Abstract
Stress was once defined as the non-specific result of the body to any demand or challenge to homeostasis. A more current view of stress is the behavioral and physiological responses generated in the face of, or in anticipation of, a perceived threat. The stress response involves activation of the sympathetic nervous system and recruitment of the hypothalamic-pituitary-adrenal (HPA) axis. When an organism encounters a stressor (social, physical, etc.), these endogenous stress systems are stimulated in order to generate a fight-or-flight response, and manage the stressful situation. As such, an organism is forced to liberate energy resources in attempt to meet the energetic demands posed by the stressor. A change in the energy homeostatic balance is thus required to exploit an appropriate resource and deliver useable energy to the target muscles and tissues involved in the stress response. Acutely, this change in energy homeostasis and the liberation of energy is considered advantageous, as it is required for the survival of the organism. However, when an organism is subjected to a prolonged stressor, as is the case during chronic stress, a continuous irregularity in energy homeostasis is considered detrimental and may lead to the development of metabolic disturbances such as cardiovascular disease, type II diabetes mellitus and obesity. This concept has been studied extensively using animal models, and the neurobiological underpinnings of stress induced metabolic disorders are beginning to surface. However, different animal models of stress continue to produce divergent metabolic phenotypes wherein some animals become anorexic and lose body mass while others increase food intake and body mass and become vulnerable to the development of metabolic disturbances. It remains unclear exactly what factors associated with stress models can be used to predict the metabolic outcome of the organism. This review will explore a variety of rodent stress models and discuss the elements that influence the metabolic outcome in order to further extend our understanding of stress-induced obesity.
Highlights
It is generally accepted that obesity has reached epidemic proportions
The present review aims to investigate the use of animal models in the study of stress and to highlight some of the factors that contribute to the metabolic outcome of these various stress paradigms
Ghrelin is capable of dampening the depressive like symptoms that normally arise following chronic social defeat (Lutter et al, 2008b). These data highlight the ability of hypothalamic feeding circuitry to influence the physiological response to stress and alter the behavioral and metabolic responses generated. It has been well-established that stressful environments are conducive to the development of obesity and related metabolic disorders
Summary
It is generally accepted that obesity has reached epidemic proportions. To some medical professionals, obesity is considered the leading preventable cause of death worldwide. More worrisome is the fact that the prevalence of obesity has drastically increased in the past 30 years, where ∼10% of the population was considered overweight in the 1970’s, a number that has risen to over 35% in the United States (Flegal et al, 2010, 2012). This estimate is accompanied by a wealth of statistics demonstrating that individuals who are overweight or obese have a much higher susceptibility to diseases such as Type II diabetes, cardiovascular disease and metabolic syndrome. CRF secretion in turn leads to the synthesis and release of adrenocorticotropic hormone (ACTH) from the anterior pituitary into the general circulation, which stimulates the release of glucocorticoids from the adrenal www.frontiersin.org
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