کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2810121 | 1158407 | 2016 | 12 صفحه PDF | دانلود رایگان |
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.
TrendsChronic stress and socioeconomic status have been associated with metabolic diseases.A beneficial metabolic potential of BAT has been identified in humans. Recent data suggest that psychological stress is a natural stimulus for BAT function, together with classically recognized cold- and diet-induced thermogenesis.Recent data also demonstrate that the dichotomous metabolic outcome of social stress can be related to differential levels of basal BAT activity and stress-induced recruitment and activation of BAT.We propose a bidirectional relation between stress and energy balance, whereby stress promotes obesity in the presence of hyperphagia and unchanged BAT function, but results in weight loss and/or obesity resistance in the presence of hypophagia or when hyperphagia is associated with enhanced BAT recruitment and/or thermogenesis.
Journal: - Volume 27, Issue 7, July 2016, Pages 504–515