MINORITY PREDOCTORAL FELLOWSHIP PROGRAM

少数族裔博士前奖学金计划

• 批准号: 7467917
• 负责人: Arion Kennedy
• 金额: $ 2.5万
• 依托单位: UNIVERSITY OF NORTH CAROLINA GREENSBORO
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-07-15 至 2009-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7467917
• 关键词: 1,2-diacylglycerol; 20 year old; Adipocytes; Adipose tissue; Adolescent; Adult; Adverse effects; Americas; Animals; Attenuated; Body Weight; Body Weight decreased; Calcium; Cardiovascular Diseases; Cell model; Chelating Agents; Child; Chronic Disease; Conjugated Linoleic Acids; Cytokine Suppression; Dairy Products; Data; Deposition; Development; Dietary Fats; Dietary Supplementation; Diglycerides; Disease; Eicosanoids; Energy Intake; Energy Metabolism; Enzymes; Epidemic; Extracellular Signal Regulated Kinases; Fatty Acids; Fatty acid glycerol esters; Fellowship Program; Fortified Food; Gene Expression; Gene Proteins; Gene Targeting; Glucose; Goals; Health; Health Care Costs; Human; Immunoblotting; Incidence; Inflammation; Inositol; Insulin Resistance; Interleukin-6; Interleukin-8; Isoenzymes; Isomerism; Knowledge; Lead; Linoleic Acids; Lipase; Lipids; Meat; Mediating; Medical; Messenger RNA; Minority; Mitogen-Activated Protein Kinases; Modeling; NF-kappaB-inducing kinase; Non-Insulin-Dependent Diabetes Mellitus; Nuclear; Nutritional; Obesity; Outcome; Overweight; Peroxisome Proliferator-Activated Receptors; Phospho-Specific Antibodies; Phospholipase A2; Phospholipase C; Phosphorylation; Phosphotransferases; Prevention; Production; Property; Prostaglandin-Endoperoxide Synthase; Prostaglandins; Protein Kinase C; Protein Kinase C Inhibitor; Publishing; Regulation; Relative (related person); Reporting; Research; Research Personnel; Research Project Grants; Risk Factors; Role; Ruminants; Safety; Signal Transduction; Specificity; Stream; Stroke; Supplementation; Testing; Triglycerides; Tumor Necrosis Factor-alpha; Tumor Necrosis Factors; Work; aged; base; beef; citrate carrier; cyclooxygenase 1; cyclooxygenase 2; cytokine; dietary supplements; enzyme activity; extracellular; glucose uptake; human TNF protein; human study; inhibitor/antagonist; innovation; insight; lipid metabolism; novel; obesity treatment; pre-doctoral; prevent; programs; protein expression; response; therapeutic target; uptake; user-friendly

DESCRIPTION (provided by applicant): The long-term goal of this research project is to identify novel dietary strategies for controlling human obesity, the most prevalent nutritional-related disease in America. The objective of this application is to identify upstream signals produced by an isomer of conjugated linoleic acid (CLA), fatty acids found in beef and dairy products and in dietary supplements for weight loss, that activate cell signals that lead to adipocyte delipidation. To complete this objective, the following specific aims will be carried out in cultures of human adipocytes: Aim #1) Determine the role of protein kinase C (PKC) in mediating CLA's activation of nuclear factor KB (NFKB) and extracellular signal-regulated kinase kinase (ERK)1/2 and delipidation; Aim #2) Identify the mechanism by which CLA increases [Ca2+]i, and its impact on NFKB and ERK1/2 signaling and delipidation; and Aim #3) Determine the extent to which CLA increases the activities of lipid metabolizing enzymes, generating signals that activate NFKB and ERK1/2 and promote delipidation. Data attained from this proposal are expected to provide critical insight for the development of therapeutic targets for the prevention and treatment of obesity and type II diabetes, and reduce health care costs related to obesity.

描述（由申请人提供）：该研究项目的长期目标是确定控制人类肥胖症的新型饮食策略，这是美国最普遍的营养相关疾病。该应用的目的是识别由共轭亚油酸（CLA）的异构体产生的上游信号，在牛肉和乳制品中发现的脂肪酸以及减肥的饮食补充剂中，从而激活了导致脂肪细胞剥落的细胞信号。为了完成这一目标，将在人脂肪细胞的培养物中进行以下特定目标：目标＃1）确定蛋白激酶C（PKC）在介导CLA激活核因子KB（NFKB）和细胞外信号受调节的受到细胞外信号激酶激酶激酶（ERK）1/2和DELIPIDED的作用；目标＃2）确定CLA增加[Ca2+] i的机制及其对NFKB和ERK1/2信号传导和删除的影响；目标＃3）确定CLA增加脂质代谢酶的活性的程度，从而产生激活NFKB和ERK1/2的信号并促进删除。预计从该提案中获得的数据将为预防和治疗肥胖和II型糖尿病的治疗靶标提供至关重要的见解，并降低与肥胖有关的医疗保健成本。