Dietary Resveratrol Ameliorates Hepatic Fatty Acid Metabolism and Jejunal Barrier in Offspring Induced by Maternal Oxidized Soybean Oil Challenge.

Increasing evidence indicates that maternal exposure to oxidized soybean oil (OSO) causes damage to the mother and offspring. The antioxidant resveratrol (Res) has a variety of health benefits. However, the protective effect of Res on mitigating offspring damage after maternal exposure to OSO and its mechanism remains unclear. Therefore, this study aimed to investigate the effect of Res on hepatic fatty acid metabolism and the jejunal barrier in suckling piglets after maternal OSO exposure. A total of 18 sows in late gestation were randomly assigned to three treatments. The sows were fed with a fresh soybean oil (FSO) diet, an OSO diet, or the OSO diet supplemented with 300 mg/kg Res (OSO + Res), respectively. The results showed that maternal supplementation of Res restored the mRNA levels of genes related to fatty acid metabolism and increased the activities of catalase (CAT) and total superoxide dismutase (T-SOD) in suckling piglets' livers under the OSO challenge. Moreover, the OSO + Res group restored the mRNA levels of occludin and claudin 4 in suckling piglet jejunum compared with the results of the OSO challenges. In summary, supplementation with Res improves hepatic fatty acid metabolism and intestinal barrier function of suckling piglets after maternal OSO challenge during late gestation and lactation.

Maternal supplementation with konjac glucomannan improves maternal microbiota for healthier offspring during lactation.

BACKGROUND: The maternal diet during gestation and lactation affects the health of the offspring. Konjac glucomannan (KGM) is a significantly functional polysaccharide in food research, possessing both antioxidant and prebiotic properties. However, the mechanisms of how KGM regulates maternal nutrition remain insufficient and limited. This study aimed to investigate maternal supplementation with KGM during late gestation and lactation to benefit both maternal and offspring generations. RESULTS: Our findings indicate that KGM improves serum low density lipoprotein cholesterol (LDL-C) and antioxidant capacity. Furthermore, the KGM group displayed a significant increase in the feed intake-related hormones neuropeptide tyrosine (NPY), Ghrelin, and adenosine monophosphate-activated kinase (AMPK) levels. KGM modified the relative abundance of Clostridium, Candidatus Saccharimonas, unclassified Firmicutes, and unclassified Christensenellaceae in sow feces. Acetate, valerate, and isobutyrate were also improved in the feces of sows in the KGM group. These are potential target bacterial genera that may modulate the host's health. Furthermore, Spearman's correlation analysis unveiled significant correlations between the altered bacteria genus and feed intake-related hormones. More importantly, KGM reduced interleukin-6 (IL-6) levels in milk, further improved IL-10 levels, and reduced zonulin levels in the serum of offspring. CONCLUSION: In conclusion, maternal dietary supplementation with KGM during late gestation and lactation improves maternal nutritional status by modifying maternal microbial and increasing lactation feed intake, which benefits the anti-inflammatory capacity of the offspring serum. © 2024 Society of Chemical Industry.

Dietary-fat supplementation alleviates cold temperature-induced metabolic dysbiosis and barrier impairment by remodeling gut microbiota.

As important components of the mammalian diet and tissues, fats are involved in a variety of biological processes in addition to providing energy. In general, the increase in basal metabolism and health risks under cold temperature conditions causes the host to need more energy to maintain body temperature and normal biological processes. The intestine and its microbiota are key components in orchestrating host metabolic homeostasis and immunity, and respond rapidly to changing environmental conditions. However, the role of dietary-fat supplementation in regulating host homeostasis of metabolism and barrier functions through gut microbiota at cold temperatures is incompletely understood. Our results showed that dietary-fat supplementation alleviated the negative effects of cold temperatures on the alpha-diversity of both ileal and colonic microbiota. Cold temperatures altered the ileal and colonic microbiota of pigs, and the extent of changes was more pronounced in the colonic microbiota. Translocation of the gut microbiota was restored after supplementation with a high-fat diet. In addition, cold temperatures exacerbated ileal mucosal damage and inflammation, and disrupted barrier function, which may be associated with decreased concentrations of butyrate and isobutyrate. Cold temperature-induced metabolic dysbiosis was manifested by altered hormone levels and upregulation of expression of multiple metabolites involved in metabolism (lipids, amino acids and minerals) and the immune response. Supplementation with a high-fat diet restored metabolic homeostasis and barrier function by improving gut-microbiota composition and increasing SCFAs concentrations in pigs. In conclusion, cold temperatures induced severe translocation of microbiota and barrier damage. These actions increased the risk of metabolic imbalance. Dietary-fat supplementation alleviated the adverse effects of cold temperatures on host metabolism by remodeling the gut microbiota.

Oxidized Soybean Oil Evoked Hepatic Fatty Acid Metabolism Disturbance in Rats and their Offspring.

The oxidation of fats and oils is an undisputed subject of science, given the effect of oxidized fats and oils on food quality and safety. This study aimed to determine whether maternal exposure to oxidized soybean oil (OSO) causes lipid metabolism disorders in the liver and whether this lipid metabolism disorder can be transmitted to offspring or even worsened. A total of 60 female Sprague-Dawley (SD) rats were divided randomly into four groups in this study. Treatment groups received a pure diet of OSO with a peroxide value of 200, 400, or 800 mEqO2/kg, while the control group received fresh soybean oil (FSO). As for our results, OSO affected serum biochemical parameters in the maternal generation (F0) and induced liver histopathology changes, inflammation, and oxidative stress. Moreover, the expression of genes related to the liver X receptor α (LXRα)─sterol regulatory element binding protein-1c (SREBP-1c) signaling pathway was changed. Similar trends were found in the livers of offspring on postnatal days 21 and 56. In conclusion, exposure to OSO during gestation and lactation can affect liver lipid synthesis. Additionally, it is detrimental to the development of the offspring's liver, affecting fatty acid metabolism and causing liver damage.

Purification and identification of xanthine oxidase inhibitory peptides from enzymatic hydrolysate of α-lactalbumin and bovine colostrum casein.

The development of food-derived Xanthine Oxidase (XO) inhibitors is critical to the treatment of hyperuricemia and oxidative stress-related disease. Few studies report on milk protein hydrolysates' XO inhibitory activity, with the mechanism of their interaction remaining elusive. Here, different commercial enzymes were used to hydrolyze α-lactalbumin and bovine colostrum casein. The two proteins hydrolyzed by alkaline protease exhibited the most potent XO inhibitory activity (bovine casein: IC50 = 0.13 mg mL-1; α-lactalbumin: IC50 = 0.28 mg mL-1). Eight potential XO inhibitory peptides including VYPFPGPI, GPVRGPFPIIV, VYPFPGPIPN, VYPFPGPIHN, QLKRFSFRSFIWR, LVYPFPGPIHN, AVFPSIVGR, and GFININSLR (IC50 of 4.67-8.02 mM) were purified and identified from alkaline protease hydrolysates by using gel filtration, LC-MS/MS and PeptideRanker. The most important role of inhibiting activity of peptides is linked to hydrophobic interactions and hydrogen bonding based on the results of molecular docking and molecular dynamics simulation. The enzymatic hydrolysate of α-lactalbumin and bovine colostrum casein could be a competitive candidates for hyperuricemia-resisting functional food.

Effects of oxidized soybean oil on the performance of sows and jejunum health of suckling piglets.

Oils provide a considerable amount of energy to the swine diet, but they are prone to lipid oxidation if not properly preserved. Consumption of oxidized oils can adversely affect the animal organism and even the offspring. This study investigated the impact of oxidized soybean oil in the diets of sows from 107 days gestation to 21 days of lactation on the performance of sows and jejunum health of suckling piglets. Sixteen sows were randomly allocated into two groups: one group (n = 8) was fed with the fresh soybean oil (FSO) diet, and another group (n = 8) was treated with the oxidized soybean oil (OSO) diet. Dietary oxidized soybean oil does not affect sow performance. Antioxidant enzyme activity in the milk was reduced significantly in the OSO group, such as the superoxide dismutase (SOD), total antioxidant capacity (T-AOC), and catalase (CAT) activities (p < 0.05). On Day 21, oxidized soybean oil increased tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and interleukin 8 (IL-8) levels in sow milk and the concentrations of TNF-α and IL-8 cytokines in plasma (p < 0.05). Suckling piglets from sows fed on OSO showed a trend towards increased IL-6 and TNF-α in plasma (p < 0.1). The mRNA expression of interleukin 1ß (IL-1ß) was augmented, whereas interleukin 10 (IL-10) was decreased, and zonula occludens-1 (ZO-1) had a tendency to be down-regulated in OSO treatment. This study revealed that the OSO of feed decreased the antioxidant capacity of milk, further contributing to the inflammatory response in the jejunum of suckling piglets.

Effects of sweet potato vine silage supplementation on meat quality, antioxidant capacity and immune function in finishing pigs.

Sweet potato vine, the byproduct of sweet potato, has a high nutritional value. Silage is an effective solution for nutrient preservation. This article explored the effects of sweet potato vine silage (SPVS) supplementation on meat quality, antioxidant capacity and immune function in finishing pigs. One hundred and eighty finishing pigs (Berkshire × Licha Black) with a body weight of 74.54 ± 3.32 kg were randomly divided into three groups. The three groups were separately fed basal diet (Ctrl), Ctrl supplemented with 2.5% SPVS (LSPVS) or 5% SPVS (HSPVS) on a dry matter basis. Results showed that the eye muscle area in the LSPVS group was significantly increased. The carcass weight in the HSPVS was significantly reduced compared with Ctrl. For the meat quality, only cooking loss in both HSPVS and LSPVS was reduced while other indexes had no significant differences. For the antioxidant capacity, the hepatic level of glutathione (GSH) peroxidase (GSH-PX) was significantly upregulated in LSPVS but downregulated in HSPVS. In the serum, HSPVS decreased GSH level and increased GSH-PX level. HSPVS significantly reduced hepatic interleukin-1ß (IL-1ß) levels and LSPVS significantly reduced IL-12 levels and increased IL-8 and IL-6 levels. Moreover, HSPVS and LSPVS promoted the secretion of immunoglobulin M (IgM) and IgG in the serum. Our data showed that low-dose SPVS supplementation improved carcass traits and high-dose SPVS supplementation increased immune function in finishing pigs, which provides a new alternative to improve animal health.

Activation of Inflammatory Networks in the Lungs Caused by Chronic Cold Stress Is Moderately Attenuated by Glucose Supplementation.

Mammals that live in cold climates endure months of exposure to low temperature in the winter. The incidence of respiratory diseases has increased. The goal of this study was to investigate the effects of chronic cold stress on lung inflammatory networks, apoptosis, and mitochondrial function via Yorkshire pig models, as well as the ameliorative effect of glucose as energy supplements. Here, two trials were conducted (chronic cold stress and glucose supplementation). The results showed that chronic cold stress induced obvious inflammatory cell infiltration in the lungs and damaged the lung tissue structure. Compared with the Y-Con group, the expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), high mobility group box 1 (HMGB1), nucleotide-binding domain, and leucine-rich repeat protein 3 (NLRP3), IL-1ß, IL-2, IL-6, and IFN-γ in the lungs of the Y-CS group was enhanced by chronic cold stress (p < 0.05). Moreover, chronic cold stress promoted the expression of the Bax and Mfn2 in lungs of Y-CS group (p < 0.05). Interestingly, dietary glucose supplementation significantly reduced inflammatory cell infiltration in the lungs. Moreover, glucose supplementation inhibited the expression of TLR4, MyD88, HMGB1, NLRP3, IL-1ß, IL-2, IL-6, IFN-γ, and Bax during chronic cold stress. In conclusion, chronic cold stress promoted inflammatory networks, apoptosis, and mitochondrial fusion in the lungs. Dietary glucose supplementation inhibited the inflammatory network during chronic cold stress.

Maternal Oxidized Soybean Oil Administration in Rats during Pregnancy and Lactation Alters the Intestinal DNA Methylation in Offspring.

As a food contaminant, oxidized oil or lipid oxidative products have been proven to exert toxicological effects on the growth and development of animals and humans. Research shows that maternal oxidative stress damage might transmit to another generation by epigenetic modulation. However, current evidence is still not clear on the mechanism of the effects of dietary oxidized oil during pregnancy on the two generations. This study employed a rat model fed with oxidized soybean oil (OSO) during pregnancy and lactation to explore the effects of the oxidative degree (0, 200, 400, and 800 mequiv of O2/kg) on the placental RNA methylation and DNA methylation in offspring jejunum. The results showed that following the ingestion of OSO, the placental genes of different m6A methylation were significantly enriched to nutrient metabolic processes and hormone activity. In addition, the intestine in offspring hypofunctioned observably, such as reducing the height of villi and the level of anti-inflammatory cytokine. Furthermore, maternal intake of OSO during pregnancy can damage the intestinal barrier function of offspring by inhibiting the proliferation and differentiation of intestinal epithelial cells and reducing the activity of intestinal DNA methyltransferase. In conclusion, this study reinforces the assertion that maternal OSO consumption during gestation and lactation negatively affects the placental health and intestinal development of suckling pups.

Response of the nuclear xenobiotic receptors to alleviate glyphosate-based herbicide-induced nephrotoxicity in weaned piglets.

Glyphosate-based herbicides (GBHs) are widely used worldwide. Glyphosate (GLP) is the main active component of GBHs. The presence of GBH residues in the environment has led to the exposure of animals to GBHs, but the mechanisms of GBH-induced nephrotoxicity are not clear. This study investigated the effects of GBHs on piglet kidneys. Twenty-eight healthy female hybrid weaned piglets (Duroc × Landrace × Yorkshire) with an average weight of 12.24 ± 0.61 kg were randomly divided into four treatment groups (n=7 piglets/group) that were supplemented with Roundup® (equivalent to GLP concentrations of 0, 10, 20, and 40 mg/kg) for a 35-day feeding trial. The results showed that the kidneys in the 40-mg/kg GLP group suffered slight damage. Roundup® significantly decreased the activity of catalase (CAT) (P=0.005) and increased the activity of superoxide dismutase (SOD) (P=0.029). Roundup® increased the level of cystatin-C (Cys-C) in the plasma (linear, P=0.002 and quadratic, P=0.015). The levels of neutrophil gelatinase-associated lipocalin (NGAL) in plasma increased linearly (P=0.007) and quadratically (P=0.003) as the dose of GLP increased. The mRNA expression of intercellular cell adhesion molecule-1 (ICAM-1) in the 20-mg/kg GLP group was increased significantly (P<0.05). There was a significant increase in the mRNA levels of pregnenolone X receptor (PXR), constitutive androstane receptor (CAR), and uridine diphosphate glucuronosyltransferase 1A3 (UGT1A3) (P<0.05). Our findings found that kidney nuclear xenobiotic receptors (NXRs) may play an important role in defense against GBHs.

Maternal oxidized soybean oil exposure in rats during lactation damages offspring kidneys via Nrf2/HO-1 and NF-κB signaling pathway.

BACKGROUND: Cooking oil is an indispensable component of the human diet. However, oils usually undergo thermal oxidation. Oxidized soybean oil (OSO) has been shown to have detrimental effects on humans and has emerged as a root cause of many chronic diseases. The objective of this work was to evaluate the effects of puerpera exposure to OSO on kidney damage in the mother and offspring using lactating rats as an experimental model. RESULTS: Pathological sections and ultrastructure showed that OSO exposure resulted in various levels of damage to lactating rats and their offspring. OSO induced oxidative stress in the kidneys of lactating rats, as evidenced by increased levels of hydrogen peroxide, interleukin (IL)-1ß, and IL-8. OSO increased the activities of glutathione peroxidase and superoxide dismutase. OSO upregulated the expression of apoptosis-related genes, nuclear factor-erythroid 2-related factor 2 (Nrf2), and nuclear factor κB-related inflammatory factor genes. In the offspring of the OSO-exposed mothers, hydrogen peroxide, malondialdehyde, IL-6, and tumor necrosis factor-alpha contents were increased. Furthermore, OSO enhanced the levels of Nrf2, NAD(P)H quinone oxidoreductase 1, heme oxygenase 1, and p65 and decreased B-cell lymphoma 2. CONCLUSION: These findings indicated that the kidneys of two generations of rats were compromised by oxidative damage when fed OSO during lactation. This study provides evidence for increasing the genes expression of the Nrf2/heme oxygenase 1 pathway to alleviate the kidney damage caused by OSO in the mother and offspring. © 2021 Society of Chemical Industry.

Lycopene Affects Intestinal Barrier Function and the Gut Microbiota in Weaned Piglets via Antioxidant Signaling Regulation.

BACKGROUND: In pig production, early and abrupt weaning frequently causes weaning stress, which manifests as oxidative damage, barrier disruption, and digestion and absorption capacity declines. Lycopene exhibits beneficial antioxidant capacity in both humans and other animal models. OBJECTIVES: The present study aimed to investigate the effects of lycopene supplementation on early weaning stress in piglets and the underlying mechanisms by examining the oxidative stress state, gut intestinal barrier function, and the gut microbiota. METHODS: Twenty-four 21-day-old weaned piglets [Duroc × (Landrace × Yorkshire); castrated males; 5.48 ± 0.10 kg initial body weight] were randomly assigned to 2 treatments. The piglets were fed a basal diet (control treatment) or a basal diet supplemented with 50 mg/kg lycopene (lycopene treatment) for 28 days. The serum lipid levels, serum and jejunum enzyme activities, jejunum morphology, mRNA and protein expression, and gut microbiota were determined. RESULTS: Compared with the control treatment, lycopene supplementation increased the serum catalase activity (P = 0.042; 62.0%); serum total cholesterol concentration (P = 0.020; 14.1%); and jejunum superoxide dismutase activity (P = 0.032; 21.4%), whereas it decreased serum (P = 0.039, 23.0%) and jejunum (P = 0.047; 20.9%) hydrogen peroxide concentrations. Additionally, lycopene increased the mRNA and protein expression of NFE2-like bZIP transcription factor 2 (214.0% and 102.4%, respectively) and CD36 (100.8% and 145.2%, respectively) in the jejunum, whereas it decreased the mRNA and protein expression of Kelch-like ECH-associated protein 1 (55.6% and 39.8%, respectively ). Lycopene also improved jejunal morphology, increasing the villus height (P = 0.018; 27.5%) and villus:crypt ratio (P < 0.001; 57.9%). Furthermore, it increased the abundances of potentially beneficial bacterial groups, including Phascolarctobacterium and Parasutterella, and decreased those of potentially pathogenic bacterial groups, including Treponema_2 and Prevotellaceae_unclassified. CONCLUSIONS: Lycopene supplementation strengthens the intestinal barrier function and improves the gut microbiota in weaned piglets by regulating intestinal antioxidant signaling.

Lycopene improves maternal reproductive performance by modulating milk composition and placental antioxidative and immune status.

Placental health and milk quality are important for maternal reproductive performance during pregnancy and lactation. Lycopene plays an important role in antioxidation, anti-inflammation and regulating lipid metabolism. The goal of the present study was to investigate the effects of dietary lycopene supplementation in the pig model on reproductive performance, placental health and milk composition during maternal gestation and lactation. In the present study, the litter size of live piglets was increased and the litter size of dead piglets was decreased by lycopene supplementation of the diet of sows. The litter weight at birth and weaning were increased in the lycopene group. Through placental proteomics, we enriched differentially expressed proteins (DEPs), gene ontology (GO) terms, and Kyoto encyclopedia of proteins and genomes (KEGG) pathways involved in immunity, anti-inflammation, antioxidants, and lipid metabolism and transport. Furthermore, in terms of placental health, we analyzed the levels of related enzymes, metabolites and mRNA expression in the placenta. Lycopene was shown to reduce mRNA expression and the levels of placental inflammatory factors, increase the content of immunoglobulin, improve the antioxidant capacity, and improve lipid metabolism and lipid transport in the placenta. In terms of sow milk composition, lycopene increased the levels of immunoglobulins in colostrum and lactose in colostrum and milk. Overall, the results of the present study demonstrate that dietary lycopene supplementation of sows during gestation and lactation improves the reproductive performance to a certain extent; this may be due to lycopene improving the placental health and milk composition of sows.

Lycopene modulates lipid metabolism in rats and their offspring under a high-fat diet.

The purpose of this study was to investigate the effects of lycopene supplementation on lipid metabolism in rats and their offspring. The experiment was conducted on 60 female rats divided into four groups: normal diet, normal diet with 200 mg kg-1 lycopene, high-fat diet, and high-fat diet with 200 mg kg-1 lycopene. The plasma levels of TG, LDL-C, AST and ALT in female rats fed a high-fat diet were significantly increased (P < 0.05). Lycopene supplementation reduced the plasma TG, LEP and AST levels (P < 0.05). In addition, the activity of ACC and mRNA expression of SREBP1c, FAS, PPARγ, CPT1, HMGCR, ACC, PLIN1 and FATP1 in the liver were also increased after feeding a high-fat diet (P < 0.05), whereas the expression of HSL was decreased (P < 0.05). Lycopene increased the activity of HSL and the expression of ATGL in the liver (P < 0.05), and the activity of ACC and mRNA expression of HMGCR and ACC were decreased (P < 0.05). For the offspring, maternal feeding of a high-fat diet reduced the plasma HDL-C levels (P < 0.05), but lycopene supplementation reduced the plasma TC levels (P < 0.05). Maternal high-fat diet also decreased the activity of HSL and the expression of CD36, PLIN1 and FATP1 in the liver while increasing the expression of PPARγ (P < 0.05). Maternal lycopene supplementation decreased the activities of ACC and FAS in the liver and decreased the expression of PPARγ, ACC and PLIN1 (P < 0.05). Maternal feeding of a high-fat diet increased the level of oxidative stress in the liver, the level of blood lipids in plasma and the rate of lipid production in the liver of rats and their offspring. Maternal lycopene supplementation can reduce the level of oxidative stress in rats and their offspring, reduce the level of blood lipids in plasma, and also reduce the rate of lipid production in the liver of rats and offspring.

Maternal Exposure to Oxidized Soybean Oil Impairs Placental Development by Modulating Nutrient Transporters in a Rat Model.

INTRODUCTION: As an exogenous food contaminant, dietary oxidized lipid impairs growth and development, and triggers chronic diseases in humans or animals. This study explores the effects of soybean oil with different oxidative degree on the placental injury of gestational rats. METHODS AND RESULTS: Thirty-two female adult rats are randomly assigned to four groups. The control group is fed the purified diet with fresh soybean oil (FSO), and the treatment groups are fed purified diets with lipid content replaced by oxidized soybean oil (OSO) at 200, 400, and 800 mEqO2 kg-1 from conception until delivery. On day 20 of gestation, OSO decreased placental and embryonic weights as the oxidative degree increased linearly and quadratically. The expression of Bax showed a linear increase, and Bcl-2 decreased as the oxidative degree increased. The expression of Fosl1 and Esx1 is linearly and quadratically decreased in OSO-treated groups than FSO group. OSO decreased the level of IL-10 but increased expression of IL-1ß in placenta and plasma. OSO remarkably upregulates levels of Fatp1 and Glut1 and decreases expression of Snat2 and Glut3. CONCLUSION: OSO aggravates placental injury by modulating nutrient transporters and apoptosis-related genes, impedes placental growth and development, and ultimately leads to the decrease of fetal weight.

Exposure to oxidized soybean oil induces mammary mitochondrial injury in lactating rats and alters the intestinal barrier function of progeny.

Similar to other food contaminants, dietary oxidized soybean oil (OSO) is also a toxic xenobiotic for animal and human nutrition. This research evaluated the effects of maternal OSO exposure during lactation on mammary mitochondrial injury and intestinal barrier of sucking progeny. Twenty-four female adult SD rats were fed a fresh soybean oil (FSO) homozygous diet (7%) or an OSO homozygous diet (7%) during lactation. On day 21 of lactation, upregulated mRNA expression of Sirt3 and PRDX3 and downregulated mRNA expression of Mfn2 were observed in mammary tissues in the OSO group compared to the control group (P < 0.05). Maternal OSO consumption increased the FasL transcriptional level in the mammary glands of rat dams (P < 0.05), while the mRNA expression of Bax, Bcl-2, Caspase3, and Fas was not different from that in the control group (P > 0.05). OSO enhanced the Nrf2 transcriptional level and decreased the expression of Keap1 and PPARα in mammary tissues (P < 0.05). In addition, the contents of CAT, MDA, SOD were not affected by dietary OSO (P > 0.05), while the concentration of H2O2 was significantly decreased in the OSO-treated mammary glands of rat dams (P < 0.05). Maternal OSO exposure during lactation did not affect the organ coefficients of pups (P > 0.05). However, maternal OSO consumption influenced the intestinal tight junction protein expression of progeny (P < 0.05). In summary, the present study demonstrated that dietary OSO may aggravate mammary injury and mitochondria dysfunction, but the OSO-induced damage was self-alleviating via the promotion of Sirt3 and PRDX3 expression and further scavenging of oxidative products.

The Effect of Increasing Neutral Detergent Fiber Level through Different Fiber Feed Ingredients throughout the Gestation of Sows.

The purpose of this study was to determine the effect of increasing dietary neutral detergent fiber (NDF) levels on pregnant sows, and to select the best feed ingredients based on reproductive performance, plasma biochemistry parameters, colostrum and milk composition, and nutrient digestibility. Seventy-two multiparous sows were randomly allotted to six dietary treatment groups (n = 12). The feeding of chicory meal (CM), wheat bran (WB), corn gluten, and rice bran meal (RBM) increased the average weaning weight of piglets compared with the control (CON) group (p < 0.05). Supplementation with CG diet increased the sow BW, weight gain, and back fat thickness compared with WB and RBM on day 107 of gestation (p < 0.05). Furthermore, Supplementation with CG diet resulted in lower plasma urea nitrogen (PUN) and higher total protein (TP) concentrations in plasma (p < 0.05). Feeding CM diet and soybean curd residue (SCR) diet reduced the total protein and globulin, and supplementation with CM diet significantly increased the PUN (p < 0.05). The apparent total tract digestibility (ATTD) of crude protein (CP), crude fat (EE), calcium (Ca), phosphorus (P), neutral detergent fiber (NDF), and acid detergent fiber (ADF) were decreased following the addition of CM, WB, or SCR to the diets (p < 0.05). The ATTD of NDF and ADF were significantly increased in the CG group (p < 0.05). In conclusion, the feeding of CG diet to sows have an excellent effect.

Effect of dietary pyrroloquinoline quinone disodium in sows on intestinal health of the offspring.

The objective of this study was to investigate the effects of dietary pyrroloquinoline quinone disodium (PQQ·Na2) supplementation in sows during gestation and lactation on intestinal health in offspring. A total of 40 cross-bred (landrace × large white crossed with Duroc boar) multiparity gestation sows with an average parity of 4.3 were used in this study. Forty sows were allotted to 2 dietary treatments after breeding. One group was the control sows, which were fed a corn-soybean meal control diet (Con treatment, n = 20), and the other group was the treatment sows fed a control diet with 20 mg kg-1 PQQ·Na2 after breeding and through gestation and lactation (PQQ treatment, n = 20). The activities of SOD and GSH-Px were significantly (P < 0.05) increased by PQQ·Na2 supplementation, and MDA activity was decreased (P < 0.05) in the plasma of piglets. CAT, SOD and GSH-Px activities were significantly (P < 0.05) increased, and MDA activity was decreased (P < 0.05) in the small intestine of piglets. The mRNA expression levels of SOD1, CAT and MGST1 in the jejunum were increased in newborn piglets (P < 0.05), and the mRNA expression levels of HO1, SOD1, CAT, SOD2, GPX4, GPX1 and GCLC in the jejunum were increased in weaned piglets (P < 0.05). The mRNA expression of ZO-1 was increased (P < 0.05) in the jejunum of newborn piglets, and the mRNA expression of Occludin and ZO-1 was increased (P < 0.05) in the jejunum of weaned piglets. The villous height of the duodenum and jejunum of weaned piglets was increased (P < 0.05) by dietary PQQ·Na2. In weaned piglets, Bacteroidetes and Firmicutes were the most prevalent phyla in both the Con and PQQ·Na2 treatment groups, and the most prevalent genera were Alloprevotella and Bacteroides. At the phylum level, the abundance of Firmicutes was significantly increased (P < 0.05), and the abundance of Proteobacteria was significantly decreased (P < 0.05). At the genus level, the abundance of Alloprevotella was significantly increased (P < 0.05), and the abundance of Actinobacillus and Escherichia was decreased (P < 0.05). In conclusion, dietary supplementation with PQQ·Na2 in sows during gestation and lactation had positive effects on intestinal health in offspring.

The Effects of Endoplasmic-Reticulum-Resident Selenoproteins in a Nonalcoholic Fatty Liver Disease Pig Model Induced by a High-Fat Diet.

The present study aimed to investigate the intervention of selenium in the oxidative stress and apoptosis of pig livers, which were induced by a high-fat diet, and the effects of four endoplasmic reticulum (ER)-resident selenoproteins in the process. A 2×4 design trial was conducted that included two dietary fat levels (BD = basal diet and HFD = high-fat diet) and four dietary Se supplementation levels (0, 0.3, 1.0, and 3.0 mg/kg of the diet, in the form of sodium selenite (Na2SeO3)). Our results indicated that the HFD significantly increased the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the serum, as well as the degree of steatosis, the content of malondialdehyde (MDA), the apoptotic rate, and the level of mRNA caspase-3 in the liver compared to their BD counterparts (p < 0.05). Moreover, these parameters in the HFD groups were more significantly reduced (p < 0.05) for a Se concentration of 1.0 mg/kg than for the other concentrations. Further, for both the BD and HFD, the groups supplemented with 1.0 mg/kg Se showed the highest mRNA level of selenoprotein S. In conclusion, the consumption of an HFD can induce oxidative damage and apoptosis in the liver. This shows that the supplementation of Se at 1.0 mg/kg may be the optimum concentration against damage induced by HFD, and Sels may play a key role in this process.

Pyrroloquinoline quinone inhibits the production of inflammatory cytokines via the SIRT1/NF-κB signal pathway in weaned piglet jejunum.

The small intestine is an important digestive organ and plays a vital role in the life of a pig. In this study, we explored the regulatory role and molecular mechanism of pyrroloquinoline quinone (PQQ) on intestinal health and to discussed the interaction between PQQ and vitamin C (VC). A total of 160 healthy piglets weaned at 21 d were randomly divided into four treatment groups according to 2 × 2 factoring. The results showed that dietary PQQ could significantly decrease the levels of plasma globulin, albumin/globulin (A/G), indirect bilirubin (IBIL), blood urea nitrogen (BUN), creatinine (CREA) (P < 0.05 for each), total bilirubin, (TBIL) (P < 0.01), diamine oxidase (DAO) (P < 0.01) and immunoglobulin G (IgG) (P < 0.0001) and increase the levels of immunoglobulin A (IgA) and immunoglobulin M (IgM) (P < 0.0001) in the plasma of weaned piglets. Similarly, dietary VC could significantly decrease the levels of plasma globulin, A/G, DAO (P < 0.05 for each) and IgG (P < 0.0001) and increase the levels of IgA and IgM (P < 0.0001) in the plasma of weaned piglets. In addition, dietary PQQ increased (P < 0.05) the mRNA levels of antioxidant genes (NQO1, UGT1A1, and EPHX1), thereby enhancing (oxidized) nicotinamide adenine dinucleotide (NAD+) concentration and sirtuin 1 (SIRT1) activity in tissues. However, the addition of 200 mg kg-1 VC to the diet containing PQQ reduced most of the effects of PQQ. We further show that PQQ reduced (P < 0.05) the expression of inflammation-related genes (IL-2, IL-6, TNF-α, and COX-2) via the SIRT1/NF-κB deacetylation signaling. In conclusion, our data reveals that PQQ exerts a certain protective effect on the intestines of piglets, but higher concentrations of VC react with PQQ, which inhibits the regulatory mechanism of PQQ.