Chronic stress increases the risk of cardiometabolic disease.
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CRH and catecholamines integrate anorexigenic-like responses to stress.
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Glucocorticoids and NPY promote adiposity after chronic stress.
The stress response mobilizes the body's energy stores in order to respond to a threatening situation. A striking observation is the diversity of metabolic changes that can occur in response to stress. On one hand acute intense stress is commonly associated with feeding suppression and reduced body weight gain. The activation of the hypothalamic–pituitary–adrenal axis and the release of corticotropin-releasing hormone (CRH) might partially explain the anorexigenic effects of acute stress. CRH can also stimulate the sympathetic nervous system and catecholamine release, inducing hypophagia and weight loss, through their effects on the liver and on white and brown adipose tissue. On the other hand, chronic stress can lead to dietary over-consumption (especially palatable foods), increased visceral adiposity and weight gain. These obesogenic effects of stress are mainly explained by the chronic release of glucocorticoids and neuropeptide Y. Stressful situations can activate all of these systems together, and the metabolic outcome of stress exposure is determined by a host of intrinsic and external factors. If we are to find new ways to limit the development of stress-linked cardiometabolic diseases, we need to discover why, in some circumstances, the pro-obesogenic effects of stress outweigh its anorexigenic effects. The equilibrium between the different components of the stress response that accompany chronic stress situations could be crucial to understand and prevent the long-lasting adverse metabolic effects induced by stress.
