This experiment was conducted to investigate the effects of inulin supplementation in low- or high-fat diets on both the reproductive performance of sow and the antioxidant defence capacity in sows and offspring. Sixty Landrace × Yorkshire sows were randomly allocated to four treatments with low-fat diet (L), low-fat diet containing 1.5% inulin (LI), high-fat diet (H) and high-fat diet containing 1.5% inulin (HI). Inulin-rich diets lowered the within-litter birth weight coefficient of variation (CV, p = 0.05) of piglets, increased the proportion of piglets weighing 1.0-1.5 kg at farrowing (p < 0.01), reduced the loss of body weight (BW) and backfat thickness (BF) during lactation (p < 0.05) and decreased the duration of farrowing as well as improved sow constipation (p < 0.05). Sows fed fat-rich diets gained more BW during gestation (p < 0.01), farrowed a greater number of total (+1.65 pigs, p < 0.05) and alive (+1.52 pigs p < 0.05) piglets and had a heavier (+2.06 kg, p < 0.05) litter weight at birth as well as a decreased weaning-to-oestrous interval (WEI, p < 0.01) compared with sows fed low-fat diets. However, it is worth noting that the H diet significantly decreased the serum activities of superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) and increased the serum malondialdehyde (MDA) levels in sows and piglets (p < 0.05). In contrast, HI diet enhanced the activities of T-SOD and GSH-Px and decreased the serum MDA concentrations (p < 0.05) in sows and piglets. In summary, the fat-rich diets fed to sows during gestation had beneficial effects on reproductive performance, but aggravated the oxidative stress in sow and piglets. Inulin-rich diets fed to sow during gestation had beneficial effects on within-litter uniformity of piglet birthweight and enhanced the antioxidant defence capacity of sows and piglets.
Background: Currently, there are many studies researched the associations between maternal serum inflammatory indicators (i.e. ferritin, C-reactive protein [CRP], C3 and C4) and preterm birth (PTB). The results, however, are inconsistent. Therefore, the aim of this study was to estimate the relationship between maternal serum inflammatory indicators and PTB in a nested case-control (NCC)study. Methods: A NCC study was conducted by Guangxi Birth Cohort Study which enrolled a total of 6203 pregnant women between 5 0/7 and 34 6/7 weeks of gestational age (wGA) from six cities in China between 2015 and 2016. There were 206women who delivered preterm (< 37 0/7 wGA), and 412 women who delivered term birth, those women were matched by maternal age, birth place, gender of infants, and wGA at blood collection. The inflammatory indicators were quantified by immunoturbidimetric methods. Results: Highest quartile concentrations of all inflammatory indicators were determined versus median. After adjusting for maternal age, high levels of CRP (CRP > 16.60 mg/L) are related to the risk of PTB (OR = 2.16, 95% CI: 1.02-4.56, p = 0.044) in the first trimester. The association of C3 was extremely related to those who delivered PTB (OR = 2.53, 95% CI: 1.14-5.64, p = 0.023) in the first trimester. Moreover, no significant associations were found in C4 (p = 0.079) and ferritin (p = 0.067) between PTB. Conclusions: Elevated concentrations of CRP and C3 in the first trimester were associated with increased risk of PTB. Inflammatory indicators may act a pivotal part in early diagnosis and prognosis of PTB.
Altered composition of the gut microbiota has been observed in many neurodegenerative diseases. LanCL1 has been proven to protect neurons and reduce oxidative stress. The present study was designed to investigate alterations of the gut microbiota in LanCL1 knockout mice and to study the interactions between gut bacteria and the brain. Wild-type and LanCL1 knockout mice on a normal chow diet were evaluated at 4 and 8-9 weeks of age. 16s rRNA sequence and untargeted metabolomics analyses were performed to investigate changes in the gut microbiota and feces metabolites. Real-time polymerase chain reaction analysis, AB-PAS staining, and a TUNEL assay were performed to detect alterations in the gut and brain of knockout mice. The serum cytokines of 9-week-old knockout mice, which were detected by a multiplex cytokine assay, were significantly increased. In the central nervous system, there was no increase of antioxidant defense genes even though there was only low activity of glutathione S-transferase in the brain of 8-week-old knockout mice. Interestingly, the gut tight junctions, zonula occludens-1 and occludin, also displayed a downregulated expression level in 8-week-old knockout mice. On the contrary, the production of mucus increased in 8-week-old knockout mice. Moreover, the compositions of the gut microbiota and feces metabolites markedly changed in 8-week-old knockout mice but not in 4-week-old mice. Linear discriminant analysis and t-tests identified Akkermansia as a specific abundant bacteria in knockout mice. Quite a few feces metabolites that have protective effects on the brain were reduced in 8-week-old knockout mice. However, N-acetylsphingosine was the most significant downregulated feces metabolite, which may cause the postponement of neuronal apoptosis. To further investigate the effect of the gut microbiota, antibiotics treatment
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