From an evolutionary perspective, the stress response system has evolved to ensure the survival of the organism and therefore of the species. Triggering the stress response system leads to several hormone-mediated metabolic alterations, aimed at exploiting energy resources and adaptive behavioral strategies to cope with real or perceived threats. In the modern highly stressed society, the majority of the stressors we face chronically are psychological. The consequent activation of the stress response system mobilizes energy resources that are not expended in the short term, but rather compromise the energetic balance of the organism for long intervals. Stress and obesity are widespread conditions that mutually interplay, as they share at the basis an intricated network of pathways that regulate the physical, behavioral, and cognitive spheres of the organism. The type of stressor, along with substantial differences in genetic, environmental, and developmental factors, are important determinants for the vulnerability to hormones-related negative consequences on metabolism, and therefore the different susceptibility to develop obesity and eventually metabolic diseases associated with an obese state, like metabolic syndrome and type 2 diabetes. The main purpose of this article is to discuss the cardinal stress-activated pathways that, combined with an impaired energy balance, result in fat mass accumulation, especially visceral, and in the onset of a chronic low-grade inflammation. These features contribute to the development of insulin resistance, and therefore to the incidence of common metabolic dysregulations which in turn represent important risk factors for other widespread and severe pathologies, such as cardiovascular diseases and tumors.

Stress, Hormones, and Metabolism / Radighieri, Giulia; Alboni, Silvia. - 1-3:(2022), pp. 502-509. [10.1016/B978-0-12-819641-0.00081-5]

Stress, Hormones, and Metabolism

Radighieri, Giulia;Alboni, Silvia
2022

Abstract

From an evolutionary perspective, the stress response system has evolved to ensure the survival of the organism and therefore of the species. Triggering the stress response system leads to several hormone-mediated metabolic alterations, aimed at exploiting energy resources and adaptive behavioral strategies to cope with real or perceived threats. In the modern highly stressed society, the majority of the stressors we face chronically are psychological. The consequent activation of the stress response system mobilizes energy resources that are not expended in the short term, but rather compromise the energetic balance of the organism for long intervals. Stress and obesity are widespread conditions that mutually interplay, as they share at the basis an intricated network of pathways that regulate the physical, behavioral, and cognitive spheres of the organism. The type of stressor, along with substantial differences in genetic, environmental, and developmental factors, are important determinants for the vulnerability to hormones-related negative consequences on metabolism, and therefore the different susceptibility to develop obesity and eventually metabolic diseases associated with an obese state, like metabolic syndrome and type 2 diabetes. The main purpose of this article is to discuss the cardinal stress-activated pathways that, combined with an impaired energy balance, result in fat mass accumulation, especially visceral, and in the onset of a chronic low-grade inflammation. These features contribute to the development of insulin resistance, and therefore to the incidence of common metabolic dysregulations which in turn represent important risk factors for other widespread and severe pathologies, such as cardiovascular diseases and tumors.
2022
17-set-2021
Encyclopedia of Behavioural Neuroscience 2e
9780128093245
Elsevier
Stress, Hormones, and Metabolism / Radighieri, Giulia; Alboni, Silvia. - 1-3:(2022), pp. 502-509. [10.1016/B978-0-12-819641-0.00081-5]
Radighieri, Giulia; Alboni, Silvia
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/1251375
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