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The impact of heat stress (HS) on production is intricately linked with feed intake. We investigated the effects of HS on intestines and diencephalic genes in Pekin ducks. One hundred and sixty adult ducks were allocated to two treatment rooms. The control room was maintained at 22°C and the HS room at 35°C for the first 10 h of the day then reduced to 29.5°C. After 3 weeks, 10 hens and 5 drakes were euthanized from each room and jejunum and ileum collected for histology. Brains were collected for gene expression analysis using qRT-PCR. Intestinal morphology data were analyzed with two-way ANOVA and diencephalic gene data were analyzed with Kruskal-Wallis test. There was an increase in villi width in the ileum (p = .0136) and jejunum (p = .0019) of HS hens compared to controls. HS drakes showed a higher crypt depth (CD) in the jejunum (p = .0198) compared to controls. There was an increase in crypt goblet cells (GC) count in the ileum (p = .0169) of HS drakes compared to HS hens. There was higher villi GC count (p = .07) in the jejunum of HS drakes compared to controls. There was an increase in the crypt GC density (p = .0054) in the ileum, not jejunum, of HS drakes compared to HS hens. Further, there were no differences in the proopiomelanocortin gene expression in either sex but there was an increase in the expression of neuropeptide Y (NPY) gene in HS hens (p = .031) only and a decrease in the corticotropin releasing hormone gene in the HS drakes (p = .037) compared to controls. These data show that there are sex differences in the effect of HS on gut morphology while the upregulation in NPY gene may suggest a role in mediating response to chronic HS., (© 2024 The Author(s). Journal of Neuroendocrinology published by John Wiley & Sons Ltd on behalf of British Society for Neuroendocrinology.)

Recent studies have highlighted the importance of maternal nutrition during gestation and lactation in modulating the gastrointestinal development and health of offspring. Therefore, the objective of this study was to determine the effects of live yeast (LY) supplementation to sows during late gestation and throughout lactation on markers of gut health of piglets prior to weaning and immediately postweaning. On day 77 of gestation, forty sows were allotted based on parity and expected farrowing dates to two dietary treatments: without (CON) or with (LY) supplementation at 0.05% and 0.1% of diet during gestation and lactation, respectively. On postnatal days (PND) 0, 10, 18, and postweaning days (PWD) 7 and 14, one piglet from each of 10 sows per treatment were selected for intestinal tissue collection (n = 10). Real-time PCR and western blotting analyses were used to determine the mucosal expression of immune and antioxidant-regulatory genes and tight junction markers of gut health in the duodenum, jejunum, and ileum. Inflammatory and tight junction markers on PND 0 were not affected by maternal dietary treatment. On PND 18, maternal LY supplementation increased (P < 0.05) mRNA expression of interleukin (IL)-6 and tended (P = 0.08) to increase expression of IL-10 in the ileal muocsa. Maternal LY supplementation also increased (P < 0.05) expression of IL-1β in the ileal mucosa on PWD 14. Likewise, expression of superoxide dismutase (SOD) 1 was increased (P < 0.05) by LY on PND 10, 18, and PWD 14, with a tendency (P = 0.09) for a greater mRNA abundance of catalase on PND 14 in the ileal mucosa. Compared to CON piglets, LY piglets had a higher (P < 0.05) protein abundance of E-cadherin in the jejunal mucosa on PND 0, PWD 7, and PWD 14. Levels of occludin and claudin-4 were also higher (P < 0.05) in the jejunum of LY piglets on PWD 14. No differences were found in jejunal histomorphological measurements between treatments. In conclusion, this study shows that maternal LY supplementation affects key markers of gut health and development in the offspring that may impact the future growth potential and health of newborn piglets., (© The Author(s) 2024. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

The presence of deoxynivalenol (DON), one of the most frequently occurring mycotoxin, in food and feed has been considered a risk factor to both human and animal health. Molecular mechanisms that regulate DON effects in tissues are still poorly understood. However, recent evidence suggests that nuclear factor erythroid 2-like 2 (Nrf2) may be a major target during mycotoxin-induced intestinal barrier dysfunction. Although quercetin, a plant-derived flavonoid, is known to induce the activation of Nrf2 signaling pathway, its potential to mitigate effects of DON and the implication of Nrf2 in its physiological effects is poorly understood. Therefore, this study was conducted to investigate the protective effects of quercetin in alleviating the DON-induced barrier loss and intestinal injuries in IPEC-J2 cells and weaned piglets and determine the potential role of Nrf2. Quercetin treatment dose-dependently increased mRNA expression of Nrf2 target gene, NQO-1 , and concomitantly increased the expression of claudin-4 at both mRNA and protein levels. Quercetin supplementation also reversed the reduction of claudin-4 caused by DON exposure in vivo and in vitro . The decreased membrane presence of claudin-4 and ZO-1 induced by DON was also blocked by quercetin. Furthermore, quercetin attenuated the endocytosis and degradation of claudin-4 caused by DON exposure. The effects of quercetin also included the restoration of transepithelial electrical resistance (TEER) and reduction of FITC-dextran permeability that have been perturbed by DON. However, the protective effects of quercetin against DON exposure were abolished by a specific Nrf2 inhibitor (brusatol), confirming the importance of Nrf2 in the regulation of TJP expression and barrier function by quercetin. In vivo study in weaned pigs showed that DON exposure impaired villus-crypt morphology as indicated by diffuse apical villus necrosis, villus atrophy and fusion. Notably, intestinal injuries caused by DON administration were partly mitigated by quercetin supplementation. Collectively, this study shows that quercetin could be used to prevent the DON-induced gut barrier dysfunction in humans and animals and the protective effects of quercetin against DON-induced intestinal barrier disruption is partly through Nrf2-dependent signaling pathway., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors.)

Background/objectives: Curcumin is a well-known phytochemical with anti-inflammatory effects. Heat shock protein (HSP) 70, an intracellular chaperone, inhibits proinflammatory signaling activation. Although curcumin has been shown to induce HSP70 expression in various cell types, whether HSP70 mediates the anti-inflammatory effects of curcumin in mature adipocytes remains unclear., Materials/methods: To assess the role of HSP70 in regulating the anti-inflammatory response to curcumin in adipocytes, fully differentiated 3T3-L1 adipocytes were treated with curcumin, lipopolysaccharide (LPS), and/or the HSP70 inhibitor pifithrin-μ (PFT-μ). The expression levels of HSP70 and proinflammatory cytokines were then measured., Results: Curcumin upregulated HSP70 expression at both protein and mRNA levels and attenuated LPS-induced Il6 , Ptx3 , and Ccl2 mRNA upregulation. PFT-μ tended to exacerbate the LPS-induced upregulation of Il6 , Ptx3 , Ccl2 , and Tnfa mRNA expression. However, on curcumin pretreatment, the tendency of PFT-μ to upregulate LPS-induced proinflammatory cytokine expression decreased or disappeared., Conclusion: These results indicate that HSP70 is involved in the regulation of inflammatory responses but may not be crucial for the anti-inflammatory effects of curcumin in 3T3-L1 adipocytes., Competing Interests: Conflict of Interest: The authors declare no potential conflicts of interests., (©2023 The Korean Nutrition Society and the Korean Society of Community Nutrition.)

The role of peroxisome proliferator activated receptor gamma (PPARγ) in the regulation of adipocyte differentiation has been well characterized. Besides adipose tissue, PPARγ is also highly expressed in the intestine. However, the functional role of PPARγ in the regulation of intestinal function still remains poorly understood. In the present study, we sought to understand the role of PPARγ activation on regulation of intestinal barrier function in intestinal porcine epithelial cells (IPEC-J2) and weaned piglets exposed to the mycotoxin, deoxynivalenol (DON). PPARγ activation by rosiglitazone and troglitazone, two pharmacological PPARγ ligands, increased the protein expression of tight junction proteins (TJP), claudin-3 and 4. PPARγ inhibition increased endocytosis of claudin-4 which was reversed by its activation with troglitazone. DON exposure decreased the protein expression of TJP, and also significantly suppressed PPARγ transcriptional activity. Interestingly, PPARγ activation reversed the reduction of claudin-3 and 4 caused by DON in vitro and in vivo. PPARγ activation also partially restored the transepithelial electrical resistance (TEER) and reduced the permeability of fluorescein isothiocyanate-dextran (FITC-dextran) that have been negatively impacted by DON. These effects were lost in the presence of a specific PPARγ antagonist or in PPARγ knockout cells, confirming the importance of PPARγ in the regulation of intestinal barrier function and integrity. Likewise, in weaned pigs exposed to DON, the PPARγ agonist pioglitazone mitigated the impaired villus-crypt morphology caused by DON. Therefore, pharmacological and natural bioactive compounds with PPARγ stimulatory activities could be effective in preventing DON-induced gut barrier dysfunction., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Fibre plays an important role in diluting dietary energy density. Fibre is also implicated in the regulation of appetite, perhaps through direct effects in the brain. However, there is little information on this effect in pigs. Therefore, this study was conducted to investigate the effect of fibre type in regulating the expression of genes involved in appetite control, inflammation and antioxidant defence in the hypothalamus of weaned piglets. A total of 64 Duroc × Landrace × Yorkshire barrows at 37 days old were blocked by body weight and allotted to two dietary treatments, supplementation with either 0.25% cellulose (Solka-Floc) or inulin (INU) for 28 days, after which animals were killed for analysis. Pigs fed INU had a tendency (p = 0.06) for reduced feed intake in the first week, although this effect disappeared in subsequent weeks. Pigs supplemented with INU had lower expression of dopamine (dopamine receptor D2), serotonin (5-hydroxytryptamine receptor 1B), free fatty acid (GPR43) and neuropeptide Y receptor Y2 receptors in the hypothalamus (p < 0.05). Expression of the tryptophan hydroxylase 2 gene in the hypothalamus also tended (p = 0.09) to be lower for pigs fed INU. The abundance of antioxidant defence genes, superoxide dismutase (SOD1) and catalase, were greater (p < 0.05) but that of a proinflammatory gene, interleukin 1β, was lower (p < 0.05) in the hypothalamus of pigs fed INU. Therefore, consumption of INU causes downregulation of inflammation in the hypothalamus and regulation of the abundance of serotonin or dopamine receptors, and may also increase antioxidant defence through upregulation of SOD and catalase in weaned piglets., (© 2022 Wiley-VCH GmbH.)

The objective of this trial was to investigate the effect of enzymatically treated yeast (ETY) on the growth performance, nutrient digestibility, immune response, and gut health of weanling pigs. A total of 192 weanling pigs (6.0 ± 1.04 kg) were allocated to 4 corn and soybean-based diets with increasing concentrations of ETY (0, 1, 2, or 4 g/kg) for a 43-d trial. There were 8 replicate pens (4 replicate pens per sex) and 6 pigs per replicate. The experiment was set up as a randomized complete block design with body weight used as a blocking factor. Pigs had ad libitum access to water and diets for the duration of the study. There was no effect of ETY supplementation on the growth performance indices of weanling pigs. At day 14, there was a quadratic decrease (P < 0.05) in the apparent total tract digestibility (ATTD) of acid detergent fiber (ADF). At day 28, there was a linear increase (P < 0.05) in the ATTD of neutral detergent fiber and a quadratic decrease (P < 0.05) in the ATTD of ADF. On day 14, there was a linear increase (P < 0.05) in serum catalase activity with ETY supplementation. There was a linear increase (P < 0.01) in the gene expression of glutathione peroxidase-4 in the ileal mucosa of pigs. Increasing dietary ETY supplementation linearly decreased (P < 0.05) the gene expression of ileal peptide transporter 1. There was a tendency for a quadratic effect (P = 0.07) in the ileal villus height to crypt depth ratio with ETY supplementation. In addition, there was a tendency for a linear increase (P = 0.06) in ileal digesta butyrate with ETY supplementation. In conclusion, the current study demonstrated that dietary ETY supplementation could partly ameliorate the deleterious effects of post-weaning stress by enhancing the antioxidative status of weanling pigs. However, prolonged supplementation of ETY may be needed to see its effect on growth performance., (© The Author(s) 2022. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Myo-inositol is a breakdown product of phytate produced in the gut through the action of phytase. Although the effect of phytase-released phosphorus (P) on growth performance of animals has been well characterized, there is still little understanding of the effect of myo-inositol. The first objective of this study was to determine the effects of added myo-inositol to a phytate-rich low-protein diet on growth performance and apparent total tract digestibility (ATTD) in growing piglets. The second objective was to determine whether myo-inositol could directly affect intestinal epithelial cell proliferation and function for which we used intestinal porcine epithelial cells (IPEC-J2). A total of 128 weanling piglets were allotted to four dietary treatments consisting of eight replicates per treatment and four piglets per replicate in a randomized complete block design for 4 wk. The four experimental diets comprised the positive control [PC; 20% crude protein (CP)], negative control (NC; 17% CP), negative control plus 2.0g/kg myo-inositol (NC+INO; 17% CP), and negative control plus 3000FTU/kg phytase (NC+PHY; 17% CP). Average daily feed intake (ADFI), average daily gain (ADG), and gain-feed ratio (G: F) were recorded. Phytase supplementation in the protein-deficient NC diet increased the G:F ratio (P < 0.05) without myo-inositol effects on growth performance. Phosphorus digestibility in the phytase-supplemented group increased compared to the PC, NC, and NC+INO groups, whereas plasma myo-inositol concentration was significantly higher (P < 0.05) in the NC+INO group. Due to the lack of myo-inositol effect on growth performance, an additional in vitro study was conducted to determine the direct effect of myo-inositol on the intestinal epithelium that might not be reflected in growth performance. Myo-inositol increased the mRNA abundance of selected nutrient transporters in a concentration-dependent manner (P < 0.05). Myo-inositol also enhanced barrier integrity in the IPEC-J2 monolayer by increasing the transepithelial electrical resistance (TEER) with reduced paracellular permeability of FITC-dextran (P < 0.05). In conclusion, despite the lack of myo-inositol effect on animal performance, the in vitro data indicate that myo-inositol may directly regulate gut barrier integrity. Addition of myo-inositol to pig diets at levels that enhance intestinal epithelial cell function may result in effects on growth performance and gut health of pigs., (© The Author(s) 2022. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Peroxisome proliferator activated receptor gamma (PPARγ) activation has been shown to protect against intestinal injury induced by different stimuli. PPARγ is known to regulate tight junction proteins (TJP) in epithelial cells. Both eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are natural PPARγ agonists, but the implication of PPARγ in their physiological effects on the gut is poorly understood. Therefore, this study was conducted to investigate the mechanism of EPA and DHA effects on intestinal epithelial cell barrier function in IPEC-J2 cells exposed to deoxynivalenol (DON), a known food mycotoxin that is toxic to both humans and animals. Exposure of cells to EPA and DHA significantly increased mRNA expression of a PPARγ target gene, AP2, and concomitantly increased the protein expression of claudin-4. Treatment with EPA and DHA also reversed the endocytosis and degradation of claudin-4 caused by DON exposure. EPA and DHA also restored the membrane presence of claudin-4 and ZO-1 that was disrupted by DON. However, the protective effects of EPA and DHA against DON exposure was abolished by a specific PPARγ antagonist (T0070907), confirming the importance of PPARγ in regulating TJP expression by the fatty acids. Effect of PPARγ activation by EPA and DHA also included the restoration of transepithelial electrical resistance (TEER) and reduction of fluorescein isothiocyanate-labeled dextran (FITC-dextran) permeability that have been perturbed by DON. However, the effectiveness of EPA and DHA in opposing DON-induced decrease in TEER and the increase in FITC-dextran permeability was not affected by PPARγ inhibition, potentially suggesting the involvement of other PPARγ-independent mechanisms in the observed benefits from EPA and DHA. Collectively, this study shows that the protective effects of EPA and DHA against DON-induced intestinal barrier disruption are through both PPARγ-dependent and-independent pathways. Therefore, EPA and DHA containing ingredients could be used to prevent the DON-induced gut barrier dysfunction in humans and animals., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Two experiments were designed to elucidate gut and hypothalamic molecular regulation of appetite by dietary phosphorus (P) concentration in broiler chickens. Birds (192 Cobb-500 broiler chickens) were randomly assigned to 3 experimental diets in experiment 1 (Exp. 1) and 24 broiler chickens were randomly assigned to 3 treatment groups in Exp. 2. Each diet comprised 8 replicate cages, with either 8 birds (Exp. 1) or 1 bird (Exp. 2) per replicate cage. In Exp. 1, diets contained 1.2 (P-deficient), 2.8 (P-marginal) or 4.4 (P-adequate) g/kg non-phytate P (nPP). In Exp. 2, birds fed the P-adequate diet were pair-fed (PF) to the feed consumption levels of birds fed the P-deficient diet. Feed intake and BW gain (P < 0.001) decreased in birds fed the P-deficient diet in Exp. 1. Birds fed the P-deficient diet had similar feed intake and BW gain with PF group fed the P-adequate diet (Exp. 2) but was significantly lower (P < 0.001) than birds fed the P-adequate diets. Sodium-phosphate cotransporter (NaPi-IIb) mRNA was upregulated (P < 0.05) in both experiments. Conversely, cholecystokinin (CCK) mRNA was downregulated (P < 0.01) in birds fed P-deficient diets. Anorexia-related hypothalamic cholecystokinin receptor (CCKAR) and melanocortin receptors (MC3R and MC4R) were upregulated (P < 0.05) in birds fed P-deficient diets, in both experiments. The current data show that dietary P deficiency decreases feed intake in broiler chickens by altering the expression of anorexigenic genes in the gut and hypothalamus of broiler chickens., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

The primary objective of the current study was to evaluate the impact of trypsin inhibitor (TI) and exogenous protease supplementation on endogenous loss of amino acids (AA) in broiler chickens. A total of 384 Cobb-500 broiler chicks were allocated to 4 nitrogen-free diets, each with 8 replicate cages and 12 birds per replicate. The diets were arranged as a 2 × 2 factorial with factors being dietary TI (0 or 8,000 TIU/g) and exogenous protease (0 or 15,000 PROT/kg). Desired dietary TI concentration was achieved by addition of commercially available, purified soybean TI. There was no effect of TI or exogenous protease or their interaction on growth performance of birds. However, the endogenous loss of nitrogen (N) and all AA increased (P < 0.05) due to dietary TI concentration except for Cys. The increase in endogenous AA due to TI ranged from 17% for Thr to 52.2% for Trp. Exogenous protease had no effect on endogenous loss of N and all AA. There was no effect of TI or exogenous protease or their interaction on the AID of P, however AID of Ca, Fe, Mg, Mn, and Cu was reduced (P < 0.05) due to dietary TI. The AID of Cu (P < 0.01) and K (P < 0.05) improved with exogenous protease supplementation. Significant interactions (P < 0.05) between exogenous protease and TI existed for Zn, Mg, Cu, and Na. The concentration (g/kg DM intake) of crude mucin and sialic acid increased (P < 0.05) with increased dietary TI. Decreased trypsin (P < 0.001) and increased chymotrypsin (P < 0.001) activity in the pancreas were observed as a result of exogenous protease supplementation. In conclusion, the current study showed that TI increases the endogenous loss of AA and reduced the digestibility of minerals in broiler chickens. Furthermore, exogenous protease did not affect endogenous AA flow, irrespective of added purified dietary TI., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

The efficacy of exogenous carbohydrases in pig diets has been suggested to depend on enzyme activity and dietary fiber composition, but recent evidence suggests other factors such as ambient temperature might be important as well. Therefore, we investigated the effect of heat stress (HS) on the efficacy of a multienzyme carbohydrase blend in growing pigs. Ninety-six (barrows: gilts; 1:1) growing pigs with initial body weight (BW) of 20.15 ± 0.18 kg were randomly assigned to six treatments, with eight replicates of two pigs per pen in a 3 × 2 factorial arrangement: three levels of carbohydrase (0, 1X, or 2X) at two environmental temperatures (20 °C or cyclical 28 °C nighttime and 35 °C day time). The 1X dose (50 g/tonne) provided 1,250 viscosimetry unit (visco-units) endo-β-1,4-xylanase, 4,600 units α-l-arabinofuranosidase and 860 visco-units endo-1,3(4)-β-glucanase per kilogram of feed. Pigs were fed ad libitum for 28 d and 1 pig per pen was sacrificed on day 28. There was no enzyme × temperature interaction on any response criteria; thus, only main effects are reported. Enzyme treatment quadratically increased (P < 0.05) BW on day 28, average daily gain (ADG) (P < 0.05), and average daily feed intake (ADFI) (P < 0.05) with the 1X level being highest. HS reduced the BW at day 14 (P < 0.01) and day 28 (P < 0.01), ADG (P < 0.01), and ADFI (P<0.001). There was a trend of increased feed efficiency (G:F) (P < 0.1) in the HS pigs. HS increased apparent jejunal digestibility of energy (P < 0.05) and apparent ileal digestibility of calcium (P < 0.01). At day 1, HS reduced serum glucose (P < 0.001) but increased nonesterified fatty acid (P < 0.01). In the jejunum, there was a trend of increased villi height by carbohydrases (P < 0.1), whereas HS reduced villi height (P < 0.05). HS increased the jejunal mRNA abundance of IL1β in the jejunum (P < 0.001). There was a trend for a reduction in ileal MUC2 (P < 0.1) and occludin (P < 0.1) by HS, and a trend for increased PEPT1 (P < 0.1). There was no effect of HS on alpha diversity and beta diversity of the fecal microbiome, but there was an increase in the abundance of pathogenic bacteria in the HS group. In conclusion, HS did not alter the efficacy of carbohydrases. This suggests that carbohydrases and HS modulate pig performance independently., (© The Author(s) 2021. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)