Obesity and metabolic diseases are linked to chronic stress and low socioeconomic status. The mechanistic link between stress and obesity has not been clarified, partly due to the inherent complexity exemplified by the bidirectional effect of stress on eating and body weight. Recent studies focusing on adaptive thermogenesis and brown adipose tissue (BAT) function support a dichotomous relation to explain the impact of stress on obesity: stress promotes obesity in the presence of hyperphagia and unchanged BAT function; stress results in weight loss and/or obesity resistance in the presence of hypophagia, or when hyperphagia is associated with BAT recruitment and enhanced thermogenesis. Mechanistically dissecting the bidirectional effects of stress on metabolic outcomes might open new avenues for innovative pharmacotherapies for the treatment of obesity-associated diseases.
Bibliographical noteFunding Information:
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.
© 2016 Elsevier Ltd.
Copyright 2017 Elsevier B.V., All rights reserved.
- Hypothalamus-pituitary-adrenocortical axis
- Social stress
- Sympathetic nervous system
- β-adrenergic receptors