How does Stress Affect Energy Balance?

Razzoli, Maria; Cero, Cheryl; Bartolomucci, Alessandro

doi:10.1002/9781118540770.ch4

Cited by 1 publication

(2 citation statements)

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“… [62] , [63] . Conversely, a functional explanation for the bidirectional effect of stress on energy balance, observed in humans and animal models, is still missing [4] , [29] , [64] , [65] , [66] , [67] , [68] , [69] . Here we demonstrated that the level of adaptive thermogenesis and the functional status of brown adipose tissue determine the resilience or the vulnerability to stress-induced obesity in mice in spite of similar level of hyperphagia, offering a key to interpret the dichotomous effect of stress on energy balance.…”

Section: Discussionmentioning

confidence: 99%

“…To model the impact of psychosocial stress on metabolism, we used a validated model of human stress-induced disease that mimics the role of socio-economic status on health [70] , [71] , [72] . Remarkably, different models of chronic psychosocial stress resulting in a similar hypothalamus-pituitary adrenocortical (HPA)-axis activation and depression-like behavior [62] , [73] induce opposite effects on energy balance [28] , [31] , [74] , reviewed in [68] , [69] . For example, in the chronic social defeat stress model (CSDS), subordinate mice consistently manifest weight and fat mass loss during the defeat phase [74] .…”

Section: Discussionmentioning

confidence: 99%

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Stress-induced activation of brown adipose tissue prevents obesity in conditions of low adaptive thermogenesis

Razzoli

Frontini

Gurney

et al. 2016

Molecular Metabolism

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BackgroundStress-associated conditions such as psychoemotional reactivity and depression have been paradoxically linked to either weight gain or weight loss. This bi-directional effect of stress is not understood at the functional level. Here we tested the hypothesis that pre-stress level of adaptive thermogenesis and brown adipose tissue (BAT) functions explain the vulnerability or resilience to stress-induced obesity.MethodsWe used wt and triple β1,β2,β3−Adrenergic Receptors knockout (β-less) mice exposed to a model of chronic subordination stress (CSS) at either room temperature (22 °C) or murine thermoneutrality (30 °C). A combined behavioral, physiological, molecular, and immunohistochemical analysis was conducted to determine stress-induced modulation of energy balance and BAT structure and function. Immortalized brown adipocytes were used for in vitro assays.ResultsDeparting from our initial observation that βARs are dispensable for cold-induced BAT browning, we demonstrated that under physiological conditions promoting low adaptive thermogenesis and BAT activity (e.g. thermoneutrality or genetic deletion of the βARs), exposure to CSS acted as a stimulus for BAT activation and thermogenesis, resulting in resistance to diet-induced obesity despite the presence of hyperphagia. Conversely, in wt mice acclimatized to room temperature, and therefore characterized by sustained BAT function, exposure to CSS increased vulnerability to obesity. Exposure to CSS enhanced the sympathetic innervation of BAT in wt acclimatized to thermoneutrality and in β-less mice. Despite increased sympathetic innervation suggesting adrenergic-mediated browning, norepinephrine did not promote browning in βARs knockout brown adipocytes, which led us to identify an alternative sympathetic/brown adipocytes purinergic pathway in the BAT. This pathway is downregulated under conditions of low adaptive thermogenesis requirements, is induced by stress, and elicits activation of UCP1 in wt and β-less brown adipocytes. Importantly, this purinergic pathway is conserved in human BAT.ConclusionOur findings demonstrate that thermogenesis and BAT function are determinant of the resilience or vulnerability to stress-induced obesity. Our data support a model in which adrenergic and purinergic pathways exert complementary/synergistic functions in BAT, thus suggesting an alternative to βARs agonists for the activation of human BAT.

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