Department of Physiological Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences, 02-766 Warsaw, Poland; Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland.
Department of Physiological Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences, 02-766 Warsaw, Poland.
Reprod Biol. 2014 Mar;14(1):51-60. doi: 10.1016/j.repbio.2014.01.005. Epub 2014 Jan 30.
The overall acceptance of pig models for human biomedical studies is steadily growing. Results of rodent studies are usually confirmed in pigs before extrapolating them to humans. This applies particularly to gastrointestinal and metabolism research due to similarities between pig and human physiology. In this context, intrauterine growth retarded (IUGR) pig neonate can be regarded as a good model for the better understanding of the IUGR syndrome in humans. In pigs, the induction of IUGR syndrome may include maternal diet intervention, dexamethasone treatment or temporary reduction of blood supply. However, in pigs, like in humans, circa 8% of neonates develop IUGR syndrome spontaneously. Studies on the pig model have shown changes in gut structure, namely a reduced thickness of mucosa and muscle layers, and delayed kinetic of disappearance of vacuolated enterocytes were found in IUGR individuals in comparison with healthy ones. Functional changes include reduced dynamic of gut mucosa rebuilding, decreased activities of main brush border enzymes, and changes in the expression of proteins important for carbohydrate, amino acids, lipid, mineral and vitamin metabolism. Moreover, profiles of intestinal hormones are different in IUGR and non-IUGR piglets. It is suggested that supplementation of the mothers during the gestation and/or the IUGR offspring after birth can help in restoring the development of the gastrointestinal tract. The pig provides presumably the optimal animal model for humans to study gastrointestinal tract structure and function development in IUGR syndrome.
猪模型在人类医学研究中的整体接受度正在稳步提高。在将啮齿动物研究结果推断至人类之前，通常会先在猪身上进行验证。由于猪和人类的生理学相似，这尤其适用于胃肠道和代谢研究。在这种情况下，宫内发育迟缓（IUGR）的新生仔猪可以被视为更好地理解人类 IUGR 综合征的良好模型。在猪中，IUGR 综合征的诱导可能包括母体饮食干预、地塞米松治疗或暂时减少血液供应。然而，与人类一样，大约 8%的仔猪会自发出现 IUGR 综合征。对猪模型的研究表明，与健康仔猪相比，IUGR 个体的肠道结构发生了变化，即黏膜和肌肉层的厚度减少，空泡化肠细胞的消失动力学延迟。功能变化包括肠道黏膜重建的动态减少、主要刷状缘酶活性降低以及对碳水化合物、氨基酸、脂质、矿物质和维生素代谢重要的蛋白质表达的变化。此外，IUGR 和非 IUGR 仔猪的肠道激素谱也不同。有人提出，在妊娠期间对母亲进行补充和/或在出生后对 IUGR 后代进行补充，可以帮助恢复胃肠道的发育。猪可能为研究 IUGR 综合征中胃肠道结构和功能发育提供了最佳的人类动物模型。
