Obesity is a major health problem worldwide. However, despite the human and economic costs of this disease, efficient anti-obesity therapies are currently lacking.
One of the avenues that might lead to gain significant insights into the causes and potential treatments of obesity is the unravelling of the biological mechanisms regulating energy balance. Integrative systems and specific fuel sensing pathways are among the mechanisms known to control energy balance. Therefore, our past 4 years of research activity has been committed to studying in an integrated way both integrative systems and specific fuel sensing pathways. In particular, among the integrative systems, we have investigated the endogenous cannabinoid system (ECS) and, among the fuel sensing mechanisms, we have studied the mammalian Target Of Rapamycin complex 1 (mTORc1) cascade. Our studies on the ECS have helped to further detail the role of this system in energy balance by showing that while food intake and energy expenditure are controlled by cannabinoid receptors type 1 (CB1) located in the central nervous system, the equilibrium between energy storage and utilization is mediated by a direct action of CB1 on peripheral tissues. At the same time, our ground-breaking studies on the mTORc1 pathway have been the first to demonstrate that mTORc1 is a critical integrator of the effects of hormones and nutrients on food intake, and that the dysregulation of this pathway favours obesity.
BACKGROUND: Spinal reactive astrocytes and microglia are known to participate to the initiation and maintenance of neuropathic pain. However, whether reactive astrocytes and microglia in thalamic nucl
OBJECTIVE: Nutrient availability modulates reactive oxygen species (ROS) production in the hypothalamus. In turn, ROS regulate hypothalamic neuronal activity and feeding behavior. The mechanistic targ
Ciliary neurotrophic factor (CNTF) potently decreases food intake and body weight in diet-induced obese mice by acting through neuronal circuits and pathways located in the arcuate nucleus (ARC) of th
The pathophysiology of body weight gain that is observed in patients suffering from myeloproliferative neoplasms treated with inhibitors of the janus kinase (Jak) 1 and 2 pathway remains unknown. Here
Dysregulated adipocyte physiology leads to imbalanced energy storage, obesity, and associated diseases, imposing a costly burden on current health care. Cannabinoid receptor type-1 (CB1) plays a cruci