Leptin and Developmental Programming of Hypothalamic Autonomic Outflow
瘦素与下丘脑自主神经流出的发育编程
基本信息
- 批准号:9185840
- 负责人:
- 金额:$ 44.3万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2016
- 资助国家:美国
- 起止时间:2016-09-03 至 2021-07-31
- 项目状态:已结题
- 来源:
- 关键词:AddressAffectBody WeightBrain regionComplexConsensusDataDevelopmentDorsalEnergy MetabolismEnvironmental Risk FactorEpidemicFatty acid glycerol estersGoalsHigh Fat DietHormonalHormonesHypothalamic structureImmunohistochemistryIndividualLactationLeptinLifeLinkMetabolicMethodsModificationMolecular GeneticsMusNeonatalNeuronsNeurosecretory SystemsNucleus solitariusNutritionalObesityPathway interactionsPatternPeripheralPhysiologicalPhysiologyPlayPredispositionProcessRegulationResearchRisk FactorsRoleSensorySignal TransductionSiteSpecific qualifier valueSpinal CordStomachStructureStructure of nucleus infundibularis hypothalamiSystemTestingThermogenesisThree-Dimensional ImageTimeTo specifyTracerVagus nerve structureVisceralbasecell motilitycritical perioddensitydevelopmental neurobiologydorsal motor nucleusenergy balancegain of functiongenetic manipulationglucose metabolismloss of functionmetabolic phenotypemother nutritionnerve supplyneuron developmentneuronal circuitrynew therapeutic targetnutritionoffspringparaventricular nucleuspostnatalprogramsrelating to nervous systemsensory input
项目摘要
PROJECT SUMMARY
Despite a growing consensus that developmental programming of metabolic regulation contributes to the
current obesity epidemic, our understanding of developmental mechanisms impacting this process remains
rudimentary. The long range goal of this line of research is to define the developmental neurobiology of central
pathways that contribute to developmental programming of metabolic phenotype. Maternal high fat diet
(MHFD) exposure represents a developmental risk factor that contributes to metabolic dysregulation and
impacts leptin sensitivity. MHFD also appears to impact leptin secretion, but it remains unknown whether it
affects the developmental actions of leptin. For the proposed studies we will focus on neuronal pathways that
connect the paraventricular hypothalamic nucleus (PVH) with two important components of the dorsal vagal
complex (DVC): the dorsal motor nucleus of the vagus nerve (DMX) and the nucleus of the solitary tract (NTS),
which regulate autonomic functions such as thermogenesis, energy expenditure and gastric motility. Inputs to
the PVH from the NTS convey visceral sensory information, and inputs from the arcuate nucleus of the
hypothalamus (ARH) and from the NTS convey hormonal signals. Integration of this information in the PVH
impacts autonomic regulation through descending projections from the PVH to the DMX and NTS. However, it
remains unknown if development of these connections is influenced by factors that program metabolic
phenotype, such as MHFD and leptin. The overall hypothesis of the proposed research is that MHFD-L
causes hyperleptinemia during a critical period of postnatal development that disrupts normal targeting of
connections between the PVH and the DVC, and that the integrity of these connections is important for
conveying signals that regulate distinct aspects of neuroendocrine physiology and autonomic function.
Molecular genetic manipulation of leptin signaling, neuroanatomical methods, and physiological profiling will be
used to address the following Specific Aims: 1) Define the impact of MHFD on formation of connections
between the PVH and DVC in offspring, and document corresponding changes in postnatal leptin secretion
and autonomic physiology; 2) Determine if leptin is required for development of bidirectional connections
between the PVH and DVC; 3) Identify the site(s) of action, and physiological consequences, for
developmental effects of leptin on formation of connections between the PVH and DVC. Completion of these
aims will advance our understanding of how environmental signals program essential components of neural
systems required to maintain normal metabolic physiology, and may identify novel therapeutic targets.
项目总结
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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RICHARD B SIMERLY其他文献
RICHARD B SIMERLY的其他文献
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{{ truncateString('RICHARD B SIMERLY', 18)}}的其他基金
Epigenetic Mechanisms and Developmental Actions of Leptin in the Hypothalamus
下丘脑瘦素的表观遗传机制和发育作用
- 批准号:
9889122 - 财政年份:2017
- 资助金额:
$ 44.3万 - 项目类别:
Epigenetic Mechanisms and Developmental Actions of Leptin in the Hypothalamus
下丘脑瘦素的表观遗传机制和发育作用
- 批准号:
9220228 - 财政年份:2017
- 资助金额:
$ 44.3万 - 项目类别:
Developmental Programming of Neural Circuits Impacting Hypothalamic Integration
影响下丘脑整合的神经回路的发育编程
- 批准号:
10617287 - 财政年份:2016
- 资助金额:
$ 44.3万 - 项目类别:
Leptin and Developmental Programming of Hypothalamic Autonomic Outflow
瘦素与下丘脑自主神经流出的发育编程
- 批准号:
9344621 - 财政年份:2016
- 资助金额:
$ 44.3万 - 项目类别:
Developmental Programming of Neural Circuits Impacting Hypothalamic Integration
影响下丘脑整合的神经回路的发育编程
- 批准号:
10445646 - 财政年份:2016
- 资助金额:
$ 44.3万 - 项目类别:
Development of Leptin-Sensitive Hypothalamic Pathways
瘦素敏感下丘脑通路的发展
- 批准号:
7998288 - 财政年份:2010
- 资助金额:
$ 44.3万 - 项目类别:
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