Weizmann Institute of Science
Exposure to acute or chronic stress is associated with derangement of metabolic and behavioral homeostasis that contributes to the clinical presentation of visceral obesity, type 2 diabetes, atherosclerosis, and metabolic syndrome.
The corticotropin-releasing factor (CRF) neuropeptide system is the primary central mediator of the central and neuroendocrine stress response and when dysregulated contributes to the etiology of stress-related metabolic and psychiatric disorders. Accordingly, the CRF receptors plays an important role in mediating the autonomic, neuroendocrine and behavioral responses to stressful challenges. Stress and energy balance share common regulatory pathways orchestrated by hypothalamic neural networks and the CRF receptors and ligands are expressed in hypothalamic neurons regulating energy homeostasis. One example is the CRFR receptor type 1 (CRFR1), which is highly expressed in the Arcuate nucleus of the hypothalamus, a major hub in integrating nutritional related information.
In this talk, I will present the CRF system and its effect on both food intake and energy expenditure. I will focus on the characterization of Arc-CRFR1 neurons and elucidating their role in protecting energy homeostasis under environmental challenges