Prevention of obesity in Infants of overweight and obese women
预防超重和肥胖女性婴儿的肥胖
基本信息
- 批准号:10409647
- 负责人:
- 金额:$ 19.26万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2021
- 资助国家:美国
- 起止时间:2021-06-01 至 2024-05-31
- 项目状态:已结题
- 来源:
- 关键词:AddressAdultAge-MonthsAnimalsBirthBody mass indexBrainBreast FeedingCaloriesChildhoodClinical TrialsCognitiveDesire for foodDevelopmentDietary intakeEatingEconomic BurdenEnergy IntakeEnvironmentEpidemicEpigenetic ProcessExhibitsExposure toFatty acid glycerol estersFood Intake RegulationFosteringGenderGenerationsGestational AgeGrowthHigh Fat DietHuman MilkHyperphagiaHypothalamic structureIncidenceInfantInfant DevelopmentInfant FoodInfant formulaIntakeInterruptionInterventionLaboratory StudyLeptin resistanceLifeLitter SizeMetabolic syndromeMilkNerve DegenerationNeurodevelopmental DisorderNeuronsNewborn InfantNon obeseNutritionalObesityOverweightPerinatalPrevention strategyPublic HealthRattusRiskSatiationSignal TransductionStructure of nucleus infundibularis hypothalamiWeightWeight GainWomanadult obesityclinical applicationearly-onset obesityexcessive weight gainfetalin uteroincreased appetiteinfant adiposityinnovationmaternal obesitymilk intakenewborn adipositynovelobese mothersobesity in childrenobesity preventionoffspringpreventprogramsrapid weight gainrelating to nervous system
项目摘要
Throughout the world, obesity and metabolic syndrome are an ongoing epidemic crisis, presenting major public health challenges and significant economic burdens. The developmental programming effects of the in-utero environment is demonstrated by the increased risk of large for gestational age (LGA) newborns and childhood and adult obesity in offspring of overweight/obese (OW/OB) mothers. Animal studies have confirmed that maternal obesity and high fat diet programs the offspring appetite center, the arcuate nucleus, resulting in offspring hyperphagia and rapid weight gain, contributing to the generational cycle of obesity. Compounding the effect of programmed hyperphagia is the impact of breast milk caloric content. Despite evidence that breastfeeding reduces the incidence of childhood obesity, breastfeed LGA infants’ childhood obesity rates are nearly 50% greater than formula fed appropriate for gestational age infants. Maternal BMI and dietary intake are highly correlated with milk total calorie and fat content. Our laboratory studies show that offspring born to and nursed by obese rat dams exhibit hyperphagia and develop early life and adult obesity. In contrast, if these offspring are cross fostered and nursed by non-obese dams (matched for gender and litter-size), the offspring grow to normal weight and BMI as adults. These studies suggest that despite programmed offspring hyperphagia at birth, the restriction to control dam milk prevents excessive newborn weight gain and obesity. We propose that normalized caloric intake and newborn growth will prevent the onset of infant obesity, hyperleptinemia (and leptin resistance), and thus normalize appetite throughout childhood. The proposed studies will 1) Confirm that OW/OB mothers’ milk has increased total calorie content and that infants of OW/OB mothers have increased milk intake, and as an intervention 2) Determine if titrated human milk or formula calorie intake prevents excessive infant weight gain in the first six months of life. This highly innovative study will examine the potential efficacy of a novel preventative strategy to prevent the development of infant obesity and interrupt the generational cycle of obesity.
在世界范围内,肥胖和代谢综合症是一场持续的流行危机,带来了重大的公共卫生挑战和巨大的经济伯恩斯。 UTERO环境的发展的编程效应证明了胎龄(LGA)新生儿,童年和成人肥胖的较大风险在超重/肥胖(OW/OB)母亲的后代。动物研究已经证实,母体肥胖和高脂饮食计划是后代食欲中心,弧形核us,导致后代的超态和体重快速增加,导致肥胖的世代循环。复杂的编程倍率的效果是母乳热量含量的影响。尽管有证据表明母乳喂养降低了儿童肥胖的发生率,但母乳喂养LGA婴儿的儿童肥胖率几乎比喂食适合妊娠婴儿的配方奶大50%。母体BMI和饮食摄入量与牛奶总卡路里和脂肪含量高度相关。我们的实验室研究表明,由肥胖大鼠大坝出生和护理的后代表现出倍感,并发展早期生活和成人肥胖。相反,如果这些后代由非肥胖大坝(与性别和垃圾大小相匹配),将后代增长到正常体重,而BMI成年。这些研究表明,尽管在生日那天对后代的脾气制作了多晶状体,但控制大坝牛奶的限制可以防止新生儿的体重增加和肥胖。我们提出,标准化的热量摄入和新生儿的生长将防止婴儿肥胖症,高瘦素血症(和瘦素耐药性)的发作,从而使整个儿童的食欲正常。拟议的研究将1)确认OW/Ob母亲的牛奶增加了卡路里的总含量,并且OW/OB母亲的婴儿增加了牛奶摄入量,而作为一项干预措施2)确定滴定的人牛奶或配方奶粉摄入量是否可以防止过量婴儿体重在生命的前六个月。这项高度创新的研究将研究一种新型预防策略的潜在有效性,以防止婴儿目标的发展并中断目标的代循环。
项目成果
期刊论文数量(2)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
TNFα-Induced Oxidative Stress and Mitochondrial Dysfunction Alter Hypothalamic Neurogenesis and Promote Appetite Versus Satiety Neuropeptide Expression in Mice.
- DOI:10.3390/brainsci12070900
- 发表时间:2022-07-09
- 期刊:
- 影响因子:3.3
- 作者:Desai, Mina;Stiles, Linsey;Torsoni, Adriana S.;Torsoni, Marcio A.;Shirihai, Orian S.;Ross, Michael G.
- 通讯作者:Ross, Michael G.
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Mina Desai其他文献
Mina Desai的其他文献
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{{ truncateString('Mina Desai', 18)}}的其他基金
Maternal Obesity Programs Offspring Hypothalamic Neurogenesis and Appetite: Mechanisms and Prevention of Hyperphagia-mediated Childhood Obesity
母亲肥胖影响后代下丘脑神经发生和食欲:进食过多介导的儿童肥胖的机制和预防
- 批准号:
10054141 - 财政年份:2020
- 资助金额:
$ 19.26万 - 项目类别:
Maternal Obesity Programs Offspring Hypothalamic Neurogenesis and Appetite: Mechanisms and Prevention of Hyperphagia-mediated Childhood Obesity
母亲肥胖影响后代下丘脑神经发生和食欲:进食过多介导的儿童肥胖的机制和预防
- 批准号:
10264059 - 财政年份:2020
- 资助金额:
$ 19.26万 - 项目类别:
Maternal Obesity Programs Offspring Hypothalamic Neurogenesis and Appetite: Mechanisms and Prevention of Hyperphagia-mediated Childhood Obesity
母亲肥胖影响后代下丘脑神经发生和食欲:进食过多介导的儿童肥胖的机制和预防
- 批准号:
10407069 - 财政年份:2020
- 资助金额:
$ 19.26万 - 项目类别:
Maternal Obesity Programs Offspring Hypothalamic Neurogenesis and Appetite: Mechanisms and Prevention of Hyperphagia-mediated Childhood Obesity
母亲肥胖影响后代下丘脑神经发生和食欲:进食过多介导的儿童肥胖的机制和预防
- 批准号:
10653772 - 财政年份:2020
- 资助金额:
$ 19.26万 - 项目类别:
Developmentally Programmed Hyperphagia and Obesity via BPA enhanced Neurogenesis
通过 BPA 增强神经发生来控制发育性贪食和肥胖
- 批准号:
8726396 - 财政年份:2013
- 资助金额:
$ 19.26万 - 项目类别:
Developmentally Programmed Hyperphagia and Obesity via BPA enhanced Neurogenesis
通过 BPA 增强神经发生来控制发育性贪食和肥胖
- 批准号:
8571418 - 财政年份:2013
- 资助金额:
$ 19.26万 - 项目类别:
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