Garza Viviana, West Sarah M, Cardoso Rodolfo C
Department of Animal Science, Texas A&M University, 2471 TAMU, College Station, TX 77843, USA.
Department of Animal Science, Texas A&M University, 2471 TAMU, College Station, TX 77843, USA.
Animal. 2023 May;17 Suppl 1:100782. doi: 10.1016/j.animal.2023.100782.
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.
青春期启动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）和促黄体生成素脉冲式释放的增加。营养是控制青春期启动时间的关键环境因素。出生后早期发育阶段的营养限制会延迟青春期，而在此期间采食量增加和肥胖则通过影响下丘脑加速青春期成熟。此外，母体在妊娠期的营养状况可对发育中胎儿的神经内分泌系统进行编程，并有可能使后代的青春期提前或延迟。瘦素是一种主要由脂肪细胞产生的激素，在向大脑传递能量状态信息和调节性成熟方面发挥着重要作用。由于GnRH神经元不含有瘦素受体，瘦素对GnRH释放的调节是由上游神经元网络介导的。位于下丘脑弓状核的两组神经元，一组表达神经肽Y（NPY，一种促食欲肽），另一组表达α-黑素细胞刺激素（αMSH，一种抑制食欲肽），它们是神经回路的核心组成部分，将抑制性（NPY）和兴奋性（αMSH）输入传递给GnRH神经元。此外，弓状核中共同表达 kisspeptin、神经激肽B（NKB）和强啡肽的KNDy神经元，也在青春期的代谢调节中发挥作用。我们对肉用小母牛的研究表明，断奶后早期（4至9月龄）体重增加率的提高会导致NPY mRNA表达降低、阿黑皮素原和 kisspeptin受体mRNA表达增加、对GnRH神经元的NPY抑制性输入减少以及对KNDy神经元的兴奋性αMSH输入增加。最后，我们的最新数据表明，母牛在妊娠最后两个阶段的营养状况也可诱导小母牛后代下丘脑神经回路的转录和结构变化，这些变化可能在出生后长期持续存在。已经开发出一些管理方法，如在妊娠期对母体进行营养补充（胎儿编程）、补饲、早期断奶和阶梯式营养方案，以利用大脑的可塑性并促进小母牛的青春期成熟。
