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Neuroendocrine Systems involved in Early-life Programming for Obesity and Diabetes

神经内分泌系统参与肥胖和糖尿病的早期规划

基本信息

批准号：
10544493
负责人：
Kathleen Alanna Page
金额：
$ 67.76万
依托单位：
UNIVERSITY OF SOUTHERN CALIFORNIA
依托单位国家：
美国
项目类别：
财政年份：
2019
资助国家：
美国
起止时间：
2019-02-13 至 2024-12-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10544493
关键词：
Age Animal Model Appetite Regulation Area Biological Body fat Body mass index Brain Child Child Support Childhood diabetes Complement Computerized Medical Record Coupled Desire for food Development Diabetes Mellitus Diagnosis Documentation Early Intervention Early identification Environment Evolution Exposure to Future Genetic Gestational Diabetes Glucose Goals Growth Health Hour Human Hyperglycemia Hypothalamic structure Impairment Insulin Resistance Intervention Life Link Longitudinal Studies Magnetic Resonance Imaging Maternal Exposure Maternal-Fetal Transmission Metabolic Diseases Mothers Neurosecretory Systems Non-Insulin-Dependent Diabetes Mellitus OGTT Obesity Oral Outcome Participant Pathway interactions Personal Satisfaction Pilot Projects Play Pregnancy Pregnancy Complications Pregnancy Trimesters Prevalence Prevention strategy Risk Role Sampling Satiation Severities Siblings Signal Transduction Structure Testing Translating Weight Gain Youth aged blood glucose regulation brain pathway cohort critical period diabetes risk energy balance fetal programming high risk in utero innovation insulin sensitivity maternal diabetes maternal obesity maternal weight metabolic phenotype next generation novel obesity in children obesity prevention obesity risk offspring prenatal exposure prepregnancy prevent response

项目摘要

! PROJECT SUMMARY/ABSTRACT The prevalence and severity of childhood obesity have increased dramatically and are coupled with alarming 30% rise in the prevalence of type 2 diabetes (T2D) in youth over the last decade. Mounting evidence suggests that exposures to maternal obesity and/or gestational diabetes mellitus (GDM) in utero contribute to these increases in childhood obesity and T2D. Studies from our group and others have shown that children who were exposed in utero to maternal obesity or GDM have greater adiposity and a higher risk for developing T2D compared to unexposed children. Studies in siblings discordant for maternal exposures suggest that the risk is in excess of that attributable to genetics and shared environment. The biological underpinnings of such maternal-fetal programming are poorly understood. Provocative studies in animal models reveal that intrauterine exposure to maternal obesity and/or diabetes results in alterations in the development of the hypothalamus, a brain area that is critical for the regulation of appetite and glucose homeostasis, leading to obesity and T2D later in life. To date, no studies have investigated the effects of exposure to maternal obesity or GDM on brain appetite pathways in humans. The overarching goal of this proposal is to test the hypothesis that in utero exposure to maternal obesity and/or GDM alters the structure and function of brain appetite pathways in ways that adversely impact energy balance and increases future risk for obesity and T2D in humans. Overall, these studies are highly innovative and have the potential to translate mechanistic findings in humans into early intervention strategies aimed at preventing the vicious cycle of maternal obesity/GDM and childhood obesity and T2D. !

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