Stress-induced alterations in estradiol sensitivity increase risk for obesity in women

• Type of Material: Article
• Authors: Vasiliki Michopoulos, Emory University
• Language: English
• Date: 2016-11-01
• Publisher: Elsevier
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2016 Elsevier Inc. All rights reserved.
• Final Published Version (URL): http://dx.doi.org/10.1016/j.physbeh.2016.05.016
• Title of Journal or Parent Work: Physiology and Behavior
• ISSN: 0031-9384
• Volume: 166
• Start Page: 56
• End Page: 64
• Grant/Funding Information: Further support was provided by the Center for Behavioral Neuroscience through the STC Program of the National Science Foundation IBN-9876754.; These studies would not have been possible without support from NIH grants HD46501, MH081816, RR00165, and F31MH085445 (VM).
• Keywords: Estradiol; CHRONIC SOCIAL STRESS; Psychology, Biological; CORTICOTROPIN-RELEASING-FACTOR; Obesity; REGIONAL FAT DISTRIBUTION; CENTRAL-NERVOUS-SYSTEM; Psychology; ESTROGEN-RECEPTOR-ALPHA; FOOD-INTAKE; Animal models; Stress axis; Science & Technology; Behavioral Sciences; Life Sciences & Biomedicine; MENSTRUAL-CYCLE; Sex differences; Glucocorticoids; Social Sciences; FEMALE RHESUS-MONKEYS; VISIBLE BURROW SYSTEM; PITUITARY-ADRENAL FUNCTION
• Research Categories: Health Sciences, Public Health; Psychology, Behavioral

Abstract

The prevalence of obesity in the United States continues to rise, increasing individual vulnerability to an array of adverse health outcomes. One factor that has been implicated causally in the increased accumulation of fat and excess food intake is the activity of the limbic-hypothalamic-pituitary-adrenal (LHPA) axis in the face of relentless stressor exposure. However, translational and clinical research continues to understudy the effects sex and gonadal hormones and LHPA axis dysfunction in the etiology of obesity even though women continue to be at greater risk than men for stress-induced disorders, including depression, emotional feeding and obesity. The current review will emphasize the need for sex-specific evaluation of the relationship between stress exposure and LHPA axis activity on individual risk for obesity by summarizing data generated by animal models currently being leveraged to determine the etiology of stress-induced alterations in feeding behavior and metabolism. There exists a clear lack of translational models that have been used to study female-specific risk. One translational model of psychosocial stress exposure that has proven fruitful in elucidating potential mechanisms by which females are at increased risk for stress-induced adverse health outcomes is that of social subordination in socially housed female macaque monkeys. Data from subordinate female monkeys suggest that increased risk for emotional eating and the development of obesity in females may be due to LHPA axis-induced changes in the behavioral and physiological sensitivity of estradiol. The lack in understanding of the mechanisms underlying these alterations necessitate the need to account for the effects of sex and gonadal hormones in the rationale, design, implementation, analysis and interpretation of results in our studies of stress axis function in obesity. Doing so may lead to the identification of novel therapeutic targets with which to combat stress-induced obesity exclusively in females.