Intra-uterine growth restriction (IUGR) impairs postnatal growth and skeletal muscle development in neonatal infants. This study evaluated whether dietary β-hydroxy-β-methylbutyrate Ca (HMB-Ca) supplementation during the early postnatal period could improve muscle growth in IUGR neonates using piglets as a model. A total of twelve pairs of IUGR and normal-birth-weight (NBW) male piglets with average initial weights (1·85 (sem 0·36) and 2·51 (sem 0·39) kg, respectively) were randomly allotted to groups that received milk-based diets (CON) or milk-based diets supplemented with 800 mg/kg HMB-Ca (HMB) during days 7–28 after birth. Blood and longissimus dorsi (LD) samples were collected and analysed for plasma amino acid content, fibre morphology and the expression of genes related to muscle development. The results indicate that, regardless of diet, IUGR piglets had a significantly decreased average daily weight gain (ADG) compared with that of NBW piglets (P<0·05). However, IUGR piglets fed HMB-Ca had a net weight and ADG similar to that of NBW piglets fed the CON diet. Irrespective of body weight (BW), HMB-Ca supplementation markedly increased the type II fibre cross-sectional area and the mRNA expression of mammalian target of rapamycin (mTOR), insulin-like growth factor-1 and myosin heavy-chain isoform IIb in the LD of piglets (P<0·05). Moreover, there was a significant interaction between the effects of BW and HMB on mTOR expression in the LD (P<0·05). In conclusion, HMB-Ca supplementation during the early postnatal period could improve skeletal muscle growth and maturity by accelerating fast-twitch glycolytic fibre development in piglets.

Melatonin (MT) is a bio-antioxidant that has been widely used to prevent pregnancy complications, such as pre-eclampsia and IUGR during gestation. This experiment evaluated the impacts of dietary MT supplementation during pregnancy on reproductive performance, maternal–placental–fetal redox status, placental inflammatory response, and mitochondrial function, and sought a possible underlying mechanism in the placenta. Sixteen fifth parity sows were divided into two groups and fed each day of the gestation period either a control diet or a diet that was the same but for 36 mg of MT. The results showed that dietary supplementation with MT increased placental weight, while the percentage of piglets born with weight < 900 g decreased. Meanwhile, serum and placental MT levels, maternal–placental–fetal redox status, and placental inflammatory response were increased by MT. In addition, dietary MT markedly increased the mRNA levels of nutrient transporters and antioxidant-related genes involved in the Nrf2/ARE pathway in the placenta. Furthermore, dietary MT significantly increased ATP and NAD⁺ levels, relative mtDNA content, and the protein expression of Sirt1 in the placenta. These results suggested that MT supplementation during gestation could improve maternal–placental–fetal redox status and reproductive performance by ameliorating placental antioxidant status, inflammatory response, and mitochondrial dysfunction.

Dietary fiber intake during pregnancy may improve offspring intestinal development. The aim of this study was to evaluate the effect of maternal high fiber intake during late gestation on intestinal morphology, microbiota, and intestinal proteome of newborn piglets. Sixteen sows were randomly allocated into two groups receiving the control diet (CD) and high-fiber diet (HFD) from day 90 of gestation to farrowing. Newborn piglets were selected from each litter, named as CON and Fiber group, respectively. Maternal high fiber intake did not markedly improve the birth weight, but increased the body length, the ileal crypt depth and colonic acetate level. In addition, maternal high fiber intake increased the -diversity indices (Observed species, Simpson, and ACE), and the abundance of Acidobacteria and Bacteroidetes at phylum level, significantly increased the abundance of Bradyrhizobium and Phyllobacterium at genus level in the colon of newborn piglets. Moreover, maternal high fiber intake markedly altered the ileal proteome, increasing the abundances of proteins associated with oxidative status, energy metabolism, and immune and inflammatory responses, and decreasing abundances of proteins related to cellular apoptosis, cell structure, and motility. These findings indicated that maternal high fiber intake could alter intestinal morphology, along with the altered intestinal microbiota composition and proteome of offspring.

This study aimed to investigate the effects of long-term maternal intake of inulin on intestinal morphology, permeability, inflammation and microbiota of offspring rats treated with dextran sulfate sodium (DSS). Sixteen female adult Sprague-Dawley rats were assigned to two groups receiving the fiber-free diet (FFD) or inulin diet (INU, 5% inulin) for three parities. The offspring weaned rats (third-parity) were fed with the same diet for four weeks until receiving 6% DSS for 7 days; the four groups were as follows: FFD, FFD + DSS, INU and INU + DSS. The results showed that maternal intake of inulin increased the histopathology score and activity of diamine oxidase (DAO) in serum, and the highest histopathology scores and activity of DAO were observed in INU + DSS rats. Maternal intake of inulin increased the activity of myeloperoxidase (MPO), mRNA expressions of inflammatory factors and protein expression of IL-1β in colonic tissues. Likewise, INU + DSS rats had the highest activity of MPO and mRNA expressions of inflammatory factors in colonic tissues. Maternal intake of inulin increased the abundances of Bacteroidetes, Bacteroides and Parasutterella, which were the highest enriched in INU + DSS rats. The level of acetate in the colonic digesta of INU + DSS rats was lower than that in FFD and INU rats. These results indicated that long-term maternal intake of inulin exacerbated the intestinal damage and inflammation of DSS-induced offspring rats, associated with the decreased level of acetate and altered intestinal microbiota.

Sows suffering excess weight loss during lactation may delay weaning to estrus interval (WEI) and have a detrimental effect on subsequent reproductive performance, however, the underlying mechanism is not completely clear. Therefore, the goal of this study was to investigate physiological profiles manifested in plasma originating from high (HWL) and low lactational weight loss (LWL) sows. The plasma biochemical parameters, hormones, antioxidant parameters, and milk compositions were assessed. Furthermore, plasma metabolites were analyzed using ultrahigh-performance liquid chromatography/time-of-flight mass spectrometry in positive and negative ion modes. Results showed that HWL sows had a lower feed intake and higher lactational weight loss and prolonged WEI, but had similar litter performance and milk composition compared to LWL sows. These changes were associated with lower plasma insulin-like growth factor 1 and higher fibroblast growth factor 21 levels in the HWL sows. Moreover, HWL led to a severe oxidative stress and metabolic damage, as accompanied by excessive protein breakdown and lipids mobilization at weaning. Metabolomic analysis revealed differences in 46 compounds between HWL and LWL sows, and the identified compounds were enriched in metabolic pathways related to amino acids metabolism, fatty acids oxidation metabolism, bile acids biosynthesis, and nucleoside metabolism. These results provide the evidence for physiological mechanism in sows with excessive lactational weight loss that delayed the WEI. Metabolomic data provides essential information and gives rise to potential targets for the development of nutritional intervention strategies.