Nutritional programming of hypothalamic development: critical periods and windows of opportunity.
Nutritional programming of hypothalamic development: critical periods and windows of opportunity.
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DOI：
10.1038/ijosup.2012.17
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发表时间：
2012-12-01
期刊：
影响因子：
--
通讯作者：
Bouret, S G
中科院分区：
文献类型：
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作者：
Bouret, S G
肥胖症在全世界以惊人的速度增加，特别是在儿童中。流行病学和实验数据表明，出生前和/或出生后的营养和生长欠佳可能在肥胖症和相关疾病的发展中起重要作用。同样，围产期营养不良可能导致终生代谢紊乱。虽然控制代谢程序的精确生物学机制尚未完全阐明，但越来越多的证据表明，肥胖和其他代谢疾病可能是由于调节能量平衡的下丘脑通路的潜在发育程序发生变化所致。下丘脑从胚胎期开始经历巨大的生长，并持续到青春期，围产期营养的改变会影响各种发育过程，包括神经发生和轴突生长，这可能导致下丘脑发育异常。代谢激素，尤其是瘦素，能够将信号传递到发育中的下丘脑，以响应营养环境的改变，并可能成为对早期代谢紊乱的潜在适应不良反应的基础。更好地了解下丘脑发育过程中的最佳围产期激素和营养环境可能有助于改善和逆转胎儿和/或新生儿的代谢编程不良。
Obesity is increasing at an alarming rate throughout the world, particularly among children. Epidemiological and experimental data have suggested that suboptimal nutrition and growth during prenatal and/or postnatal life can have a significant role in the development of obesity and related diseases. Similarly, exposure to malnutrition during perinatal life can result in lifelong metabolic disorders. Although the precise biological mechanisms governing metabolic programming have not been fully elucidated, there is growing evidence that obesity and other metabolic diseases may result from a change in the underlying developmental program of the hypothalamic pathways that regulate energy balance. The hypothalamus undergoes tremendous growth beginning in the embryonic period and continuing through adolescence, and an alteration in perinatal nutrition can affect various developmental processes, including neurogenesis and axon growth, which can lead to abnormal hypothalamic development. Metabolic hormones, particularly leptin, are capable of transmitting signals to the developing hypothalamus in response to alterations in the nutritional environment and may underlie potential maladaptive responses to early metabolic perturbations. A better understanding of the optimal perinatal hormonal and nutritional environment during hypothalamic development may help ameliorate and reverse the metabolic malprogramming of the fetus and/or neonate.