Depression and Insulin Sensitivity in Adolescents

青少年的抑郁和胰岛素敏感性

• 批准号: 9924530
• 负责人: LAUREN BERGER SHOMAKER
• 金额: $ 52.92万
• 依托单位: COLORADO STATE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2017
• 资助国家: 美国
• 起止时间: 2017-06-01 至 2022-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9924530
• 关键词: Accounting; Address; Adolescence; Adolescent; Adolescent obesity; Adrenal Gland Hyperfunction; Adult; Affect; Aftercare; Aggressive course; Award; Behavior; Behavioral; Beta Cell; Cell physiology; Child; Cognitive; Communities; Consultations; Control Groups; Data; Depressive disorder; Deterioration; Diabetes Mellitus; Diabetes prevention; Disadvantaged; Disease; Diurnal Rhythm; Doctor of Philosophy; Eating; Ethnic group; Face; Failure; Family; Family history of; Female Adolescents; Goals; Health; Health education; Healthcare; High Prevalence; Human; Hydrocortisone; Insulin; Insulin Resistance; Intervention; Knowledge; Link; Longevity; Mediator of activation protein; Medicine; Mental Depression; Mission; Modeling; Monitor; Non-Insulin-Dependent Diabetes Mellitus; Obesity; Outcome; Output; Overweight; Pathogenesis; Physical activity; Physiological; Physiology; Play; Population; Prevention; Psychosocial Stress; Puberty; Public Health; Randomized Controlled Trials; Recording of previous events; Research; Risk; Risk Factors; Role; Scientist; Sleep; Sleep disturbances; Stress; Structure; Structure of beta Cell of islet; Symptoms; Testing; Time; United States National Institutes of Health; Work; cardiometabolic risk; cardiometabolism; child depression; comorbidity; cost effective; depressive symptoms; diabetes risk; early onset; effective intervention; ethnic diversity; experience; follow-up; girls; high risk; high-risk adolescents; improved; innovation; insulin secretion; insulin sensitivity; lifestyle intervention; moderate-to-vigorous physical activity; modifiable risk; multidisciplinary; physical inactivity; preservation; prevent; program costs; programs; prospective; psychosocial; racial and ethnic; response; sedentary; statistics; stress symptom; symptomatic improvement; theories; young adult

Project Summary/Abstract There has been rapid escalation of type 2 diabetes (T2D) rates in adolescents. Early-onset T2D (<20y) typically shows a more aggressive course than adult-onset T2D and disproportionately affects girls from disadvantaged, racial/ethnic groups. This group of girls also is at heightened risk for depression, and depression and T2D are linked. Depressive symptoms often manifest in adolescence and are a prospective risk factor for worsening of insulin sensitivity, the major physiological precursor—in combination with deterioration of pancreatic β-cell ca- pacity to secrete insulin—in the path to T2D. The effects of depression on poor insulin sensitivity remain even after accounting for adiposity. In theory, depressive symptoms may worsen insulin sensitivity through stress- induced behaviors (e.g., disinhibited eating, [physical inactivity], sleep disturbance) and stress-induced phys- iological causal mechanisms (e.g., hypercortisolism). The central theme of our proposal is that intervening to reduce depressive symptoms in adolescents at-risk for T2D may offer an innovative, targeted approach to ame- liorate insulin resistance and to, consequently, preserve β-cell function and lessen T2D risk. In preliminary data from an NIH K99/R00 Award, the PI found initial evidence that a 6-week cognitive-behavioral group decreased depressive symptoms and prevented worsening of insulin sensitivity 1 year later in overweight and obese girls with moderate depressive symptoms and a family history of T2D, in comparison to a 6-week health education control group. Directly extending these findings, the aims of this R01 proposal are: 1) to assess the efficacy of a 6-week cognitive-behavioral depression group vs. a 6-week health education control group for improving insulin sensitivity and preserving β-cell function in racially/ethnically diverse adolescent girls at-risk for T2D with mod- erate depressive symptoms over a 1-year follow-up; 2) to evaluate changes in eating, [physical activity], and sleep as behavioral explanatory mediators underlying the relationship between decreases in depressive symp- toms and improvements in insulin sensitivity and β-cell function over 1 year and 3) to test changes in cortisol awakening response, diurnal cortisol rhythm, and total daily cortisol output as physiological mechanisms explain- ing the relationship between decreases in depressive symptoms and improvements in insulin sensitivity and β- cell function over 1 year. We have assembled a strong, multidisciplinary team of scientists with expertise in depression, obesity, eating (PI: Lauren Shomaker, PhD), [child and adolescent insulin sensitivity and secre- tion] (Co-I: Kristen Nadeau, MD, MS), [puberty, precursors of early-onset T2D] (Co-I: Megan Kelsey, MD, MS), and statistics (Co-I: Sangeeta Rao, PhD), as well as consultation from experts on [ambulatory physical activity monitoring (Andrea Kriska, PhD, MS)], sleep medicine (Kenneth Wright Jr, PhD), [and adolescent depression (Eric Stice, PhD)]. Our long-term goal is to identify feasible, cost-effective public health solutions that have high potential for effective dissemination in communities at-risk for cardiometabolic disease and to understand the mechanisms by which alleviating psychosocial stress facilitates more positive health outcomes.

项目摘要/摘要 青少年中2型糖尿病(T2D)的发病率迅速上升。早发性T2D(&lt；20y)通常 显示出比成人起病的T2D更具侵略性的病程，并且对弱势女孩的影响不成比例， 种族/民族群体。这组女孩患抑郁症的风险也很高，抑郁症和T2D是 已链接。抑郁症状通常出现在青春期，并是恶化的潜在危险因素 胰岛素敏感性，主要的生理前体-结合胰腺β细胞的恶化。 分泌胰岛素的速度-在T2D的道路上。抑郁对胰岛素敏感性差的影响仍然是一样的。 在考虑了肥胖症之后。从理论上讲，抑郁症状可能会通过压力恶化胰岛素敏感性-- 诱导性行为(例如，不禁止进食、[身体不活动]、睡眠障碍)和应激诱导性物理行为- 生物学原因机制(例如，皮质醇过多症)。我们建议的中心主题是干预 减少T2D高危青少年的抑郁症状可能提供一种创新的、有针对性的方法来治疗AME- 减轻胰岛素抵抗，从而保护β细胞功能，降低T2D风险。在初步数据中 从NIH K99/R00奖中，PI发现了6周认知行为组减少的初步证据 超重和肥胖女孩的抑郁症状和预防1年后胰岛素敏感性恶化 有中度抑郁症状和T2D家族史的患者与接受6周健康教育的患者进行比较 对照组。直接扩展这些发现，本R01提案的目的是：1)评估 6周认知行为抑郁组与6周健康教育对照组的胰岛素改善 不同种族/民族的T2D合并MOD的青春期女孩的敏感性和β细胞功能的保护 在一年的随访中消除抑郁症状；2)评估饮食、[体力活动]和 睡眠作为行为解释因子在抑郁症状减少之间的关系-- 一年和三年的TOM和胰岛素敏感性和β细胞功能的改善，以测试皮质醇的变化 唤醒反应，每日皮质醇节律，和每日皮质醇总排出量，这是生理机制解释的- 抑郁症状的减轻与胰岛素敏感性和β的改善之间的关系 细胞功能1年以上。我们已经组建了一支强大的、多学科的科学家团队，他们拥有 抑郁，肥胖，饮食(PI：Lauren Shomaker，PhD)，[儿童和青少年胰岛素敏感性和安全感- [青春期，早发性T2D的先兆](共同-I：梅根·凯尔西，医学，医学博士， Ms)和统计(Co-I：Sangeeta Rao，PhD)，以及[非卧床体检]专家的咨询 活动监测(Andrea Kriska，博士，硕士)]，睡眠医学(小Kenneth Wright Jr，博士)，[和青少年 抑郁症(Eric Stices，博士)]。我们的长期目标是找到可行的、具有成本效益的公共卫生解决方案 在心脏代谢性疾病的高危社区有效传播的潜力很高 了解缓解心理社会压力促进更积极的健康结果的机制。