Impact of Catechol-O-methyltransferase in the neuro-immune regulation of metabolic disorders
Aging is associated with maladaptive chronic inflammation, increasing the risk of multiple chronic diseases such as diabetes, heart disease, cognitive dysfunction, certain cancers and immune disorders. With age, adipose tissue loses its ability to perform lipolysis efficiently, leading to a higher accumulation of lipids and participating in the development of chronic inflammation. Adipose macrophages are key mediator of inflammation as well as regulation of lipolysis through the degradation of catecholamines, the main inducer of lipolytic enzymes. Dr. Leveau’s previous work shows that macrophages ability to degrade catecholamines is impaired with age. By using a murine model deficient for the enzyme responsible of catecholamine degradation, her lab seeks to determine whether increasing bioavailability of catecholamines will improve lipolysis response and inflammation in aging. Moreover, she proposes to study the putative detrimental impact of catecholamine degradation byproducts on inflammation. Her work has the potential to reveal new therapeutic approaches to target metabolic dysfunction and chronic inflammation.
