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Updated: Jan 27, 2026

Multidisciplinary Approach to Obesity Management: A Case Report
Published on: May 30, 2025
Glucocorticoids, stress and obesity.
Renato Pasquali1,2, Valentina Vicennati1, Alessandro Agostini1
1a Division of Endocrinology, Department of Clinical Medicine, S. Orsola-Malpighi Hospital, University Alma Mater Studiorum, Via Massarenti 9, 40138 Bologna, Italy.
Chronic stress can lead to obesity through neuroendocrine dysregulation, particularly involving the hypothalamic-pituitary-adrenal (HPA) axis and comfort food consumption. Specific individual phenotypes may be predisposed to obesity following stressful events.
Area of Science:
- Neuroendocrinology
- Metabolic Syndrome Research
- Stress Physiology
Background:
- Obesity and metabolic syndrome are linked to chronic stress and neuroendocrine axis dysregulation.
- The hypothalamic-pituitary-adrenal (HPA) axis is central to stress response and homeostasis.
- Stress-related neural centers also regulate feeding behavior.
Purpose of the Study:
- To explore the link between chronic stress, neuroendocrine axes, and obesity development.
- To investigate the role of comfort food consumption in stress adaptation and obesity.
- To propose a specific phenotype susceptible to stress-induced obesity.
Main Methods:
- Review of clinical experience and experimental animal studies.
- Analysis of the neuroendocrine regulation of stress and feeding behavior.
- Examination of the endocannabinoid system's role in stress and reward.
Main Results:
- Chronic stress, mediated by the HPA axis, can lead to obesity.
- Comfort food consumption may adapt reward systems but promote obesity.
- The endocannabinoid system influences HPA axis activity and reward mechanisms.
Conclusions:
- A specific individual phenotype may be predisposed to obesity due to major stressful events.
- Dysregulation of neuroendocrine axes, particularly the HPA axis, is implicated in stress-induced obesity.
- Understanding these mechanisms may inform targeted interventions for obesity prevention.
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