Association between workaholism and fasting glucose/insulin, insulin sensitivity, and lipids.

项目摘要 2型糖尿病（T2 D）的发生和发展与多种因素有关。这些因素 包括饮食、锻炼、遗传学、环境暴露、社会经济学、年龄、性别、地理 行为模式在行为模式中，新出现的证据表明，工作狂是一种促成因素。 冠心病和中风，这两种疾病往往是大血管并发症和/或 并伴有长期的T2 D工作狂远远超出了工作的小时数-它是 以强迫性需求为特征（即，专注于工作）工作过度努力（即，永久 工作参与度），它跨越了白领和蓝领工人。工作狂的角色可能 在T2 D病因学中的作用尚不清楚。我们的长期目标是建立 工作狂促进T2 D发展的机制。此R15应用程序的目标是 通过调查工作狂和工作狂之间的关系， 血糖、胰岛素和脂质的循环水平。我们将重点关注健康和糖尿病前期的受试者 范围，以避免T2 D的混淆效应。整体压力、工作压力、 睡眠问题、总热量摄入和总体力活动对工作狂与 还将检查受损的代谢结果。我们假设工作狂与 葡萄糖/胰岛素失调，是胰岛素抵抗（T2 D的标志）的主要驱动因素，以及 血脂异常与胰岛素抵抗相关，并导致T2 D及其 并发症目的1：探讨工作狂与空腹血糖、空腹胰岛素、 和胰岛素敏感性。目的2：研究工作狂与空腹低密度脂蛋白（LDL）、高密度脂蛋白（HDL）、总胆固醇（TC）、总胆固醇（TC）、总胆固醇（TC）的关系。 胆固醇和甘油三酯。影响：拟议的研究通过调查一个新的领域， 工作狂与空腹血糖、空腹胰岛素、计算的胰岛素敏感性和血脂的关系 使用客观和严格的评估来调查工作狂的健康水平。建立 工作狂和特定代谢结果之间的关系将为测试提供基础 旨在改变工作狂行为及其对胰岛素抵抗的潜在影响的干预措施， 糖尿病前期，最终是T2 D。此外，我们的工作将为未来的纵向研究奠定基础， 将在工作狂和糖尿病前期/T2 D之间建立机械水平的因果关系。最后，一致 以R15应用为目标，将为学生提供强有力的跨学科培训 （特别是来自少数群体）与工业/组织心理学，统计学， 生物医学科学

PROJECT SUMMARY A range of factors contribute to the development and progression of type 2 diabetes (T2D). These factors include diet, exercise, genetics, environmental exposures, socioeconomics, age, sex, geography, and behavioral patterns. Among behavioral patterns, emerging evidence suggests workaholism is a contributing factor in coronary heart disease and stroke, two diseases that are often macrovascular complications of and/or complicated by prolonged T2D. Workaholism goes well beyond the number of hours worked—it is characterized by a compulsive need (i.e., preoccupation with work) to work excessively hard (i.e., perpetual work involvement), and it spans across white-collar and blue-collar workers alike. The role workaholism may play in contributing toward the etiology of T2D is not known. Our long-term objective is to establish mechanisms by which workaholism contributes to the development of T2D. The goal of this R15 application is to take the first steps toward our long-term goal by investigating the relationship between workaholism and circulating levels of glucose, insulin, and lipids. We will focus on subjects across the healthy and prediabetic range to avoid the confounding effects of T2D. The potential mediating roles of overall stress, work stress, sleep problems, total caloric intake, and total physical activity on the association between workaholism and impaired metabolic outcomes will also be examined. We hypothesize workaholism is associated with glucose/insulin dysregulation, which are major drivers of insulin resistance (a hallmark of T2D), and dyslipidemia, which is associated with insulin resistance and contributes to the etiology of T2D and its complications. Aim 1 will determine the relationship between workaholism and fasting glucose, fasting insulin, and insulin sensitivity. Aim 2 will determine the relationship between workaholism and fasting LDL, HDL, total cholesterol, and triglycerides. Impact: The proposed research breaks new ground by investigating a relationship between workaholism and fasting glucose, fasting insulin, calculated insulin sensitivity, and lipid levels using objective and rigorous assessments to investigate the health of workaholics. Establishing a relationship between workaholism and specific metabolic outcomes will provide the basis for testing interventions designed to modify workaholic behaviors and its potential impact on insulin resistance, prediabetes, and ultimately T2D. Furthermore, our work will set the basis for future longitudinal studies which will establish causality at a mechanistic level between workaholism and prediabetes/T2D. Finally, consistent with the objectives of an R15 application, strong interdisciplinary training will be provided to students (particularly from minority groups) with the fusion of industrial/organizational psychology, statistics, and biomedical sciences.