Abstract：
Pubertal attainment is an intricate biological process that involves maturation of the reproductive neuroendocrine axis and increased pulsatile release of gonadotropin-releasing hormone (GnRH) and luteinizing hormone. Nutrition is a critical environmental factor controlling the timing of puberty attainment. Nutrient restriction during early postnatal development delays puberty, whereas increased feed intake and adiposity during this period hasten pubertal maturation by imprinting the hypothalamus. Moreover, the dam\'s nutrition during gestation can program the neuroendocrine system in the developing fetus and has the potential to advance or delay puberty in the offspring. Leptin, a hormone produced primarily by adipose cells, plays an important role in communicating energy status to the brain and regulating sexual maturation. Leptin\'s regulation of GnRH release is mediated by an upstream neuronal network since GnRH neurons do not contain the leptin receptor. Two groups of neurons located in the arcuate nucleus of the hypothalamus that express neuropeptide Y (NPY), an orexigenic peptide, and alpha melanocyte-stimulating hormone (αMSH), an anorexigenic peptide, are central elements of the neural circuitry that relay inhibitory (NPY) and excitatory (αMSH) inputs to GnRH neurons. Moreover, KNDy neurons, neurons in the arcuate nucleus that co-express kisspeptin, neurokinin B (NKB), and dynorphin, also play a role in the metabolic regulation of puberty. Our studies in beef heifers demonstrate that increased rates of BW gain during early postweaning (4-9 mo of age) result in reduced expression of NPY mRNA, increased expression of proopiomelanocortin and kisspeptin receptor mRNA, reduced NPY inhibitory inputs to GnRH neurons, and increased excitatory αMSH inputs to KNDy neurons. Finally, our most recent data demonstrate that nutrition of the cow during the last two trimesters of gestation can also induce transcriptional and structural changes in hypothalamic neurocircuitries in the heifer progeny that likely persist long-term after birth. Managerial approaches, such as supplementation of the dam during gestation (fetal programming), creep feeding, early weaning, and stair-step nutritional regimens have been developed to exploit brain plasticity and advance pubertal maturation in heifers.
摘要：
青春期发育是一个复杂的生物学过程，涉及生殖神经内分泌轴的成熟以及促性腺激素释放激素（GnRH）和黄体生成素的脉冲释放增加。营养是控制青春期时间的关键环境因素。出生后早期发育期间的营养限制会延迟青春期，而在此期间增加的采食量和肥胖会通过印记下丘脑来加速青春期成熟。此外，妊娠期间的营养可以对发育中的胎儿神经内分泌系统进行编程，并有可能促进或延迟后代的青春期。瘦素,一种主要由脂肪细胞产生的激素，在向大脑传达能量状态和调节性成熟方面发挥着重要作用。瘦素对GnRH释放的调节是由上游神经元网络介导的，因为GnRH神经元不含瘦素受体。两组位于下丘脑弓状核的神经元表达神经肽Y（NPY），一种促食欲肽，和α黑素细胞刺激素（αMSH），一种厌食肽，是将抑制性（NPY）和兴奋性（αMSH）输入传递给GnRH神经元的神经回路的中心元素。此外，KNDy神经元，弓状核中共表达kisspeptin的神经元，神经激肽B(NKB),和强啡肽,还在青春期的代谢调节中发挥作用。我们在牛母牛中的研究表明，断奶后早期（4-9个月）BW增加率导致NPYmRNA表达降低，原黑皮质素和kisspeptin受体mRNA的表达增加，减少对GnRH神经元的NPY抑制输入，增加了对KNDy神经元的兴奋性αMSH输入。最后,我们的最新数据表明,母牛在妊娠最后两个三个月的营养也可以诱导母牛后代下丘脑神经回路的转录和结构变化,这种变化可能在出生后长期持续.管理方法，例如在妊娠期间补充大坝（胎儿编程），蠕变进料,早期断奶,已经开发了阶梯式营养方案，以利用小母牛的大脑可塑性和促进青春期成熟。
