Molecular mechanisms and individual vulnerability in an animal model (Mus musculus) of obesity induced by chronic social stress

Vulnerability to stress is given by our genetic make-up and our experiences, therefore it differs between individuals since we are not genetically identical and do not experience the same life events. Moreover, even though stress has been associated obesity, some subjects lose weight instead under stressful conditions. The goal of this thesis is to undercover some of the molecular mechanisms underlying the individual susceptibility to stress which will allow us to better understand how individuals cope better than others. To answer our question we investigated key molecular player involved in adipogenesis, lipolysis, diabetogenesis, sympathetic and insulin signaling markers in metabolically active tissue coming from different strains of mice following exposure to chronic psychosocial stress. Our results showed that a stress induced a complex profile of pro-adipogenic and lipolytic-markers’ expression with a fat depot-specificity as well as strain specificity allowing the contemporary activation of catabolic and anabolic pathways to cope better with stress.