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LOUISIANA COBRE: P4: MECHANISMS OF AGING-INDUCED LEPTIN RESISTANCE AND OBESITY

LOUISIANA COBRE: P4: MECHANISMS OF AGING-INDUCED LEPTIN RESISTANCE AND OBESITY
路易斯安那 COBRE:P4:衰老引起的瘦素抵抗和肥胖的机制
批准号:
8167952
负责人:
Christopher D Morrison
金额:
$20.58万
依托单位国家:
美国
项目类别:
财政年份:
2010
资助国家:
美国
项目状态:
已结题
起止时间:
2010-07-01 至 2011-06-30

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项目成果

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中文摘要
翻译
这个子项目是众多研究子项目之一
英文摘要
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. A. Specific Aims Specific Aim 1: Test the hypothesis that aging enhances the negative effects of high fat diet (HFD) on brain leptin signaling, metabolism and behavior. Specific Aim 2: Test the hypothesis that aging will impair the ability of the animal to reduce body adiposity and recover normal brain leptin signaling following cessation of a HFD. Specific Aim 3: Test the hypothesis that leptin protects against oxidative stress in hypothalamic and hippocampal neurons by enhancing antioxidant enzyme activity via NRF2 signaling. Specific Aim 4: Determine the functional interaction between leptin signaling and oxidative stress within areas of the hippocampus and hypothalamus.
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Preclinical
FGF21-dependent mechanisms driving changes in energy expenditure during dietary protein restriction
Neural circuits coordinating protein intake: Role of FGF21
Preclinical
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