Abstract

Obesity and metabolic dysfunction are risk factors for a number of chronic diseases, such as type 2 diabetes, hypertension, heart disease, stroke, and certain forms of cancers. Both animal studies and human population-based and clinical studies have suggested that chronic stress is a risk factor for metabolic disorders. A good social support system is known to exert positive effects on the mental and physical well-being of an individual. On the other hand, long-term deprivation of social contacts may represent a stressful condition that has negative effects on health. In the present study, we investigated the effects of chronic social isolation on metabolic parameters in adult C57BL/6 mice. We found that individually housed mice had increased adipose mass compared to group-housed mice, despite comparable body weight. The mechanism for the expansion of white adipose tissue mass was depot-specific. Notably, food intake was reduced in the social isolated animals, which occurred around the light-dark phase transition periods. Similarly, reductions in heat generated and the respiratory exchange ratio were observed during the light-dark transitions. These phase-specific changes due to long-term social isolation have not been reported previously. Our study shows social isolation contributes to increased adiposity and altered metabolic functions.

Highlights

  • Social isolation (SI) has been shown to induce an increase in emotionality and hypothalamic-pituitary-adrenal axis reactivity in mice [1, 2]

  • Brown adipose tissue (BAT) weight was increased by 1.54-fold (P < 0.01)

  • It remains possible that longer duration of social isolation may eventually lead to significant increases in body weight gain, our study shows that there was a change in body composition and a preferential accumulation of adipose tissues even before any observable body weight gain

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Summary

Introduction

Social isolation (SI) has been shown to induce an increase in emotionality and hypothalamic-pituitary-adrenal axis reactivity in mice [1, 2]. Given the association between stress and obesity [7, 8], efforts have been made in developing and characterizing animal stress models for the study of metabolic dysfunctions. These models include unpredictable chronic stress model, social defeat model, and the use of various chronic stressors [9,10,11]. The hypothalamo-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) are the main effector pathways of the stress system and both affects energy metabolism. Activation of the SNS triggers the release of epinephrine, which mediates a number of physiological changes to prepare the body for “fight or flight” response

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