Trends in Endocrinology & Metabolism
ReviewThe Dichotomous Effect of Chronic Stress on Obesity
Section snippets
The Dichotomous Consequences of Stress on Energy Balance
Over the past few decades, obesity-associated metabolic diseases have become a pandemic, seemingly due to the widespread consumption of a Western-type diet combined with sedentary lifestyle and increased psychoemotional stress [1]. However, industrialized societies also suffer from stress-associated eating disorders that can negatively impact energy balance, such as anorexia nervosa, characterized by self-starvation and excessive weight loss, and bulimia, characterized by periods of excessive
Central Mechanisms of Stress-Induced Positive Energy Balance
Laboratory rodents can respond with hyperphagic behavior to several psychological and physical stress models. For example, chronic mild stress and chronic social stress (see Glossary) have been linked to sustained hyperphagia and binge eating-like disorders 17, 18, 19. During chronic stress and the corresponding hyperactivation of the HPA axis, glucocorticoids and insulin increase craving for calorie-rich meals [20]. The preference for palatable food ingestion has been proposed to reduce the
Adaptive Thermogenesis and BAT Function at the Core of the Stress-Induced Regulation of Obesity
A major factor hindering the understanding of the dichotomous metabolic responses to stress reviewed above is the intrinsic complexity of the physiologic regulation of metabolism [67]. In this context, the CNS has a key role by exerting efferent control on adipose depot functions. The autonomic innervation of WAT is fundamental in the regulation of adipogenesis and lipolysis [48] and, under certain conditions, thermogenesis [68]. Sympathectomy causes the increased accumulation of lipids in WAT
The Dichotomous Effect of Stress on Obesity: An Energy Balance Perspective
The main components of energy balance are food intake, nutrients absorption, and energy expenditure. Energy expenditure is classically subdivided into three main components: basal thermogenesis, physical activity-related thermogenesis, and adaptive thermogenesis [13]. We propose that there are two main factors promoting stress-induced vulnerability versus resilience to obesity: (i) changes in food intake; and (ii) recruitment and/or activation of BAT and its impact on nutrient clearance and
Concluding Remarks and Future Perspectives
The metabolic effects of chronic stress in rodents are heterogeneous and reminiscent of human data. While progress has been made on the identification of the mediators of stress-induced metabolic effects using classical neuroendocrine approaches, the mechanistic understanding of how stress affects energy balance is still at an early stage (see Outstanding Questions). Accumulated evidence now supports a major role for sympathetically derived factors in brown adipocyte function. Classically,
Acknowledgments
We would like to thank past and current members of the laboratory as well as colleagues and collaborators for help generating the experimental data discussed in the review and for helpful discussions. We apologize to those authors whose papers could not be cited owing to space constraints. A.B. is supported by NIH/NIDDK R01DK102496, NIH/NIA R01AG043972.
Glossary
- Chronic mild stress
- sequential exposure of experimental animals to a variety of mild stressors (e.g., overnight illumination; periods of food and/or water deprivation; cage tilt; or change of cage mate).
- Chronic social stress
- two male mice are paired and allowed to aggressively interact for a short period of time daily; they are thereafter in sensory contact allowed by a perforated partition in the housing cage for up to 6 weeks. A dominant mouse and a subordinate mouse are identified by
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