Ji Yun, Wu Zhenlong, Dai Zhaolai, Wang Xiaolong, Li Ju, Wang Binggen, Wu Guoyao
State Key Laboratory of Animal Nutrition, China Agricultural University, Beijing, 100193 China.
Henan Yinfa Animal Husbandry Co., Ltd., Xinzheng, Henan 451100 China.
J Anim Sci Biotechnol. 2017 May 5;8:42. doi: 10.1186/s40104-017-0173-5. eCollection 2017.
Maternal undernutrition or overnutrition during pregnancy alters organ structure, impairs prenatal and neonatal growth and development, and reduces feed efficiency for lean tissue gains in pigs. These adverse effects may be carried over to the next generation or beyond. This phenomenon of the transgenerational impacts is known as fetal programming, which is mediated by stable and heritable alterations of gene expression through covalent modifications of DNA and histones without changes in DNA sequences (namely, epigenetics). The mechanisms responsible for the epigenetic regulation of protein expression and functions include chromatin remodeling; DNA methylation (occurring at the 5´-position of cytosine residues within CpG dinucleotides); and histone modifications (acetylation, methylation, phosphorylation, and ubiquitination). Like maternal malnutrition, undernutrition during the neonatal period also reduces growth performance and feed efficiency (weight gain:feed intake; also known as weight-gain efficiency) in postweaning pigs by 5-10%, thereby increasing the days necessary to reach the market body-weight. Supplementing functional amino acids (e.g., arginine and glutamine) and vitamins (e.g., folate) play a key role in activating the mammalian target of rapamycin signaling and regulating the provision of methyl donors for DNA and protein methylation. Therefore, these nutrients are beneficial for the dietary treatment of metabolic disorders in offspring with intrauterine growth restriction or neonatal malnutrition. The mechanism-based strategies hold great promise for the improvement of the efficiency of pork production and the sustainability of the global swine industry.
孕期母体营养不足或营养过剩会改变器官结构，损害猪的产前和新生儿生长发育，并降低瘦肉组织生长的饲料效率。这些不良影响可能会延续到下一代或更久。这种跨代影响的现象被称为胎儿编程，它是由DNA和组蛋白的共价修饰导致基因表达的稳定和可遗传改变介导的，而DNA序列不变（即表观遗传学）。负责蛋白质表达和功能表观遗传调控的机制包括染色质重塑；DNA甲基化（发生在CpG二核苷酸内胞嘧啶残基的5´位置）；以及组蛋白修饰（乙酰化、甲基化、磷酸化和泛素化）。与母体营养不良一样，新生仔猪期的营养不足也会使断奶后仔猪的生长性能和饲料效率（增重：采食量；也称为增重效率）降低5-10%，从而增加达到上市体重所需的天数。补充功能性氨基酸（如精氨酸和谷氨酰胺）和维生素（如叶酸）在激活雷帕霉素哺乳动物靶点信号传导以及调节DNA和蛋白质甲基化的甲基供体供应方面起着关键作用。因此，这些营养素有利于对患有子宫内生长受限或新生仔猪营养不良的后代进行代谢紊乱的饮食治疗。基于机制的策略对于提高猪肉生产效率和全球养猪业的可持续性具有巨大潜力。
