Sustaining factors for stress-induced emotional feeding in females

女性应激性情绪喂养的维持因素

• 批准号: 8652449
• 负责人: Mark E Wilson
• 金额: $ 75.43万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2013
• 资助国家: 美国
• 起止时间: 2013-04-17 至 2016-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8652449
• 关键词: Acute; Adult; Animals; Attenuated; Behavior; Behavioral; Biological; Brain; Calories; Chronic; Comorbidity; Consumption; Coupled; Data; Desire for food; Diet; Dopamine; Eating; Emotional; Energy Intake; Environment; Estradiol; Exhibits; Exposure to; Fatty acid glycerol esters; Female; Goals; Health; Hormones; Housing; Human; Hyperphagia; Individual; Intake; Intervention; Lead; Life Style; Longitudinal Studies; Macaca mulatta; Metabolic; Metabolism; Modeling; Monkeys; Obesity; Outcome; Ovarian; Pathway interactions; Pattern; Phenotype; Physiological; Population; Precipitating Factors; Predisposition; Premenopause; Psychosocial Stress; Reducing diet; Relative (related person); Reporting; Research Design; Rewards; Risk; Self Medication; Social status; Stress; System; Testing; Therapeutic Intervention; Time; Weight; Woman; coping; dopamine system; environmental intervention; feeding; genetic variant; good diet; improved; men; neurochemistry; novel; obesity risk; psychologic; psychosocial; public health relevance; receptor; receptor binding; response; restraint; social; social stress; stressor

DESCRIPTION (provided by applicant): Emotional feeding resulting from chronic exposure to psychosocial stressors is likely a key factor for excess food intake. This may be particularly important for women, who consistently report more stress-induced eating and have higher rates of obesity. The well-accepted notion is that emotional feeding of calorically dense diets is a form of self-medication to relieve the behavioral and physiological manifestations of stress. While this may be the case, it is also probable that emotional feeding is the result of compromised dopamine (DA) reward pathways, as exposure to chronic psychosocial stress increases susceptibility to an addictive phenotype by reducing DA 2 receptors (D2R) in mesolimbic regions, producing a hypodopaminergic condition. Furthermore, simply eating a calorically dense diet reduces D2R in these regions but only in some animals. Thus, self-medicating with high caloric diets may further compromise the stress-induced hypofunctional DA system. Clearly, this is not a healthy coping strategy for unresolved stress. An issue particularly important for women attempting to diet is whether these stress-induced changes, including impaired DA function, persist in the face of life style changes. Our preliminary data using social subordination in female rhesus monkeys as a model of chronic psychosocial stress in women suggests this may be the case, as subordinate females consume significantly more calories when given a high caloric diet (HCD) and this hyperphagia persists when a healthier diet is exclusively available. What is not known, however, is how this pattern continues under these healthy dietary conditions. Similarly, it is unknown if the alleviation of chronic psychosocial stress will restore caloric restraint, or if changes in systems regulating appetite, including DA, persist even after stress is resolved. Using socially housed female rhesus monkeys as a translational model for women, this project will identify mechanisms that sustain emotional feeding. Aim 1 will determine whether chronic social stress induced by social subordination sustains excessive intake of a HCD and whether this is exacerbated by exposure to acute stressors. Aim 2 will test the hypothesis that intake of a calorically dense diet will reduce DR2 availability in mesolimbic regions and this will be exacerbated by social subordination. Aim 3 will test the hypothesis that estradiol will be more effective suppressing caloric intake in dominant females when a LCD is available but will promote caloric intake when an HCd is available, particularly in subordinate females. in a Aim 4 will use two intervention strategies to further elucidate how social stress sustains emotional feeding: 1) despite replacing a HCD with a healthier low caloric diet, hyperphagia and reduced D2R binding potential in subordinates will persist; and 2) reducing social stress by changing social status will improve but not normalize D2R availability or food intake Together, these studies will increase our understanding of factors that sustain emotional feeding, even in a healthy dietary environment.

描述（由申请人提供）：长期暴露于心理社会压力源导致的情绪化进食可能是过量食物摄入的关键因素。这对女性来说可能特别重要，因为她们经常报告更多的压力引起的饮食，肥胖率也更高。普遍接受的观点是，高热量饮食的情感喂养是一种形式， 自我药疗以缓解压力的行为和生理表现。虽然这 可能是这种情况，也可能情绪喂养是受损的多巴胺（DA）奖赏途径的结果，因为暴露于慢性心理社会应激通过减少中脑边缘区的DA 2受体（D2 R）而增加对成瘾表型的易感性，从而产生多巴胺能减退的状况。此外，简单地吃高热量的饮食会降低这些区域的D2 R，但仅在某些动物中。因此，高热量饮食的自我治疗可能会进一步损害应激诱导的功能减退的DA系统。显然，这不是应对未解决压力的健康策略。对于试图节食的女性来说，一个特别重要的问题是，这些压力引起的变化，包括DA功能受损，是否会在生活方式改变的情况下持续存在。我们使用雌性恒河猴的社会从属关系作为女性慢性心理社会压力模型的初步数据表明，情况可能是这样的，因为当给予高热量饮食（HCD）时，从属女性消耗更多的卡路里，并且当只提供更健康的饮食时，这种暴食症仍然存在。然而，目前尚不清楚的是，这种模式如何在这些健康的饮食条件下继续下去。同样，我们也不知道慢性心理社会压力的缓解是否会恢复热量的限制，或者调节食欲的系统（包括DA）的变化是否会在压力缓解后持续存在。使用社会圈养的雌性恒河猴作为女性的翻译模型，该项目将确定维持情绪喂养的机制。目标1将确定由社会从属地位引起的慢性社会压力是否会维持HCD的过量摄入，以及暴露于急性压力源是否会加剧这种情况。目标2将测试这一假设，即摄入高热量的饮食会降低中脑边缘区的DR 2可用性，这将加剧社会从属地位。目标3将 测试以下假设：当LCD可用时，雌二醇将更有效地抑制占主导地位的女性的热量摄入，但当HCd可用时，雌二醇将促进热量摄入，特别是在从属女性中。在目标4中，将使用两种干预策略来进一步阐明社会压力如何维持情绪喂养：1）尽管用更健康的低热量饮食取代了HCD，但下属的摄食过多和D2 R结合潜力降低仍将持续;和2）通过改变社会地位来减少社会压力将改善但不会使D2 R可用性或食物摄入正常化。这些研究将增加我们对维持情绪喂养的因素的理解，即使是在健康的饮食环境中。