Stress induced obesity: lessons from rodent models of stress

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.

Air Pollution and Insulin Resistance: Do All Roads Lead to Rome?

“…A growing body of evidence supports the hypothesis that ozone exposure induces a neuronal response that activates stress-sensitive centers in the nucleus tractus solitarius (10,11). Activation of catecholaminergic neurons in the nucleus tractus solitariuscentral to systemic sympathetic stimulation-can mediate an immediate action (fight-or-flight response), activate a hypothalamus-pituitary-adrenal-mediated release of hormones from the adrenal cortex (12), and result in a release of glucose, free fatty acids, and branched-chain amino acids into the circulation (Fig. 1) (13).…”

Attachment Strategies and Neuroendocrine Biomarkers in Obese Children

“…6,13,14 The environmental factors contributing to cortisol reactivity and associated neuroendocrine changes have yet to be documented in people with obesity.…”

“…There is evidence that variance in hypothalamic-pituitary-adrenal (HPA) axis activity varies with weight. 6 In the present study, the quality of attachment was examined in relation to various neuroendocrine biomarkers, including cortisol and thyroid stimulating hormone (TSH).…”

Sex Differences in Ileal Somatostatin-Response after Stress Conditioning in Rats

“…Previous studies have reported that there is a close relationship between stress and feeding behavior [1][2][3]. Usually evidenced in both human and animal studies, stress has been shown to affect food intake feeding behavior in a bidirectional fashion, inducing either increases or decreases in food intake [4].…”