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Cell Cycle Regulators in Diabetes and Obesity

Cell Cycle Regulators in Diabetes and Obesity
糖尿病和肥胖症中的细胞周期调节剂
批准号：
8553543
负责人：
Sushil Rane
金额：
$34.63万
依托单位：
NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES
依托单位国家：
美国
项目类别：
财政年份：
--
资助国家：
美国
项目状态：
未结题
起止时间：
至
来源：
https://reporter.nih.gov/project-details/8553543
关键词：
AddressAnimal ModelCell CycleCell Cycle ProgressionCell DeathDataDiabetes MellitusDiabetic mouseEpidemiologyFuture GenerationsGoalsGrowth and Development functionHomeostasisInvestigationMalignant NeoplasmsMetabolicMusMuscleMuscle DevelopmentMuscle functionMutationObesityObesity associated diseaseOrganPathogenesisPathway interactionsProcessPublic HealthRoleblood glucose regulationcancer riskenergy balanceglucose tolerancelipid biosynthesismouse modelnon-diabetic

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中文摘要
翻译
在这项提案中，我们将使用CDK4基因突变的小鼠模型。CDK4-/-小鼠患有糖尿病且身材瘦弱，相比之下，CDK4R24C小鼠没有糖尿病且体重较重。这些观察结果与Rb/E2F途径在脂肪形成和肌肉分化中的作用是一致的。我们假设，CDK4活性可能调节脂肪生成、肌肉发育和功能，进而调节整体能量平衡。我们正在通过评估CDK4小鼠不同代谢器官中依赖CDK4的功能来研究糖耐量和能量平衡的机制。这些发现揭示了CDK4在调节能量平衡过程中的重要作用。
英文摘要
In this proposal we will use mouse models that have mutations in the Cdk4 locus. Cdk4-/- mice are diabetic and lean, and in contrast, Cdk4R24C mice are non-diabetic and heavier. These observations are consistent with a role of the RB/E2F pathway in adipogenesis amd muscle differentiation. We hypothesize that Cdk4 activity may regulate adipogenesis and muscle development and function, and, by extension, overall energy balance. We are studying mechanisms of glucose tolerance and energy homeostasis by evaluating CDk4-dependent functions in different metabolic organs in the Cdk4 mice. The findings are revealing important role of Cdk4 in processes that modulate energy balance.
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