to the onset of these metabolic diseases. Notably, changes in the nutritional and/or hormonal environment during gestation and/or lactation (e.g. maternal obesity/malnutrition or diabetes) can permanently alter the development of “brain-metabolic” pathways. Those alterations will in turn lead to life-long changes in homeostatic functions and predisposes individuals to develop metabolic diseases later in life.

We are focusing on uncovering new mechanisms underlying the developmental programming of metabolic neuronal networks. Altogether, we intend to pinpoint novel brain-metabolic pathways sensitive to abnormal perinatal milieus that could ultimately contribute to the onset of metabolic dysfunctions.

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