Dimethylglycine Sodium Salt Alleviates Intrauterine Growth Restriction-Induced Low Growth Performance, Redox Status Imbalance, and Hepatic Mitochondrial Dysfunction in Suckling Piglets

Abstract

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This study aimed to investigate the mechanism of redox status imbalance and hepatic mitochondrial dysfunction induced by intrauterine growth restriction (IUGR) and relieve this condition through dimethylglycine sodium salt (DMG-Na) supplementation during the suckling period. Thirty normal birth weight (NBW) and 30 IUGR newborns were selected from 20 sows. Briefly, 1 NBW and 1 IUGR newborn were obtained from each litter of 10 sows, and 10 NBW and 10 IUGR newborns were obtained. Additionally, 2 NBW and 2 IUGR newborns were obtained from each litter of another 10 sows, and 20 NBW newborns were allocated to the N [basic milk diets (BMDs)] and ND (BMDs+0.1% DMG-Na) groups. Furthermore, 20 IUGR newborns were assigned to the I (BMDs) and ID (BMDs+0.1% DMG-Na) groups. The results revealed that the growth performance, serum and hepatic redox status, and hepatic gene and protein expression levels were lower (P < 0.05) in the I group compared to the N group. Additionally, supplementation with DMG-Na (ND and ID groups) improved (P < 0.05) these parameters compared to the non-supplemented groups (N and I groups). In conclusion, the activity of Nrf2/SIRT1/PGC1α was inhibited in IUGR newborns, and this led to their hepatic dysfunctions. Supplementation with DMG-Na activated Nrf2/SIRT1/PGC1α in IUGR newborns, thereby improving their performance.

Keywords

• intrauterine growth restriction
• suckling piglets
• hepatic
• redox status
• mitochondrial dysfunction
• dimethylglycine sodium salt