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Review
. 2016 Jul;27(7):504-515.
doi: 10.1016/j.tem.2016.04.007. Epub 2016 May 5.

The Dichotomous Effect of Chronic Stress on Obesity

Maria Razzoli  1 , Alessandro Bartolomucci  2
Affiliations
Review

The Dichotomous Effect of Chronic Stress on Obesity

Maria Razzoli et al. Trends Endocrinol Metab. 2016 Jul.

Abstract

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.

Keywords: hypothalamus-pituitary-adrenocortical axis; purinergic; social stress; sympathetic nervous system; β-adrenergic receptors.

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Figures

Figure 1
Figure 1. Proposed model to explain the dichotomous effect of stress on energy balance
We propose that the metabolic outcome (exemplified by an obese/diabetic and a lean mouse) of chronic psycho-emotional stress is mediated by changes in food intake and recruitment/activation of the brown adipose tissue (BAT) and their impact on nutrient clearance and thermogenesis. Stress promotes obesity in the presence of increased caloric intake and unchanged BAT recruitment and function. Stress results in weight loss or resistance to obesity in the presence of hypophagia or hyperphagia, the latter paralleled by increased thermogenesis and BAT recruitment/function.
Figure 2
Figure 2. Model of the impact of stress-induced sympathetic and neuroendocrine function on BAT activation and recruitment
Stress acutely enhances BAT activation and thermogenesis (top graph) and chronically induces BAT recruitment (lower panel) as a function of the intensity of the sympathetic and neuroendocrine activation. Experimental evidences support a model in which the basal pre-stress adaptive thermogenesis requirements modulate the capacity of stress stimuli to elicit BAT recruitment. Specifically, in subjects characterized by high thermogenesis requirement, only stress leading to maximal sympathetic/neuroendocrine activation will enhance BAT recruitment and thermogenic capacity. Conversely, in subjects characterized by low thermogenesis requirement even stress of mild intensity will induce a sympathetic/neuroendocrine activation effectual for BAT recruitment. CPS= Chronic Psychosocial Stress; CSD= Chronic Social Defeat.
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