Dietary fat supplementation relieves cold temperature-induced energy stress through AMPK-mediated mitochondrial homeostasis in pigs.

BACKGROUND: Cold stress has negative effects on the growth and health of mammals, and has become a factor restricting livestock development at high latitudes and on plateaus. The gut-liver axis is central to energy metabolism, and the mechanisms by which it regulates host energy metabolism at cold temperatures have rarely been illustrated. In this study, we evaluated the status of glycolipid metabolism and oxidative stress in pigs based on the gut-liver axis and propose that AMP-activated protein kinase (AMPK) is a key target for alleviating energy stress at cold temperatures by dietary fat supplementation. RESULTS: Dietary fat supplementation alleviated the negative effects of cold temperatures on growth performance and digestive enzymes, while hormonal homeostasis was also restored. Moreover, cold temperature exposure increased glucose transport in the jejunum. In contrast, we observed abnormalities in lipid metabolism, which was characterized by the accumulation of bile acids in the ileum and plasma. In addition, the results of the ileal metabolomic analysis were consistent with the energy metabolism measurements in the jejunum, and dietary fat supplementation increased the activity of the mitochondrial respiratory chain and lipid metabolism. As the central nexus of energy metabolism, the state of glycolipid metabolism and oxidative stress in the liver are inconsistent with that in the small intestine. Specifically, we found that cold temperature exposure increased glucose transport in the liver, which fully validates the idea that hormones can act on the liver to regulate glucose output. Additionally, dietary fat supplementation inhibited glucose transport and glycolysis, but increased gluconeogenesis, bile acid cycling, and lipid metabolism. Sustained activation of AMPK, which an energy receptor and regulator, leads to oxidative stress and apoptosis in the liver; dietary fat supplementation alleviates energy stress by reducing AMPK phosphorylation. CONCLUSIONS: Cold stress reduced the growth performance and aggravated glycolipid metabolism disorders and oxidative stress damage in pigs. Dietary fat supplementation improved growth performance and alleviated cold temperature-induced energy stress through AMPK-mediated mitochondrial homeostasis. In this study, we highlight the importance of AMPK in dietary fat supplementation-mediated alleviation of host energy stress in response to environmental changes.

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.

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.

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.

Non-12α-Hydroxylated Bile Acids Improve Piglet Growth Performance by Improving Intestinal Flora, Promoting Intestinal Development and Bile Acid Synthesis.

As an emulsifier and bioactive substance, bile acids (BAs) participate in the absorption of nutrients and in various physiological processes. The objective of this experiment was to investigate the effects of non-12α-hydroxylated BAs (including hyocholic acid, hyodeoxycholic acid and chenodeoxycholic acid, from now on referred to as NBAs) on growth performance, BAs metabolism and the intestinal flora of piglets. The experiment included four groups, with eight piglets per group. The four groups of pigs were fed 0, 60, 120 and 180 mg/kg of NBAs, respectively. The results show that adding NBAs significantly increased the final weight (FW), average daily feed intake (ADFI), average daily gain (ADG), and digestibility of crude fat (EE) and organic matter (OM) in piglets (p < 0.05). Adding NBAs significantly increased the villus height (VH) of the jejunum and ileum (p < 0.05). In addition, NBAs supplementation increased the content of urea nitrogen (BUN) and creatinine (CREA) as well as the ratio of urea nitrogen to creatinine (BUN/CREA) in serum (p < 0.05). Adding NBAs can affect the genes related to BAs enterohepatic circulation. Specifically, adding NBAs significantly decreased the relative mRNA abundance of FXR in the liver (p < 0.05), significantly increased the relative mRNA abundance of CYP27A1 (p < 0.05), and significantly increased the relative mRNA abundance of NTCP (p < 0.05). Adding NBAs also significantly decreased the relative mRNA abundance of FXR in the ileum (p < 0.05). In the full-length 16S rDNA sequencing analysis, ten biomarkers were found from the gate to the species level. NBAs mainly enriched Lactobacillus_Johnsonii and decreased the abundance of Streptococcus_alactolyticus. Short-chain fatty acids (SCFAs) content in the colon was significantly increased (p < 0.05). These results indicate that NBAs supplementation can improve the growth performance of piglets, promote the development of the bile acid replacement pathway and improve intestinal flora.

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.

Characteristics of glucose and lipid metabolism and the interaction between gut microbiota and colonic mucosal immunity in pigs during cold exposure.

BACKGROUND: Cold regions have long autumn and winter seasons and low ambient temperatures. When pigs are unable to adjust to the cold, oxidative damage and inflammation may develop. However, the differences between cold and non-cold adaptation regarding glucose and lipid metabolism, gut microbiota and colonic mucosal immunological features in pigs are unknown. This study revealed the glucose and lipid metabolic responses and the dual role of gut microbiota in pigs during cold and non-cold adaptation. Moreover, the regulatory effects of dietary glucose supplements on glucose and lipid metabolism and the colonic mucosal barrier were evaluated in cold-exposed pigs. RESULTS: Cold and non-cold-adapted models were established by Min and Yorkshire pigs. Our results exhibited that cold exposure induced glucose overconsumption in non-cold-adapted pig models (Yorkshire pigs), decreasing plasma glucose concentrations. In this case, cold exposure enhanced the ATGL and CPT-1α expression to promote liver lipolysis and fatty acid oxidation. Meanwhile, the two probiotics (Collinsella and Bifidobacterium) depletion and the enrichment of two pathogens (Sutterella and Escherichia-Shigella) in colonic microbiota are not conducive to colonic mucosal immunity. However, glucagon-mediated hepatic glycogenolysis in cold-adapted pig models (Min pigs) maintained the stability of glucose homeostasis during cold exposure. It contributed to the gut microbiota (including the enrichment of the Rikenellaceae RC9 gut group, [Eubacterium] coprostanoligenes group and WCHB1-41) that favored cold-adapted metabolism. CONCLUSIONS: The results of both models indicate that the gut microbiota during cold adaptation contributes to the protection of the colonic mucosa. During non-cold adaptation, cold-induced glucose overconsumption promotes thermogenesis through lipolysis, but interferes with the gut microbiome and colonic mucosal immunity. Furthermore, glucagon-mediated hepatic glycogenolysis contributes to glucose homeostasis during cold exposure.

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.

Resveratrol alleviates oxidative stress induced by oxidized soybean oil and improves gut function via changing gut microbiota in weaned piglets.

BACKGROUND: Oxidized soybean oil (OSO) has been shown to impair growth and exacerbate inflammation, leading to intestinal barrier injury in animals. Recent evidence suggests important roles for resveratrol (RES) in the promoting growth performance, antioxidant capacity, anti-inflammatory, and regulate intestinal barriers in animals. Therefore, The objectives of this study are to investigate the effects of dietary RES (purity 98%) supplementation on the growth performance, antioxidant capacity, inflammatory state, and intestinal function of weaned piglets challenged with OSO. METHODS: A total of 28 castrated weaned male piglets with a similar body weight of 10.19 ± 0.10 kg were randomly assigned to 4 dietary treatments for 28-d feeding trial with 7 replications per treatment and 1 piglet per replicate. Treatments were arranged as a 2 × 2 factorial with oil type [3% fresh soybean oil (FSO) vs. 3% OSO] and dietary RES (0 vs. 300 mg/kg). RESULTS: The results showed that relative to the FSO group, OSO stress tended to decrease the average daily feed intake (ADFI), and decreased the activity levels of lipase, villus/crypt ratio (VCR), the mRNA expression of FABP1, SOD2, IL-10 and ZO-1 in the jejunum, and SOD2, GPX1, occludin and ZO-1 in the colon, the levels of acetic acid in the colonic digesta, whereas up-regulated the mRNA expression of IL-1ß and TNF-α in the jejunum (P < 0.05). Moreover, dietary supplementation with RES increased ether extract (EE), the activity levels of sucrase, lipase, α-amylase, villus height (VH) and VCR, the mRNA expression of FABP1, SOD2, IL-10 and occludin in the jejunum, and FABP1, PPAR-γ, GPX1, occludin and ZO-1 in the colon, and the abundance of Firmicutes, acetic and propionic acid, but decreased the levels of D-lactic acid in the plasma, the abundance of Bacteroidetes in the colonic digesta of weaned piglets compared to the non-RES group (P < 0.05). Meanwhile, in the interaction effect analysis, relative to the OSO group, dietary RES supplementation in the diets supplemented with OSO increased the activity levels of trypsin, VH in the jejunum, the abundance of Actinobacteria, the levels of butyric acid of weaned piglets, but failed to influence the activity levels of trypsin and VH, Actinobacteria abundance, the levels of butyric acid when diets were supplemented with FSO (interaction, P < 0.05). Relative to the OSO group, dietary RES supplementation in the diets supplemented with OSO decreased the activity levels of DAO in the plasma of weaned piglets but failed to influence the activity levels of DAO when diets were supplemented with FSO (interaction, P < 0.05). Relative to the FSO group, dietary RES supplementation in the diets supplemented with FSO decreased the level of propionic acid, whereas RES supplementation failed to influence the level of propionic acid when the diet was supplemented with OSO (interaction, P < 0.01). CONCLUSIONS: Inclusion of OSO intensified inflammatory states and impaired the intestinal health characteristics of weaned piglets. Dietary RES supplementation improved the antioxidant capacity, anti-inflammatory activity, and intestinal morphology. Further studies showed that the protective effects of RES on gut health could be linked to the decreased abundance of Prevotella_1, Clostridium_sensu_stricto_6, and Prevotellaceae_UCG003 and increased levels of acetic and propionic acid.

Low-fat ice cream model system: impact of incorporation of alcalase hydrolyzed zein.

Research on fat substitutes with low calories and good flavor is important to reduce the fat content in food. In this paper, the selection of fat substitutes and the preparation of low-fat ice cream were carried out through looking at the emulsion properties of the enzymatic hydrolysis of zein. The results showed that the emulsifying activity of zein after enzymatic hydrolysis for 10 min was 66.76 m2 g-1, and the emulsifying stability was 78.51 min, showing the best emulsifying properties. Enzymatic hydrolysis of zein can effectively reduce the degree of lipid oxidation. The protein digestibility in intestinal juice was also significantly improved, and the release rate of free fatty acids in the emulsion reached more than 80%. The viscosity, shear stress, elastic modulus, electronic nose and electronic tongue of ice cream with 10% oil substitute were close to those of full-fat ice cream. It is expected to provide a basis for the development of functional foods.

Glucose supplementation improves intestinal amino acid transport and muscle amino acid pool in pigs during chronic cold exposure.

Mammals in northern regions chronically suffer from low temperatures during autumn-winter seasons. The aim of this study was to investigate the response of intestinal amino acid transport and the amino acid pool in muscle to chronic cold exposure via Min pig models (cold adaptation) and Yorkshire pig models (non-cold adaptation). Furthermore, this study explored the beneficial effects of glucose supplementation on small intestinal amino acid transport and amino acid pool in muscle of cold-exposed Yorkshire pigs. Min pigs (Exp. 1) and Yorkshire pigs (Exp. 2) were divided into a control group (17 °C, n = 6) and chronic cold exposure group (7 °C, n = 6), respectively. Twelve Yorkshire pigs (Exp. 3) were divided into a cold control group and cold glucose supplementation group (8 °C). The results showed that chronic cold exposure inhibited peptide transporter protein 1 (PepT1) and excitatory amino acid transporter 3 (EAAT3) expression in ileal mucosa and cationic amino acid transporter-1 (CAT-1) in the jejunal mucosa of Yorkshire pigs (P < 0.05). In contrast, CAT-1, PepT1 and EAAT3 expression was enhanced in the duodenal mucosa of Min pigs (P < 0.05). Branched amino acids (BCAA) in the muscle of Yorkshire pigs were consumed by chronic cold exposure, accompanied by increased muscle RING-finger protein-1 (MuRF1) and muscle atrophy F-box (atrogin-1) expression (P < 0.05). More importantly, reduced concentrations of dystrophin were detected in the muscle of Yorkshire pigs (P < 0.05). However, glycine concentration in the muscle of Min pigs was raised (P < 0.05). In the absence of interaction between chronic cold exposure and glucose supplementation, glucose supplementation improved CAT-1 expression in the jejunal mucosa and PepT1 expression in the ileal mucosa of cold-exposed Yorkshire pigs (P < 0.05). It also improved BCAA and inhibited MuRF1 and atrogin-1 expression in muscle (P < 0.05). Moreover, dystrophin concentration was improved by glucose supplementation (P < 0.05). In summary, chronic cold exposure inhibits amino acid absorption in the small intestine, depletes BCAA and promotes protein degradation in muscle. Glucose supplementation ameliorates the negative effects of chronic cold exposure on amino acid transport and the amino acid pool in muscle.

Dietary full-fat rice bran prevents the risk of heart ferroptosis and imbalance of energy metabolism induced by prolonged cold stimulation.

The threat to human health from cold stimulation is increasing due to the frequent occurrence of temperature extremes. It is a challenge for people to resist the negative effects of prolonged cold stimulation on the heart. In this study, we created prolonged cold stimulation pig models to investigate the cardiac energy metabolism and injury during prolonged cold stimulation, and the molecular mechanisms by which dietary supplementation with full-fat rice bran reduces cardiac injury. The results showed that lesions in the morphological structure of the heart were detected under prolonged cold stimulation. At the same time, dystrophin was downregulated under the effect of prolonged cold stimulation. Cardiac fatty acid transport and utilization were promoted, and oxidative stress was increased under prolonged cold stimulation. It also increased MDA content and decreased T-AOC level in the heart, while promoting the mRNA expression of Nrf2 and NQO1, as well as the protein content of Nrf2 and HO-1. Prolonged cold stimulation induced mitochondrial lesions, mitochondrial fusion, and mitophagy in the heart. Prolonged cold stimulation promoted the mRNA expression of PTGS2, TLR4, MyD88, NLRP3, and IL-1ß; and protein expression of PTGS2, NLRP3, and mature-IL-1ß. GCH1 and FtH inhibited by prolonged cold stimulation caused the activation of heart ferroptosis. In addition, dietary supplementation with full-fat rice bran improved oxidative stress in the heart and inhibited mitophagy, ferroptosis, and pyroptosis. In conclusion, prolonged cold stimulation heightens the risk of cardiac ferroptosis and imbalance of energy metabolism, whereas dietary supplementation with full-fat rice bran mitigates the adverse effects of prolonged cold stimulation on the heart.

The early faecal microbiota transfer alters bile acid circulation and amino acid transport of the small intestine in piglets.

The purpose of this study was to investigate the effects of faecal microbiota transfer (FMT) with lactation Min sows as faecal donor on blood immunity, small intestine amino acid transport capacity, bile acid circulation, and colon microbiota of recipient piglets. From Days 1 to 10, the recipient group (R group) was orally inoculated with a faecal suspension. The control group (Con group) was orally inoculated with sterile physiological saline. On Day 21, the results showed that the immunoglobulin A (IgA) concentration in plasma of the R group was increased (p < 0.05). The expression of 4F2hc in the jejunal mucosa and ileum mucosa of the R group was ameliorated (p < 0.05). The relative abundance of Synergistetes in the colon of the R group was increased, Proteobacteria was diminished by FMT (p < 0.05). On Day 40, the concentrations of IgA, IgG, and interleukin-2 detected in the plasma of the R group were increased (p < 0.05). FXR and fibroblast growth factor 19 gene expression was upregulated in ileum mucosa, CYP7A1 and Na+ taurocholate cotransporter polypeptide gene expression were downregulated in the liver and organic solute transporters α/ß was downregulated in colonic mucosa (p < 0.05). The relative abundance of Proteobacteria and Spirochaetes in the colon of the R group was decreased (p < 0.05). In conclusion, an early FMT with lactation Min sows as faecal donors can alter the small intestine amino acid transport capacity, bile acid circulation, and colonic microbiota of recipient piglets during lactation and after weaning.

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.

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.

Perinatal exposure to high concentration glyphosate-based herbicides induces intestinal apoptosis by activating endoplasmic reticulum stress in offspring.

Glyphosate-based herbicides (GBHs), the most widely used pesticide worldwide, have been reported to impair organ function in humans and animals. However, research on the effect of maternal GBHs exposure on the intestinal health of offspring has received little attention. Based on the glyphosate limits defined by Codex Alimentarius Commission and European Food Safety Authority, this study established pregnant sow exposure models to investigate the influence of low (L-GBHs, 20 mg/kg) and high concentration GBHs (H-GBHs, 100 mg/kg) on the intestinal health of offspring and proposed the protective mechanism mediated by betaine. The results showed that the intestinal morphology and barrier function of suckling piglets were damaged in the H-GBHs group. H-GBHs increased the activity of glutathione peroxidase (GPX) and levels of methane dicarboxylic aldehyde (MDA), hydrogen peroxide (H2O2) and inflammatory factors (tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), interleukin-6 (IL-6), interleukin-10 (IL-10)) in suckling piglets and activated Nrf2-mediated antioxidant signaling pathway. Subsequently, we found that exposure to H-GBHs triggered endoplasmic reticulum stress (ERS) and further induced apoptosis by upregulating the expression of Bcl-2-associated X protein (Bax), Caspase3, Caspase9 and Caspase12. Moreover, H-GBHs exposure perturbed mitochondrial membrane fusion and electron transport in mitochondrial respiratory chains by increasing the mRNA expression of mitofusin-2 (MFN2) and succinate dehydrogenase subunit A (SDHA), causing mitochondrial dysfunction. Dietary supplementation with betaine provided modest protection against GBHs-induced intestinal damage in suckling piglets. These findings reveal the mechanism of GBHs-induced intestinal damage in offspring, improving our understanding of the risk of GBHs exposure in pregnant women and suggesting the potential protective effects of betaine against GBHs poisoning.

Supplementation with Complex Dietary Fiber during Late Pregnancy and Lactation Can Improve Progeny Growth Performance by Regulating Maternal Antioxidant Status and Milk Quality.

This study investigated the nutritional benefits of complex dietary fiber (beta-glucan and fructo-oligosaccharides, CDF) supplementation in sows and piglets during late pregnancy and lactation. Twenty-four sows were randomly divided into two groups: the control group was fed a basal diet (n = 12), and the experimental group was fed a CDF diet (0.25% CDF replaced the same proportion of corn in the basal diet, n = 12). Dietary treatment was given from day 107 of pregnancy to day 25 of lactation. The results of this experiment showed that CDF increased the average daily feed intake (ADFI) of sows during lactation and the weaning body weight (BW) and average daily gain of piglets. Dietary CDF supplementation improved the antioxidant capacity and immune level of sows and decreased the serum zonulin level. Dietary supplementation with CDF increased the levels of antioxidant activity, immunoglobulin, and anti-inflammatory factor interleukin-10 (IL-10) in milk. Meanwhile, piglets in the CDF group had increased serum antioxidant activity, immunoglobulin, and growth-related hormone levels; decreased malondialdehyde (MDA), interleukin-6 (IL-6), and D-lactic acid (D-LA) levels; and increased fecal short-chain fatty acid content. In addition, the CDF group increased the diversity of microorganisms in sow feces. In conclusion, the supplementation of a diet with CDF in late pregnancy and lactation can alleviate the oxidative stress of sows, improve milk quality, and have significant positive effects on the antioxidant capacity and growth performance of piglets.

Perinatal exposure to glyphosate-based herbicides impairs progeny health and placental angiogenesis by disturbing mitochondrial function.

Glyphosate-based herbicides (GBHs) are the most widely used pesticide worldwide and can provoke placental injury. However, whether and how GBHs damage angiogenesis in the placenta is not yet known. This work evaluated the safety of glyphosate on pregnant sows based on the limit level by governments and investigated the effects and mechanism of Low-GBHs (20 mg/kg) and High-GBHs (100 mg/kg) exposure on placental angiogenesis. Results showed that gestational exposure to GBHs decreased placental vessel density and cell multiplication by interfering with the expression of VEGFA, PLGF, VEGFr2 and Hand2 (indicators of angiogenesis), which may be in relation to oxidative stress-induced disorders of mitochondrial fission and fusion as well as the impaired function of the mitochondrial respiratory chain. Additionally, GBHs destroyed barrier function and nutrient transport in the placenta, and was accompanied by jejunum oxidative stress in newborn piglets. However, GBHs exposure had no significant differences on sow reproductive performance. As a natural antioxidant, betaine treatment protected placenta and newborn piglets against GBHs-induced damage. In conclusion, GBHs impaired placental angiogenesis and function and further damaged the health of postnatal progeny, these effects may be linked to mitochondrial dysfunction. Betaine treatment following glyphosate exposure provided modest relief.

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.