Dalle Molle R, Bischoff A R, Portella A K, Silveira P P
1Departamento de Pediatria, Faculdade de Medicina,Universidade Federal do Rio Grande do Sul,Porto Alegre,Brazil.
2Programa de Residência Médica em Pediatria,Hospital de Clínicas de Porto Alegre,Porto Alegre,Brazil.
J Dev Orig Health Dis. 2016 Jun;7(3):222-230. doi: 10.1017/S2040174415007187. Epub 2015 Sep 28.
Increased energy consumption is one of the major factors implicated in the epidemic of obesity. There is compelling evidence, both clinical and experimental, that fetal paucity of nutrients may have programming effects on feeding preferences and behaviors that can contribute to the development of diseases. Clinical studies in different age groups show that individuals born small for their gestational age (SGA) have preferences towards highly caloric foods such as carbohydrates and fats. Some studies have also shown altered eating behaviors in SGA children. Despite an apparent discrepancy in different age groups, all studies seem to converge to an increased intake of palatable foods in SGA individuals. Small nutrient imbalances across lifespan increase the risk of noncommunicable diseases in adult life. Homeostatic factors such as altered responses to leptin and insulin and alterations in neuropeptides associated with appetite and satiety are likely involved. Imbalances between homeostatic and hedonic signaling are another proposed mechanism, with the mesocorticolimbic dopaminergic pathway having differential reward and pleasure responses when facing palatable foods. Early exposure to undernutrition also programs hypothalamic-pituitary-adrenal axis, with SGA having higher levels of cortisol in different ages, leading to chronic hyperactivity of this neuroendocrine axis. This review summarizes the clinical and experimental evidence related to fetal programming of feeding preferences by SGA.
能量消耗增加是肥胖流行的主要因素之一。有令人信服的临床和实验证据表明，胎儿期营养缺乏可能对进食偏好和行为产生编程效应，进而导致疾病的发生。针对不同年龄组的临床研究表明，小于胎龄儿（SGA）对高热量食物（如碳水化合物和脂肪）有偏好。一些研究还表明，SGA儿童存在饮食行为改变。尽管不同年龄组之间存在明显差异，但所有研究似乎都表明SGA个体对美味食物的摄入量增加。一生中微小的营养失衡会增加成年后患非传染性疾病的风险。可能涉及一些稳态因素，如对瘦素和胰岛素的反应改变以及与食欲和饱腹感相关的神经肽变化。稳态信号与享乐信号之间的失衡是另一种提出的机制，当中脑边缘多巴胺能通路面对美味食物时会有不同的奖赏和愉悦反应。早期暴露于营养不良也会对下丘脑 - 垂体 - 肾上腺轴进行编程，SGA在不同年龄段的皮质醇水平较高，导致该神经内分泌轴长期过度活跃。本综述总结了与SGA胎儿进食偏好编程相关的临床和实验证据。
