Relationship between stress, inflammation and metabolismSeematter, Géralda,b; Binnert, Christopheb; Martin, Jean-Lucb; Tappy, LucbCurrent Opinion in Clinical Nutrition & Metabolic Care: March 2004 - Volume 7 - Issue 2 - p 169-173 Nutrition in the intensive care unit Abstract Author Information Purpose of review Various threatening stimuli, such as pain, low blood pressure, or infection, elicit a set of neuroendocrine responses that include an increased secretion of catecholamines and glucocorticoid from the adrenal gland and activation of the sympathetic nervous system. These hormonal secretions allow a ‘fight or flight’ response by mobilizing endogenous substrate. They also exert anti-insulin actions, and may in the long term induce a state of insulin resistance. In addition, stress stimulates inflammatory mediators in mononuclear cells. Given the possible role of low-grade inflammation in chronic metabolic disorders, this suggests that stress may be a factor in the development of insulin resistance and the metabolic syndrome. Recent findings Studies reviewed in this article cover: (1) the metabolic and haemodynamic effects of stress in healthy and insulin-resistant individuals; (2) the relationship between stress and inflammation and the role of the autonomic nervous system; and (3) some factors known to modulate the neuroendocrine responses to stress. Future perspectives, together with some hints regarding the role of neurotrophins such as brain-derived neurotrophic factor, are delineated. Summary Recent work performed in the field has indicated that stress may be a significant factor in the pathogenesis of metabolic disorders. Nutritional intervention or pharmacological agents targeted at modulating stress should be investigated. aService of Anesthesiology, Lausanne University Hospital; and bDepartment of Physiology, University of Lausanne, Lausanne, Switzerland Correspondence to Luc Tappy, Département de Physiologie, 7 rue du Bugnon, 1005 Lausanne, Switzerland Fax: +41 021 692 55 95; e-mail: firstname.lastname@example.org © 2004 Lippincott Williams & Wilkins, Inc.