White Adipose Tissue Physiology, Mitochondrial Function and Adiponectin
白色脂肪组织生理学、线粒体功能和脂联素
基本信息
- 批准号:8847709
- 负责人:
- 金额:$ 46.43万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2013
- 资助国家:美国
- 起止时间:2013-07-05 至 2016-04-30
- 项目状态:已结题
- 来源:
- 关键词:AdipocytesAdipose tissueAmyloidAreaAttentionBiogenesisBlood CirculationCarbohydratesCardiovascular DiseasesCatalogingCatalogsCell physiologyDataDietElectron TransportEtiologyFGF21 geneFatty acid glycerol estersFunctional disorderGeneric DrugsHealthHomeostasisInsulin ResistanceInterventionLeadLinkLipidsMediatingMembrane PotentialsMetabolicMetabolic DiseasesMetabolismMitochondriaMitochondrial Membrane ProteinMitochondrial ProteinsModelingNon-Insulin-Dependent Diabetes MellitusObesityOuter Mitochondrial MembraneOxidative StressPathway interactionsPhasePhysiologyPlayProcessProductionProtein ImportProtein PrecursorsProteinsResearch InfrastructureRoleSurveysSystemTestingVascular Endothelial Growth Factorsadiponectinbasecopingcytochrome c oxidasediabeticdicarboxylate-binding proteinglucose metabolismlipid metabolismloss of functionmitochondrial dysfunctionmitochondrial membranemouse modeloxidationprogramsrespiratory
项目摘要
DESCRIPTION (provided by applicant): Over the past decade, efforts in the field have focused on the connection between mitochondrial dysfunction and the etiology of obesity, insulin resistance and the progression of type 2 diabetes mellitus (T2DM). Numerous studies indicate that such metabolic disorders are accompanied by reduced mitochondrial content, compromised mitochondrial respiratory capacity, heightened oxidative stress, impaired -oxidation and, consequently, altered whole-body lipid and glucose metabolism. In parallel, both the production and the release of the adipokine adiponectin are frequently impaired as well. Our data indicate that altered mitochondrial activity and adiponectin production are tightly linked. In
the studies outlined in this proposal, we will better define the impact of mitochondrial function o white adipose tissue physiology and establish which metabolic intermediates are the critical drivers connecting mitochondrial activity and adiponectin production. We propose to approach these questions by surveying the effects of a number of different manipulations of mitochondrial activity in adipocytes and cataloguing the common denominators and distinct features between the models that lead to systemic metabolic benefits and the induction of adiponectin. We will approach this in a hierarchical fashion by focusing on broad inducers of the mitochondrial program in the white adipocyte (Aim 1), followed by a more specific manipulation of mitochondrial activity (Aim 2) in which we employ gain and loss of function models of two critical mitochondrial proteins, mitoNEET and the mitochondrial dicarboxylate carrier. This will allow us to effectively manipulate mitochondrial activity in a very-targeted fashion. In the last aim (Aim 3, we will develop a system that will allow us to acutely phase out overall mitochondrial function selectively in adipocytes in a highly-titratable fashion. Combined, these studies enable us to carefully dissect the effects of altered mitochondrial function on adiponectin production and overall cellular physiology of the white adipocyte. While the established role of mitochondrial function in brown adipocytes is well appreciated, our data argues that the relevance of mitochondrial function in the white adipocyte has been mistakenly undervalued. We have generated a unique toolset that allows us to systematically approach the question of "mitochondrial dysfunction" and, in fact, helps us to methodically define the term "dysfunction". We also have the desire to better understand the mechanisms governing adiponectin production and release. Based upon our preliminary data, we strongly believe that mitochondrial activity plays an essential role in this process. Results from our studies will help us define mechanistically why adipocytes regulate adiponectin release into circulation by gauging mitochondrial activity, leading to a better teleological understanding of the role of adiponectin within the system.
描述(由申请人提供):在过去的十年中,该领域的努力集中在线粒体功能障碍与肥胖病因、胰岛素抵抗和2型糖尿病(T2DM)进展之间的联系。大量研究表明,这种代谢紊乱伴随着线粒体含量降低、线粒体呼吸能力受损、氧化应激升高、氧化受损,从而导致全身脂质和葡萄糖代谢改变。同时,脂肪因子脂联素的产生和释放也经常受损。我们的数据表明,线粒体活性的改变和脂联素的产生密切相关。在
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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PHILIPP E SCHERER其他文献
PHILIPP E SCHERER的其他文献
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{{ truncateString('PHILIPP E SCHERER', 18)}}的其他基金
Physiological Role of Dedifferentiating Dermal Adipose Tissue
真皮脂肪组织去分化的生理作用
- 批准号:
10348609 - 财政年份:2021
- 资助金额:
$ 46.43万 - 项目类别:
Physiological Role of Dedifferentiating Dermal Adipose Tissue
真皮脂肪组织去分化的生理作用
- 批准号:
10532175 - 财政年份:2021
- 资助金额:
$ 46.43万 - 项目类别:
White Adipose Tissue Physiology, Mitochondrial Function and Adiponectin
白色脂肪组织生理学、线粒体功能和脂联素
- 批准号:
9920126 - 财政年份:2013
- 资助金额:
$ 46.43万 - 项目类别:
White Adipose Tissue Physiology, Mitochondrial Function and Adiponectin
白色脂肪组织生理学、线粒体功能和脂联素
- 批准号:
8557828 - 财政年份:2013
- 资助金额:
$ 46.43万 - 项目类别:
White Adipose Tissue Physiology, Mitochondrial Function and Adiponectin
白色脂肪组织生理学、线粒体功能和脂联素
- 批准号:
10395460 - 财政年份:2013
- 资助金额:
$ 46.43万 - 项目类别:
White Adipose Tissue Physiology, Mitochondrial Function and Adiponectin
白色脂肪组织生理学、线粒体功能和脂联素
- 批准号:
8696859 - 财政年份:2013
- 资助金额:
$ 46.43万 - 项目类别:
Novel Mechanisms Regulating the Adipocyte-Brain Hepatocyte Axis
调节脂肪细胞-脑肝细胞轴的新机制
- 批准号:
8308565 - 财政年份:2010
- 资助金额:
$ 46.43万 - 项目类别:
Novel Mechanisms Regulating the Adipocyte-Brain-Hepatocyte Axis
调节脂肪细胞-脑-肝细胞轴的新机制
- 批准号:
9100718 - 财政年份:2010
- 资助金额:
$ 46.43万 - 项目类别:
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