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Park2,impaired lipid absorption and protection from diet-induced obesity

Park2，脂质吸收受损并防止饮食引起的肥胖

基本信息

批准号：
9229747
负责人：
Michael J. Jurczak
金额：
$ 7.74万
依托单位：
UNIVERSITY OF PITTSBURGH AT PITTSBURGH
依托单位国家：
美国
项目类别：
财政年份：
2017
资助国家：
美国
起止时间：
2017-02-01 至 2019-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9229747
关键词：
Acute Address Body Weight Complex Data Diet Diet Monitoring Dietary Fats Enterobacteria phage P1 Cre recombinase Enterocytes Enzymes Epithelial Cells Esterification Excision Fatty acid glycerol esters Feasibility Studies Functional disorder Future Gene Expression Generations Genes Genotype High Fat Diet Homeostasis Impairment Inflammatory Intestines Knockout Mice Knowledge Lipids Longitudinal Studies Malabsorption Syndromes Measurement Mediating Metabolic Metabolism Midbrain structure Mitochondria Mitochondrial DNA Modeling Mus Nutritional Obesity Pathway interactions Peripheral Pharmacology Phenotype Pilot Projects Plasma Play Predisposition Regulation Regulatory Element Reporting Research Research Design Research Support Resistance Role Signal Transduction Small Intestines Stress Technology Testing Tissues Transgenic Mice Triglycerides Ubiquitin Weight Gain absorption cell growth regulation differential expression energy balance feeding in vivo Model intestinal epithelium lipid metabolism metabolic phenotype microbiome mouse model novel obesity treatment proteostasis stem cell niche tool ubiquitin-protein ligase uptake villin

项目摘要

Project summary The studies designed in this application will result in the generation of two unique experimental tools for understanding a newly identified regulator of intestinal lipid absorption and how intestinal lipid absorption contributes to whole-body energy balance. Specifically, we will differentially modulate the intestinal expression of a gene whose deletion results in resistance to diet induced obesity and perform baseline studies to determine 1) if restoring intestinal expression of the gene in mice that lack the gene in all tissues reverses the resistance to diet induced obesity; and 2) if deleting the gene specifically in intestine confers resistance to diet induced obesity. This new experimental technology and pilot studies will serve as the basis for more in depth studies and application for further research support. The knowledge acquired through these studies may lend itself to developing a novel treatment option for obesity.

项目摘要本申请中设计的研究将产生两种独特的实验工具，了解一种新发现的肠道脂质吸收调节剂以及肠道脂质吸收有助于全身能量平衡。具体来说，我们将差异调节肠表达一个基因的缺失导致对饮食诱导的肥胖的抵抗，并进行基线研究，确定1）如果在所有组织中都缺乏该基因的小鼠中恢复该基因的肠表达，对饮食诱导的肥胖症的抗性;和2）如果在肠中特异性地删除基因赋予对饮食的抗性诱发性肥胖这项新的实验技术和试点研究将作为更深入的基础研究和申请进一步的研究支持。通过这些研究获得的知识可能有助于为肥胖症开发一种新的治疗选择。