Liver Of Piglets Research Articles

Aberrant Cholesterol Metabolic Genes Regulation in a Negative Feedback Loop Induced by an Alphacoronavirus.

Porcine epidemic diarrhea virus (PEDV) is an alphacoronavirus that causes acute inflammation and severe diarrhea in newborn piglets with a high mortality rate. Given that cholesterol is required for coronavirus infection in vitro, the role of endogenous cholesterol metabolism in regulating coronavirus infection and the mechanism behind it ought to be elucidated. In this study, we found that the levels of cholesterol and bile acids were both elevated in the livers of PEDV-infected piglets compared to those of the control group. Consistently, in the livers of PEDV-infected piglets, the expression of key genes involved in cholesterol metabolism was significantly increased. Transcriptomic analysis indicated that the cholesterol homeostasis pathway was among the most enriched pathways in the livers of PEDV-infected piglets. Unexpectedly, the expression of key genes in the cholesterol metabolic pathway was downregulated at the messenger RNA (mRNA) level, but upregulated at the protein level. While the primary transcriptional factors (TFs) of cholesterol metabolism, including SREBP2 and FXR, were upregulated at both mRNA and protein levels in response to PEDV infection. Further Chromatin Immunoprecipitation Quantitative Real-time PCR (ChIP-qPCR) analysis demonstrated that the binding of these TFs to the locus of key genes in the cholesterol metabolic pathway was remarkably inhibited by PEDV infection. It was also observed that the occupancies of histone H3K27ac and H3K4me1, at the locus of the cholesterol metabolic genes HMGCR and HMGCS1, in the livers of PEDV-infected piglets, were suppressed. Together, the PEDV triggers an aberrant regulation of cholesterol metabolic genes via epigenetic inhibition of SREBP2/FXR-mediated transcription, which provides a novel antiviral target against PEDV and other coronaviruses.

Increased Ingestion of Hydroxy-Methionine by Both Sows and Piglets Improves the Ability of the Progeny to Counteract LPS-Induced Hepatic and Splenic Injury with Potential Regulation of TLR4 and NOD Signaling.

Methionine, as an essential amino acid, play roles in antioxidant defense and the regulation of immune responses. This study was designed to determine the effects and mechanisms of increased consumption of methionine by sows and piglets on the capacity of the progeny to counteract lipopolysaccharide (LPS) challenge-induced injury in the liver and spleen of piglets. Primiparous sows (n = 10/diet) and their progeny were fed a diet that was adequate in sulfur amino acids (CON) or CON + 25% total sulfur amino acids as methionine from gestation day 85 to postnatal day 35. A total of ten male piglets were selected from each treatment and divided into 2 groups (n = 5/treatment) for a 2 × 2 factorial design [diets (CON, Methionine) and challenge (saline or LPS)] at 35 d old. After 24 h challenge, the piglets were euthanized to collect the liver and spleen for the histopathology, redox status, and gene expression analysis. The histopathological results showed that LPS challenge induced liver and spleen injury, while dietary methionine supplementation alleviated these damages that were induced by the LPS challenge. Furthermore, the LPS challenge also decreased the activities of GPX, SOD, and CAT and upregulated the mRNA and(or) protein expression of TLR4, MyD88, TRAF6, NOD1, NOD2, NF-kB, TNF-α, IL-8, p53, BCL2, and COX2 in the liver and (or) spleen. The alterations of GPX and SOD activities and the former nine genes were prevented or alleviated by the methionine supplementation. In conclusion, the maternal and neonatal dietary supplementation of methionine improved the ability of piglets to resist LPS challenge-induced liver and spleen injury, potentially through the increased antioxidant capacity and inhibition of TLR4 and NOD signaling pathway.

Pathological changes in the liver of piglets under the influence of mycotoxins in feed in sows

Pathological changes in the liver of piglets under the influence of mycotoxins in feed in sows

Taurine Prevents LPS-Induced Liver Injury in Weaned Piglets.

This study employed taurine as a feed additive to explore the prophylactic effect of taurine on LPS-induced hepatic injury in piglets. The pathological shifts within hepatic tissue were observed by HE staining. Serum levels of ALT and AST together with SOD, CAT, GSH-PX activity, and MDA serum and liver levels were detected. TUNEL was used to detect apoptosis, while qPCR was employed to detect HO-1, Nrf-2, Bcl2, BAX, Caspase-3, and NF- κB p65 transcriptomic expression levels. TRL4, Caspase-3, Nrf-2, and NF- κB p-p65/NF- κB p65 were detected by Western blot. The results revealed that taurine reduces LPS-induced pathological damage of hepatic tissue and reduces the levels of ALT and AST in pig serum. The transcriptomic expression levels of HO-1 and Nrf-2 were upregulated, and proteomic expression of Nrf-2 was increased. SOD, CAT, and GSH-PX activity was elevated, while MDA content was reduced in serum and liver. The levels of mRNA of BAX and Caspase-3 were downregulated, but mRNA content of Bcl2 was increased, and the protein levels of TRL4, NF-κB p-p65/NF-κB p65, and Caspase-3 were diminished. Overall, the degree of hepatocyte apoptosis was also significantly reduced. In conclusion, taurine reduces LPS-induced injury of piglet liver, while reducing hepatocyte apoptotic levels. These data provide a scientific basis for the selection of animal feed additives and lay a foundation for the healthy and sustainable development of the porcine industry.

ULTRASOUND IMAGING OF THE SPLEEN, STOMACH, LIVER, KIDNEYS, BLADDER, AND PROSTATE IN PIGLETS (Sus scrofa domestica)

This study aims to describe ultrasonographic imaging of the spleen, stomach, liver, kidney, bladder, and prostate in piglets (Sus scrofa domestica). Ultrasonography was performed on six male piglets aged 1 month with a body weight of 4-8 kg. Ultrasonography of the spleen, stomach, liver, urinary bladder, and prostate was observed in the dorsal-recumbency position, and the kidney was observed in the lateral-recumbency position. The ultrasound examination used the Chison EBit 60, which is a linear type transducer with a frequency of 9 MHz, transverse and sagittal positions, and a gain of about 55-80. Ultrasonography of the spleen showed that the shape of the spleen head varied in each individual. The results of gastric ultrasonography showed the gastric lining clearly and the similarity of the position, shape, structure, echogenicity, and size of the stomach. The results of liver ultrasonography showed that the echogenicity of the liver tended to be hyperechoic, the kidneys were hyperechoic, and the bladder was hypoechoic due to the use of improper gain. The average length of the right kidney was 4.73±0.50 cm and the left kidney was 4.08±0.26 cm. The bladder wall thickness was 1.3±0.31 mm. Imaging of the bladder showed changes in wall size and echogenicity. Prostate ultrasound results obtained an average length of 2.68±0.45 cm, width 1.69±0.35 cm. The results of this study can be used as a reference for normal data on organ position, organ structure, and organ echogenicity of the spleen, stomach, liver, kidney, bladder, and prostate in piglets.

MicroRNA Expression Profiling in Porcine Liver, Jejunum and Serum upon Dietary DON Exposure Reveals Candidate Toxicity Biomarkers.

Deoxynivalenol (DON), a frequent mycotoxin worldwide, impairs human and animal health. The response of microRNAs, small non-coding RNAs, to DON has been scarcely investigated, but holds remarkable potential for biomarker applications. Hence, we aimed to investigate DON-induced changes in the microRNA expression in porcine liver, jejunum and serum by combining targeted and untargeted analyses. Piglets received uncontaminated feed or feed containing 900 µg/kg and 2500 µg/kg DON for four weeks, followed by a wash-out period. In tissue, only slight changes in microRNA expression were detected, with ssc-miR-10b being downregulated in liver of DON-exposed piglets. In serum, several microRNAs were differentially expressed upon DON exposure, four of which were validated by qPCR (ssc-miR-16, ssc-miR-128, ssc-miR-451, ssc-miR-205). The serum microRNA response to DON increased over time and declined after removal of contaminated diets. Receiver operating curve analyses for individual microRNAs were significant, and a combination of the four microRNAs increased the predictive capacity for DON exposure. Predicted microRNA target genes showed enrichment of several pathways including PIK3-AKT, Wnt/β-catenin, and adherens junctions. This study gives, for the first time, a comprehensive view of the porcine microRNA response to DON, providing a basis for future research on microRNAs as biomarkers for mycotoxins.

Nano-Selenium and Macleaya cordata Extracts Improved Immune Functions of Intrauterine Growth Retardation Piglets under Maternal Oxidation Stress.

Intrauterine growth retardation (IUGR) is the main death cause of newborn piglets in large-scale farms. To investigate the effects of maternal nano-selenium (nano-Se) and Macleaya cordata extracts (MCE) on immune functions of IUGR piglets in large scale farms, a 2 × 2 factorial design was adopted in this test, and two factors were nano-Se (0, 0.50mg/kg) and MCE (0, 500mg/kg). A total of 32 ternary hybrid sows (Landrace × Yorkshire × Duroc, parity 2) were used in this 25-day trial from day 90 of pregnancy to delivery. The dietary treatments were as follows: (1) CON group, basic diet (0.0mg/kg Se); (2) Nano-Se group, basic diet + 0.50mg/kg added Se (nano-Se); (3) MCE group, basic diet + 500mg/kg added MCE; (4) Combined group, basic diet + 0.50mg/kg added nano-Se and 500mg/kg added MCE. Maternal nano-Se or combination of nano-Se and MCE diets extremely increased the superoxide dismutase (SOD), catalase (CAT), superoxide dismutase (GSH-Px) contents in the serum and liver of IUGR offspring (P < 0.05), and MCE supplementation in sow diets remarkably increased the serum superoxide dismutase (SOD), catalase (CAT), and superoxide dismutase (GSH-Px) contents of IUGR piglets (P < 0.05). Adding nano-Se, MCE, or nano-Se and MCE to sow diets decreased the malondialdehyde (MDA) content in the serum and liver of IUGR piglets (P < 0.05). The supplementation of nano-Se and combined diets extremely increased the activities of immunoglobulin G (IgG) and immunoglobulin A (IgA) in the serum and liver of IUGR offspring (P < 0.05). Maternal nano-Se, MCE, and combined diets greatly decreased the levels of tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), and interleukin-1β (IL-1β) in the serum and liver of IUGR piglets (P < 0.05). Together, the application of nano-Se and/or MCE to sow diets improved antioxidant capacities and immune functions of IUGR offspring, and alleviated oxidative stress.

Early Weaning Affects Liver Antioxidant Function in Piglets.

Simple SummaryEarly weaning is used to improve efficiency in pig production. However, early weaning may trigger liver oxidative stress in piglets. In this study, we evaluated the effects of early weaning on the development and antioxidant function of the liver in piglets. Our findings show that early weaning significantly decreases piglet body weight and suppresses liver development. We find that early weaning also suppresses the activities of superoxide dismutase (SOD) and catalase (CAT) (p < 0.05). It could be concluded that weaning may reduce the growth performance and liver antioxidant function of piglets.This study examined the impact of early weaning on antioxidant function in piglets. A total of 40 Duroc × Landrace × Large White, 21-day-old piglets (half male and half female) were divided into suckling groups (SG) and weaning groups (WG). Piglets in WG were weaned at the 21st day, while the piglets in SG continued to get breastfed. Eight piglets from each group were randomly selected and slaughtered at 24th-day (SG3, WG3) and 28th-day old (SG7, WG7). The body weight, liver index, hepatocyte morphology, antioxidant enzymes activity, gene expression of antioxidant enzymes, and Nrf2 signaling in the liver of piglets were measured. The results showed that weaning caused decreased body weight (p < 0.01), lower liver weight (p < 0.01), and decreased the liver organ index (p < 0.05) of piglets. The area and size of hepatocytes in the WG group was smaller than that in the SG group (p < 0.05). We also observed that weaning reduced the activity of superoxide dismutase (SOD) and catalase (CAT) (p < 0.05) in the liver of piglets. Relative to the SG3 group, the gene expression of GSH-Px in liver of WG3 was significantly reduced (p < 0.05). The gene expression of Nrf2 in the SG3 group was higher than that in the WG3 group (p < 0.01). The gene expression of NQO1 in the SG7 group was higher than that in the WG7 group (p < 0.05). In conclusion, weaning resulted in lower weight, slowed liver development, and reduced antioxidant enzymes activity, thereby impairing liver antioxidant function and suppressing piglet growth.

The Influence of Fusarium Mycotoxins on the Liver of Gilts and Their Suckling Piglets.

Simple SummaryMycotoxins are toxic secondary metabolites of fungi that frequently contaminate animal feed and human food in different combinations; therefore, it is of great importance to determine the effects of mycotoxin co-contamination. Pigs are one of the most sensitive animal species to Fusarium mycotoxins, and the liver is an important site of mycotoxin metabolism. The objective of the present research was to determine histopathological changes, apoptosis, and proliferation in the liver of gilts fed with Fusarium mycotoxin-contaminated feed for a prolonged time at the end of their pregnancy and until weaning of their piglets. Additionally, the same parameters were evaluated in the liver of their piglets to determine whether Fusarium mycotoxins would affect the offspring. The results revealed increased hepatocellular necrosis and apoptosis as well as sinusoidal leukocytosis with inflammatory infiltrates of hepatic lobules in experimental gilts, but no significant changes were observed in the piglet livers, implying that the utilized concentrations and duration of exposure did not cause detrimental effects on them. Interestingly, the amount of interlobular connective tissue in the liver of experimental gilts was significantly decreased. The obtained results emphasized the need to evaluate Fusarium mycotoxin concentrations in feed because even at low concentrations, they can cause adverse effects, but there is less concern for severe detrimental effects on the offspring.Mycotoxins are common fungal secondary metabolites in both animal feed and human food, representing widespread toxic contaminants that cause various adverse effects. Co-contamination with different mycotoxins is frequent; therefore, this study focused on feed contaminated with Fusarium mycotoxins, namely, deoxynivalenol (5.08 mg/kg), zearalenone (0.09 mg/kg), and fusaric acid (21.6 mg/kg). Their effects on the liver of gilts and their piglets were chosen as the research subject as pigs are one of the most sensitive animal species that are also physiologically very similar to humans. The gilts were fed the experimental diet for 54 ± 1 day, starting late in their pregnancy and continuing until roughly a week after weaning of their piglets. Livers of gilts and their piglets were assessed for different histopathological changes, apoptosis, and proliferation activity of hepatocytes. On histopathology, gilts fed the experimental diet had a statistically significant increase in hepatocellular necrosis and apoptosis (p = 0.0318) as well as sinusoidal leukocytosis with inflammatory infiltrates of hepatic lobules (p = 0.0004). The amount of interlobular connective tissue in the liver of experimental gilts was also significantly decreased (p = 0.0232), implying a disruption in the formation of fibrous connective tissue. Apoptosis of hepatocytes and of cells in hepatic sinusoids, further assessed by the terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) assay, showed a statistically significant increase (p = 0.0224 and p = 0.0007, respectively). No differences were observed in piglet livers. These results indicated that Fusarium mycotoxins elicited increased apoptosis, necrosis, and inflammation in the liver of gilts, but caused no effects on the liver of piglets at these concentrations.

Orphan Nuclear Receptor RORγ Modulates the Genome-Wide Binding of the Cholesterol Metabolic Genes during Mycotoxin-Induced Liver Injury.

Maintaining lipid homeostasis is crucial to liver function, the key organ that governs the whole-body energy metabolism. In contrast, lipid dysregulation has been implicated in mycotoxin-induced liver injury, by which the pathophysiological regulation and the molecular components involved remain elusive. Here we focused on the potential roles of orphan nuclear receptor (NR) RORγ in lipid programming, and aimed to explore its action on cholesterol regulation in the liver of mycotoxin-exposed piglets. We found that liver tissues were damaged in the mycotoxin-exposed piglets compared to the healthy controls, revealed by histological analysis, elevated seral ALT, AST and ALP levels, and increased caspase 3/7 activities. Consistent with the transcriptomic finding of down-regulated cholesterol metabolism, we demonstrated that both cholesterol contents and cholesterol biosynthesis/transformation gene expressions in the mycotoxin-exposed livers were reduced, including HMGCS1, FDPS, SQLE, EBP, FDFT1 and VLDLR. Furthermore, we reported that RORγ binds to the cholesterol metabolic genes in porcine hepatocytes using a genome-wide ChIP-seq analysis, whereas mycotoxin decreased the RORγ binding occupancies genome-wide, especially at the cholesterol metabolic pathway. In addition, we revealed the enrichment of co-factors p300 and SRC, the histone marks H3K27ac and H3K4me2, together with RNA Polymerase II (Pol-II) at the locus of HMGCS1 in hepatocytes, which were reduced by mycotoxin-exposure. Our results provide a deep insight into the cholesterol metabolism regulation during mycotoxin-induced liver injury, and propose NRs as therapeutic targets for anti-mycotoxin treatments.

Impact of Dietary Crude Protein Level on Hepatic Lipid Metabolism in Weaned Female Piglets.

Simple SummaryIt has been reported that a high crude protein diet could reverse the diet-induced lipid accumulation in the liver of mice and rodents. However, in vivo data supporting a functional role of a high crude protein diet on hepatic lipid metabolism-associated genes and proteins in weaned piglets is not available. In the present study, we aimed to provide a mechanistic insight into alterations in the hepatic lipid lipogenesis, lipolysis, oxidation, and gluconeogenesis in response to different dietary crude protein levels. Our results demonstrated that dietary crude protein could regulate hepatic lipid metabolism through regulating hepatic lipid lipogenesis, lipolysis, oxidation, and gluconeogenesis. The result indicated an important role of dietary crude protein in regulating hepatic lipid metabolism in weaned piglets.Amino acids serve not only as building blocks for proteins, but also as substrates for the synthesis of low-molecular-weight substances involved in hepatic lipid metabolism. In the present study, eighteen weaned female piglets at 35 days of age were fed a corn- and soybean meal-based diet containing 20%, 17%, or 14% crude protein (CP), respectively. We found that 17% or 20% CP administration reduced the triglyceride and cholesterol concentrations, while enhanced high-density lipoprotein cholesterol (HDL-C) concentration in serum. Western blot analysis showed that piglets in the 20% CP group had higher protein abundance of hormone-sensitive triglyceride lipase (HSL) and peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), as compared with other groups. Moreover, the mRNA expression of sterol regulatory element binding transcription factor 1 (SREBPF1), fatty acid synthase (FASN), and stearoyl-CoA desaturase (SCD) were lower in the 17% or 20% CP group, compared with those of the piglets administered with 14% CP. Of note, the mRNA level of acetyl-CoA carboxylase alpha (ACACα) was lower in the 17% CP group, compared with other groups. Additionally, the mRNA level of lipoprotein lipase (LPL), peroxisome proliferator-activated receptor alpha α (PPARα), glucose-6-phosphatase catalytic subunit (G6PC), and phosphoenolpyruvate carboxykinase 1 (PKC1) in the liver of piglets in the 20% CP group were higher than those of the 14% CP group. Collectively, our results demonstrated that dietary CP could regulate hepatic lipid metabolism through altering hepatic lipid lipogenesis, lipolysis, oxidation, and gluconeogenesis.

The Farnesoid X Receptor Agonist Tropifexor Prevents Liver Damage in Parenteral Nutrition-fed Neonatal Piglets.

Intestinal failure-associated liver disease (IFALD) is a life-threatening complication for patients with intestinal failure who receive long-term parenteral nutrition (PN). We evaluated the effects of the farnesoid X receptor agonist tropifexor on a neonatal piglet model of IFALD fed with PN. The piglets received PN and tropifexor for 14 days, then levels of liver enzymes, bile acid metabolism, inflammation, and intestinal barrier markers were assessed using quantitative real-time PCR. Fibroblast growth factor (FGF) 19 serum levels were determined using enzyme-linked immunosorbent assays. Bile acids were determined in liver, serum, and intestinal contents, and the microbiome was sequenced in different intestinal segments. The PN model was established in newborn piglets. The levels of serum liver enzymes, pro-inflammatory factors, and oxidative stress increased in the livers of piglets fed with PN, but not in those fed with PN and tropifexor. Tropifexor stimulated FGF19 expression in ileal epithelial cells, increased portal FGF19 levels, then inhibited cholesterol 7α-hydroxylase expression in the liver. Tropifexor increased the relative abundance of bacteria associated with bile salt hydrolase and 7α-dehydrogenation in the contents of ileum and altered the composition of bile acids in serum, liver, and intestinal contents. Tropifexor also inhibited intestinal inflammation, alleviated intestinal mucosal atrophy, and improved the intestinal barrier. Tropifexor might prevent liver damage in neonatal piglets receiving PN by altering the composition of intestinal microbiota and bile acids. Tropifexor also alleviates intestinal inflammation and preserves the intestinal barrier.

Swine Inflammation and Necrosis Syndrome Is Associated with Plasma Metabolites and Liver Transcriptome in Affected Piglets.

Simple SummarySwine inflammation and necrosis syndrome (SINS) is a newly identified syndrome associated with inflammatory and necrotic signs in different body parts of suckling piglets, weaners, and fatteners. While the proven inflammatory basis of the disease and the development of signs in even newborns indicate a primarily endogenous etiology, the mechanisms underlying SINS development are largely unknown. In this study, the hypothesis was tested that SINS is indirectly triggered by the translocation of gut-derived microbial components into the liver, thereby causing derangements of liver metabolism, by comparing the hepatic transcriptome and plasma metabolome of SINS-affected and unaffected piglets. Apart from demonstrating that hepatic inflammation occurs in SINS-affected piglets, the study clearly shows for the first time that several metabolic derangements are induced in SINS-affected piglets that may contribute to the clinical and histopathological signs of SINS.Swine Inflammation and Necrosis Syndrome can lead to severe clinical signs, especially in tails, ears, teats, and claws in pigs. Clinical and histopathological findings in newborn piglets with intact epidermis indicate a primarily endogenous etiology, and microbial-associated molecular patterns (MAMPs), such as lipopolysaccharide (LPS) are assumed to play a central role in the development of the syndrome. We hypothesized that swine inflammation and necrosis syndrome (SINS) is indirectly triggered by gut-derived MAMPs entering the circulatory system via the liver and thereby causing derangements on liver metabolism. To test this hypothesis, metabolomes, candidate genes of the liver and liver transcriptomes of 6 piglets with high-grade clinical signs of SINS (SINS high) were examined and compared with 6 piglets without significant signs of SINS (SINS low). Several hepatic pro-inflammatory genes and genes involved in stress response were induced in piglets of the SINS high group. The most striking finding from hepatic transcript profiling and bioinformatic enrichment was that the most enriched biological processes associated with the approximately 220 genes induced in the liver of the SINS high group were exclusively related to metabolic pathways, such as fatty acid metabolic process. Within the genes (≈390) repressed in the liver of the SINS high group, enriched pathways were ribosome biogenesis, RNA processing, RNA splicing, spliceosome, and RNA transport. The transcriptomic findings were supported by the results of the metabolome analyses. These results provide the first evidence for the induction of an inflammatory process in the liver of piglets suffering from SINS, accompanied by lipid metabolic derangement.

Serine Supplementation in the Diets of Late Gestating and Lactating Sows Improves Selenium Nutritional Status in Sows and Their Offspring.

Serine can regulate selenoprotein expression, and dietary serine is correlated with the contents of plasma selenoprotein P (Sepp1) and milk selenium (Se) in lactating mothers. Based on this, we investigated the effects of serine supplementation in the diets of late gestating and lactating sows on Sepp1 and Se contents in sows and their offspring. A total of 72 sows were assigned to four groups. During the experiment, sows were fed either a basal diet or basal diets supplemented with three different levels of serine. The results showed that maternal dietary serine had no effect on the Se content in the serum of sows and their offspring, whereas it significantly increased the Se content in the liver of piglets at the age of 21 days. Maternal dietary serine significantly increased Sepp1 content, either in the serum of sows or that in their offspring at the ages of 3 days, 7 days, and 21 days. Additionally, maternal dietary serine significantly increased litter weight and the average body weight of piglets at the age of 11 days. Notably, a positive correlation was found between the average body weight of piglets at the age of 11 days and serum Sepp1 content in piglets, at the age of either 3 days or 7 days. In conclusion, maternal dietary serine supplementation could improve Se nutritional status in sows and their offspring. These beneficial changes may contribute to the higher body weight of the offspring.

Tolerable upper intake level of iron damages the liver of weaned piglets.

Iron is one of the essential trace elements, which is often supplemented as an additive to meet the growing needs of toddlers and young animals. Recommended nutrient intake (RNI) and tolerable upper intake levels (UL) are always set when the iron is supplemented. The purpose of this study was to evaluate the subacute (28days) toxicity of UL iron to weaned piglet liver. Thirty 23-day-old weaned piglets were divided into three groups and, respectively, supplemented with 100, 300 or 3000 (UL) mg/kg iron. UL iron caused significant weight loss in 4th week (p<0.05). Divalent metal transporter 1(DMT1) decreased significantly, ferroportin 1 and ferritin increased significantly in the liver of UL iron group (p<0.05). Although there was no significant effect on liver morphology, UL iron significantly increased hepatic iron, reactive oxygen species (ROS), malondialdehyde (MDA) and protein carbonyl (p<0.05). UL iron significantly reduced glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT) and total anti-oxidation capacity (T-AOC) in the liver (p<0.05). Nuclear factor erythroid 2-related factor 2 (Nrf2) activated subunits of glutamate cysteine ligase (Gclc) and glutathione S-transferase A1 (Gsta1) upregulation in the UL iron group liver, thereby increasing resistance to oxidative stress. In conclusion, UL iron supplementation altered iron metabolism, generated free radicals, reduced antioxidant enzyme activity and activated Nrf2 signalling pathway in the weaned piglet liver.

O-GlcNAc / Akt pathway regulates glucose metabolism and reduces apoptosis in liver of piglets with acute cold stress

Cold stress is one of the serious factors restricting the development of animal husbandry in cold areas. Cold exposure can easily lead to cold stress, slow growth and even death of newborn animals. O-GlcNAcylation modification can act as type of “stress receptor” and“nutrition sensor” in a variety of stress responses, however, it is not clear how O-GlcNAcylation can regulate glucose metabolism in the liver of piglets under cold stress. In this study, piglets 21 days of age were exposed to 4 °C for 4 h or 8 h in a phytotron. Serum cortisol and other stress hormones were used to assess body status to establish a cold stress piglet model. The changes of glycogen in liver were detected by PAS. FDP and PA were also measured to study the glycolysis level of liver. To characterize potential mechanisms of O-GlcNAcylation on the livers of cold stress piglets, AKT, GSK3β, GS, PFKFB2, AS160 and their corresponding phosphorylation were determined by Western blotting. Results show O-GlcNAcylation increased and apoptosis levels increased in the liver following cold exposure during excessive CORT or metabolic dysfunction. It is suggested that the acute cold exposure of piglets induced a sequential change in the level of O-GlcNAcylation, which may be one of the factors mediating liver cell apoptosis and glucose metabolism regulation by the O-GlcNAc/AKT pathway. These findings provide new insight into the mechanisms of the cold stress response, which can facilitate the development of new strategies to combat the effects of hypothermia.

Fecal Microbiota Transplantation Shows Marked Shifts in the Multi-Omic Profiles of Porcine Post-weaning Diarrhea.

Weaning is the most critical phase in pig production and is generally associated with significant impacts on intestinal morphology, structure, physiology, and immune responses, which can lead to subsequent production inefficiencies such as decreases in growth and intake and increases in morbidity and mortality. In the present study, we attempted to explore the effects of fecal microbiota transplantation (FMT) on the fecal microbiota, fecal metabolites, and transcriptome in the jejunum, colon, liver, spleen, and oral mucosa in piglets with post-weaning diarrhea and to evaluate the therapeutic potential of FMT in piglets with post-weaning diarrhea. We found that FMT partially relieved the symptoms of diarrhea in piglets, and microbiota analysis results indicated that unclassified_f_Prevotellaceae was identified as an FMT-associated bacterial family at 66 day and that the Shannon index in the healthy group at 34, 38, and 66 days were higher than that at 21 day. Functional enrichment analysis of the oral mucosa, liver, jejunum, and colon showed that most of the differentially expressed genes (DEGs) were enriched in the terms metabolic process, immune response, and inflammatory response. Moreover, the enriched fecal metabolites focused mostly on apoptosis, beta-alanine metabolism, glutathione metabolism, and sphingolipid metabolism. We tried to detect specific “metabolite-bacterium” pairs, such as “g_Catenisphaera-stigmastentriol,” “p_Bacteroidetes-(6beta,22E)-6-hydroxystigmasta-4,22-dien-3-one,” and “g_Prevotellaceae_NK3B31_group-stenocereol.” Overall, the present study provides a theoretical basis for the alleviation of weaning stress and contributes to the realization of effective and sustainable application of FMT in the pig production industry in the future.

Metabolomic profiling reveals the effects of early-life lactoferrin intervention on protein synthesis, energy production and antioxidative capacity in the liver of suckling piglets.

This study aimed to determine the effects of an early-life lactoferrin (LF) intervention on liver metabolism in suckling piglets. Sixty newborn piglets with an average initial body weight (BW) of 1.51 ± 0.05 kg were assigned to a control (CON) group and an LF group. At age 1 to 7 days, the piglets in the LF group were orally administered LF solution (0.5 g per kg BW daily), whereas the piglets in the CON group were orally administered the same dose of physiological saline. Plasma, jejunum and liver samples were collected on days 8 and 21. The LF piglets showed a decreased plasma urea nitrogen level on day 8 and an increased plasma albumin level on day 21. Pathway analysis of the metabolomic profiles showed that the LF treatment affected amino acid metabolism in the liver. In addition, the LF treatment upregulated the gene expression levels of proteolytic enzymes and amino acid transporters (APA, APN, EAAC1, Pept1, CAT1, B0AT1 and ASCT2) in the jejunum, and it enhanced the phosphorylation levels of mTOR and p70S6K in the liver. The LF treatment also upregulated the expression of a β-oxidation-related gene (CPT1) and affected the tricarboxylic acid cycle in the liver on day 21. Furthermore, the LF piglets showed a decreased level of malondialdehyde and increased levels of GSH, GSH-Px and GCLC in the liver mitochondria. Overall, the early-life LF intervention affected the protein synthesis, energy production and antioxidative capacity in the liver of the neonatal piglets.

ГИСТОЛОГИЧЕСКИЕ ОСОБЕННОСТИ ПЕЧЕНИ НОВОРОЖДЕННЫХ ПОРОСЯТ ПОРОДЫ ЛАНДРАС

ГИСТОЛОГИЧЕСКИЕ ОСОБЕННОСТИ ПЕЧЕНИ НОВОРОЖДЕННЫХ ПОРОСЯТ ПОРОДЫ ЛАНДРАС

Assessing antibiotic residues in piglet liver and kidney samples: How to manage the results obtained

The use of antibiotics in livestock production has become a common practice. In the EU, the use of antibiotics as growth promoters is forbidden. However, the (mis)use of antibiotics may lead to antimicrobial resistance, which adversely affects humans, animals and the environment. Thus, the present study, using a previously validated multiclass and multi-residue UHPLC-ToF-MS methodology for the determination of 43 antibiotics, presents an assessment of data obtained from 60 piglets, using their livers and kidneys as samples. Eleven antimicrobials from different families were detected, which included ciprofloxacin, danofloxacin, doxycycline, enrofloxacin, oxytetracycline, spiramycin, sulfisomidine, sulfachloropyridazine, sulfadiazine, tilmicosin, and trimethoprim. The obtained concentrations ranged from 0.3 to 438.7 μg kg−1, confirming that both kidney and liver matrices are relevant in monitoring drug residue control programs.