{"title":"发育、大脑可塑性和奖励:早期高脂肪饮食暴露容易导致肥胖——从椅子上看","authors":"C-D Walker","doi":"10.1038/ijosup.2012.14","DOIUrl":null,"url":null,"abstract":"<p><p>The significant increase in childhood obesity has become a particular concern, and it is recognized that the programming of obesity can arise from events occurring in the peri-conception period, prenatally and/or during the early postnatal period. In particular, high intake of dietary fat by the mother has long-term effects that are worse than once thought. This symposium was designed to outline some of the important consequences of maternal high-fat feeding during gestation and lactation, as well as exposure to a high-fat diet (HFD) after weaning, on the programming of homeostatic and hedonic regulation of food intake in both rodents and nonhuman primates (NHPs). Although a consensus emerges that high-fat feeding in early development increases the risk of developing obesity and the metabolic syndrome in adulthood, there is less agreement on the mechanisms through which this risk is conferred. Epigenetic modifications in specific gene promoters within the dopaminergic reward pathways and on the histone code will be discussed. We will also examine the effects of metabolic hormones such as leptin and ghrelin to shape the early development of hypothalamic projections that are critical to control food intake; finally, the importance of placental function in increasing obesity risk in NHP fetus from HFD mothers will be debated. </p>","PeriodicalId":14202,"journal":{"name":"International journal of obesity supplements","volume":"2 Suppl 2","pages":"S3-6"},"PeriodicalIF":0.0000,"publicationDate":"2012-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1038/ijosup.2012.14","citationCount":"6","resultStr":"{\"title\":\"Development, brain plasticity and reward: early high-fat diet exposure confers vulnerability to obesity-view from the chair.\",\"authors\":\"C-D Walker\",\"doi\":\"10.1038/ijosup.2012.14\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The significant increase in childhood obesity has become a particular concern, and it is recognized that the programming of obesity can arise from events occurring in the peri-conception period, prenatally and/or during the early postnatal period. In particular, high intake of dietary fat by the mother has long-term effects that are worse than once thought. This symposium was designed to outline some of the important consequences of maternal high-fat feeding during gestation and lactation, as well as exposure to a high-fat diet (HFD) after weaning, on the programming of homeostatic and hedonic regulation of food intake in both rodents and nonhuman primates (NHPs). Although a consensus emerges that high-fat feeding in early development increases the risk of developing obesity and the metabolic syndrome in adulthood, there is less agreement on the mechanisms through which this risk is conferred. Epigenetic modifications in specific gene promoters within the dopaminergic reward pathways and on the histone code will be discussed. We will also examine the effects of metabolic hormones such as leptin and ghrelin to shape the early development of hypothalamic projections that are critical to control food intake; finally, the importance of placental function in increasing obesity risk in NHP fetus from HFD mothers will be debated. </p>\",\"PeriodicalId\":14202,\"journal\":{\"name\":\"International journal of obesity supplements\",\"volume\":\"2 Suppl 2\",\"pages\":\"S3-6\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2012-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1038/ijosup.2012.14\",\"citationCount\":\"6\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International journal of obesity supplements\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1038/ijosup.2012.14\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2012/12/11 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of obesity supplements","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1038/ijosup.2012.14","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2012/12/11 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
Development, brain plasticity and reward: early high-fat diet exposure confers vulnerability to obesity-view from the chair.
The significant increase in childhood obesity has become a particular concern, and it is recognized that the programming of obesity can arise from events occurring in the peri-conception period, prenatally and/or during the early postnatal period. In particular, high intake of dietary fat by the mother has long-term effects that are worse than once thought. This symposium was designed to outline some of the important consequences of maternal high-fat feeding during gestation and lactation, as well as exposure to a high-fat diet (HFD) after weaning, on the programming of homeostatic and hedonic regulation of food intake in both rodents and nonhuman primates (NHPs). Although a consensus emerges that high-fat feeding in early development increases the risk of developing obesity and the metabolic syndrome in adulthood, there is less agreement on the mechanisms through which this risk is conferred. Epigenetic modifications in specific gene promoters within the dopaminergic reward pathways and on the histone code will be discussed. We will also examine the effects of metabolic hormones such as leptin and ghrelin to shape the early development of hypothalamic projections that are critical to control food intake; finally, the importance of placental function in increasing obesity risk in NHP fetus from HFD mothers will be debated.