There are few studies on the mechanism of redox status imbalance and intestinal dysfunction in intrauterine growth restricted (IUGR) newborn piglets. Here, we investigated the mechanism of jejunum dysfunction in weaned piglets with IUGR and the mechanism through which dimethylglycine sodium salt (DMG-Na) supplementation improving the imbalance of their redox status. In this work, a total of 10 normal birth weight (NBW) newborn piglets and 20 IUGR newborn piglets were obtained. After weaning at 21 d, they were assigned to 3 groups (n = 10/group): NBW weaned piglets fed standard basal diets (NBWC); one IUGR weaned piglets fed standard basal diets (IUGRC); another IUGR weaned piglets from the same litter fed standard basal diets plus 0.1% DMG-Na (IUGRD). The piglets in these 3 groups were sacrificed at 49 d of age, and the blood and jejunum samples were collected immediately. The growth performance values in the IUGRC group were lower (P < 0.05) than those in the NBWC group. Jejunum histomorphological parameters, inflammatory cytokines, and digestive enzyme activity as well as serum immunoglobulin were lower (P < 0.05) in the IUGRC group than those in the NBWC group. Compared with these in the NBWC group, the redox status of serum, jejunum, and mitochondria and the expression levels of jejunum redox status-related, cell adhesion-related, and mitochondrial function-related genes and proteins were suppressed in the IUGRC group (P < 0.05). However, compared with those in the IUGRC group, the growth performance values, jejunum histomorphological parameters, inflammatory cytokines, digestive enzyme activity, serum immunoglobulin, redox status of serum, jejunum, and mitochondria, and the expression levels of jejunum redox status-related, cell adhesion-related, and mitochondrial function-related genes and proteins were improved (P < 0.05) in the IUGRD group. In conclusion, dietary DMG-Na supplementation alleviates redox status imbalance and intestinal dysfunction in IUGR weaned piglets mainly by activating the sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptorγcoactivator-1α (PGC1α) pathway, thereby improving their unfavorable body state.

关于宫内生长受限（IUGR）新生仔猪氧化还原状态失衡和肠道功能障碍的机制研究较少。在这里，我们研究了 IUGR 断奶仔猪空肠功能障碍的机制以及补充二甲基甘氨酸钠盐 (DMG-Na) 改善其氧化还原状态失衡的机制。本工作共获得10头正常出生体重（NBW）新生仔猪和20头IUGR新生仔猪。21 d断奶后，分3组（n = 10/组）：NBW断奶仔猪饲喂标准基础日粮（NBWC）；1 头 IUGR 断奶仔猪饲喂标准基础日粮 (IUGRC)；另一只 IUGR 从同一窝断奶的仔猪饲喂标准基础日粮和 0.1% DMG-Na (IUGRD)。这3组仔猪在49日龄处死，立即采集血液和空肠样本。IUGRC 组的生长性能值低于 NBWC 组（P  < 0.05）。空肠组织形态学参数、炎性细胞因子、消化酶活性及血清免疫球蛋白均较低（P < 0.05) IUGRC 组优于 NBWC 组。与NBWC组相比，IUGRC组血清、空肠和线粒体的氧化还原状态以及空肠氧化还原状态相关、细胞粘附相关、线粒体功能相关基因和蛋白的表达水平受到抑制（P  < 0.05)。但与 IUGRC 组相比，生长性能值、空肠组织形态学参数、炎性细胞因子、消化酶活性、血清免疫球蛋白、血清、空肠和线粒体的氧化还原状态，以及与空肠氧化还原状态相关的表达水平，细胞粘附相关和线粒体功能相关的基因和蛋白质得到改善（P < 0.05) 在 IUGRD 组中。总之，日粮补充DMG-Na主要通过激活sirtuin 1（SIRT1）/过氧化物酶体增殖物激活受体γcoactivator-1α（PGC1α）通路来缓解IUGR断奶仔猪的氧化还原状态失衡和肠道功能障碍，从而改善其不利的身体状态。