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The intestinal epithelial barrier, composed of epithelial cells, tight junction proteins and intestinal secretions, prevents passage of luminal substances and antigens through the paracellular space. Dysfunction of the intestinal barrier integrity induced by toxins and pathogens is associated with a variety of gastrointestinal disorders and diseases. Although butyrate is known to enhance intestinal health, its role in the protection of intestinal barrier function is poorly characterized. Therefore, we investigated the effect of butyrate on intestinal epithelial integrity and tight junction permeability in a model of LPS-induced inflammation in IPEC-J2 cells. Butyrate dose-dependently reduced LPS impairment of intestinal barrier integrity and tight junction permeability, measured by trans-epithelial electrical resistance (TEER) and paracellular uptake of fluorescein isothiocyanate-dextran (FITC-dextran). Additionally, butyrate increased both mRNA expression and protein abundance of claudins-3 and 4, and influenced intracellular ATP concentration in a dose-dependent manner. Furthermore, butyrate prevented the downregulation of Akt and 4E-BP1 phosphorylation by LPS, indicating that butyrate might enhance tight junction protein abundance through mechanisms that included activation of Akt/mTOR mediated protein synthesis. The regulation of AMPK activity and intracellular ATP level by butyrate indicates that butyrate might regulate energy status of the cell, perhaps by serving as a nutrient substrate for ATP synthesis, to support intestinal epithelial barrier tight junction protein abundance. Our findings suggest that butyrate might protect epithelial cells from LPS-induced impairment of barrier integrity through an increase in the synthesis of tight junction proteins, and perhaps regulation of energy homeostasis.

Short chain fatty acids (SCFA), products of microbial fermentation of dietary fiber, exert multiple metabolic effects in cells. Previously, we had demonstrated that soluble fiber influenced fat mass accumulation, gut microbial community structure and SCFA production in pigs. The current study was designed to identify effects of SCFA treatment during adipogenic differentiation of porcine stromovascular cells on lipid metabolism and adipokine expression. Differentiating cells were treated with varying concentrations of butyrate. Results show that butyrate treatment enhanced adipogenesis and lipid accumulation, perhaps through upregulation of glucose uptake and de novo lipogenesis and other mechanisms that include induction of SREBP-1c, C/EBPα/β, GLUT4, LPL, PPARγ, GPAT4, DGAT1 and DGAT2 expression. In addition, butyrate induced adiponectin expression, resulting in activation of downstream target genes, such as AMPK and AKT. Activation of AMPK by butyrate led to phosphorylation of ACC. Although increased ACO gene expression was seen with butyrate treatment, experiments with the peroxisomal fatty acid inhibitor, thioridazine, suggest that butyrate may have an inhibitory effect on peroxisomal fatty acid oxidation. Our studies also provide evidence that butyrate may inhibit lipolysis, perhaps in an FFAR3-dependent manner. Therefore, this study presents a novel paradigm for butyrate action in adipocytes and shows that adipocytes are capable of utilizing butyrate, leading to increased expression of adiponectin for enhanced glucose uptake and improved insulin sensitivity.

Calcium cycling induced by the SERCA2b–RyR2 pathway in beige fat cells allows for thermogenic activity independent of UCP1. Uncoupling protein 1 (UCP1) plays a central role in nonshivering thermogenesis in brown fat; however, its role in beige fat remains unclear. Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca 2+ cycling by sarco/endoplasmic reticulum Ca 2+ -ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2). Inhibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in pigs, a species that lacks a functional UCP1 protein. Conversely, enhanced Ca 2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b–RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes. In the absence of UCP1, beige fat dynamically expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss. Our study uncovers a noncanonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca 2+ cycling.

Obesity leads to changes in the gut microbial community which contribute to the metabolic dysregulation in obesity. Dietary fat and fiber affect the caloric density of foods. The impact of dietary fat content and fiber type on the microbial community in the hind gut is unknown. Effect of dietary fat level and fiber type on hindgut microbiota and volatile fatty acid (VFA) profiles was investigated. Expression of metabolic marker genes in the gut, adipose tissue and liver was determined. A 2 × 2 experiment was conducted in pigs fed at two dietary fat levels (5% or 17.5% swine grease) and two fiber types (4% inulin, fermentable fructo-oligosaccharide or 4% solka floc, non-fermentable cellulose). High fat diets (HFD) resulted in a higher (P<0.05) total body weight gain, feed efficiency and back fat accumulation than the low fat diet. Feeding of inulin, but not solka floc, attenuated (P<0.05) the HFD-induced higher body weight gain and fat mass accumulation. Inulin feeding tended to lead to higher total VFA production in the cecum and resulted in a higher (P<0.05) expression of acyl coA oxidase (ACO), a marker of peroxisomal β-oxidation. Inulin feeding also resulted in lower expression of sterol regulatory element binding protein 1c (SREBP-1c), a marker of lipid anabolism. Bacteria community structure characterized by DGGE analysis of PCR amplified 16S rRNA gene fragments showed that inulin feeding resulted in greater bacterial population richness than solka floc feeding. Cluster analysis of pairwise Dice similarity comparisons of the DGGE profiles showed grouping by fiber type but not the level of dietary fat. Canonical correspondence analysis (CCA) of PCR- DGGE profiles showed that inulin feeding negatively correlated with back fat thickness. This study suggests a strong interplay between dietary fat level and fiber type in determining susceptibility to obesity.

Background Black soldier fly larvae meal (BSFLM) stands out as a promising nutritional resource due to its rich bioactive substances and favorable protein profile. Nonetheless, its potential to mitigate coccidia infection in broilers remains uncertain. This study aimed to evaluate the impact of partially defatted BSFLM (pBSFLM) on growth performance, nutrient utilization, and intestinal health, focusing on morphology, immunology, and cecal fermentation in coccidia-infected broilers. Methods Over the initial 13 d, 480 newly-hatched Cobb 500 male birds were allocated to three diets with increasing pBSFLM concentrations (0, 60, or 120 g/kg). At d 13 post hatching, chicks within each dietary group were further allotted to non-challenge or challenge subsets, generating six treatments in a 3 × 2 factorial arrangement. Challenged birds were orally administered oocysts of E. maxima , E. acervulina , and E. tenella (25,000:125,000:25,000). Results During the infection phase (d 13 to 19), linear interactions between Eimeria and pBSFLM were observed in gain to feed ratio (G:F) ( P  < 0.05) and cecal interferon-γ (IFN-γ, P  < 0.05), with a tendency in cecal acetate concentration ( P  = 0.06). A quadratic interaction was observed in crypt depth (CD, P  < 0.05). Incremental pBSFLM inclusion negatively affected G:F, CD, IFN-γ, and acetate productions in the ceca under coccidia challenge. Conversely in non-challenged birds, the impact of pBSFLM varied from neutral (e.g. G:F) to potentially advantageous (e.g. acetate). Challenged birds exhibited decreased ( P  < 0.01) BW, BW gain, feed intake (FI), and the apparent ileal digestibility and total tract nutrient utilization of DM, gross energy, and nitrogen (N). Eimeria challenge reduced ( P  < 0.01) serum carotenoid concentrations, decreased the villus height to crypt depth ratio (VH:CD, P  < 0.01), and increased concentrations of branched-chain fatty acids, specifically isobutyrate ( P  = 0.059) and isovalerate ( P  < 0.05) in the cecum. Dietary pBSFLM addition linearly reduced ( P  < 0.05) BW, FI, and N utilization. Tendencies ( P  < 0.06) were observed where pBSFLM linearly decreased VH:CD and reduced goblet cell density. Conclusions Increasing pBSFLM supplementation, particularly at 12%, adversely affected growth, ileal morphology, cecal acetate production, and downregulated key cytokine expression in response to coccidia infection.

The objective of this study was to compare the effect of sodium selenite (SS) and selenium yeast (SY) on performance, egg quality, and selenium concentration in eggs and serum biochemical indices in laying hens. Seven hundred twenty healthy Roman laying hens (21 weeks old, 18 weeks in lay) with a similar laying rate (90.27% ± 1.05%) were randomly divided into 5 groups with 6 replicates of 24 hens each. Five diets were prepared as a 1+2×2 factorial arrangement with control and two sources of Se at two levels. Control diet (control) was prepared without adding exogenous selenium (analyzed basal Se content of 0.178 mg/kg). The other four diets were prepared with the control diet supplemented with SY or SS at 0.3 mg/kg (low; L) or 0.5 mg/kg (high; H) to give 5 diets designated as control, SY-L, SY-H, SS-L, and SS-H. The analyzed selenium content in the SY-L, SY-H, SS-L, and SS-H diets were 0.362, 0.572, 0.323, and 0.533 mg/kg respectively. The pre-trial period lasted 7 d, and the experimental period lasted 56 d (30 weeks old), during which the egg production, egg quality, and hen serum parameters were measured. Results showed that selenium source and level had no effect (P > 0.05) on average daily egg weight and feed conversion ratio (FCR). However, the laying rate was different at the L and H levels of supplementation, regardless of source, such that hens that were supplemented had a higher performance than that of the control, and the H level of supplementation lead to a higher laying rate than that of the L level (P < 0.05). There was a difference in average daily feed intake (ADFI) with an interaction in selenium source and level (P < 0.05), such that SS-L was higher than other selenium supplemented treatment or control. There were no significant differences in egg quality (P > 0.05); at the high level, SY had higher egg yolk selenium compared with SS. However, within SY, adding 0.5 mg/kg selenium led to higher egg yolk selenium than 0.3 mg/kg selenium (P < 0.05). Moreover, adding 0.3 mg/kg SY, 0.3 mg/kg, or 0.5 mg/kg SS to the basal diet had no significant effect on the selenium content in the egg (P > 0.05). There were no significant differences in serum biochemical indices among the five groups (P > 0.05). In conclusion, adding a high level of selenium in the diet of laying hens significantly increased egg production, and addition of a high level of selenium in the form of SY led to a higher deposition of selenium in the yolk than that of SS. These results indicate that adding 0.5 mg/kg of SY in the diet of laying hens would result in Se-enriched eggs.

Mycotoxin contamination in foods is a major risk factor for human and animal health due to its prevalence in cereals and their by-products. Deoxynivalenol (DON), mainly produced by Fusarium genera, is the most common mycotoxin detected in cereal products. Deoxynivalenol disrupts intestinal barrier function and decreases protein levels of tight junction proteins (TJP). However, the overall mechanism by which DON regulates specific TJP turnover and epithelial cell integrity remains unclear. Herein, we show that DON (2 μM) decreases the protein stability and accelerates the degradation of TJP in the lysosome. Interestingly, pretreatment of cells with dynasore (a dynamin-dependent endocytosis inhibitor) protected against DON-induced degradation of claudin-3 and 4. Immunofluorescence analysis also shows that the decreased membrane presence of claudin-4 and ZO-1 induced by DON is reversible with dynamin inhibition, whereas the pretreatment with cytochalasin D (an actin-dependent endocytosis inhibitor) reverses the degradation of claudin-1 and 4 induced by DON. We also show that the endocytosis and degradation of claudin-1 is regulated by p38 mitogen-activated protein kinase (MAPK), whereas the endocytosis of claudin-4 and ZO-1 is mediated by c-Jun-N-terminal kinase (JNK). Resveratrol, with JNK inhibitory activity, also prevents the endocytosis and degradation of claudin-4 and ZO-1 and protects against DON-induced decrease in transepithelial electrical resistance (TEER) and increase in FITC–dextran permeability. Collectively, this study, for the first time, shows that DON accelerates the endocytosis and degradation of TJP and this is regulated by the activation of p38 MAPK and JNK signaling pathways. Therefore, natural bioactive compounds with p38 MAPK and JNK inhibitory activities may be effective in preventing the DON-induced TJP disruption and preserve gut barrier function in vivo.

This study was conducted to investigate the effects of different patterns and sources of Zn, Fe, Cu, Mn, and Se on performance, mineral deposition (liver, kidney, pancreas, spleen, pectorals muscle, and tibia), and excretion of laying hens, then to find an optimal dietary supplemental pattern of trace elements in laying hens. A total of 864 healthy laying hens with similar laying rate (Roman, 26-week-old) were randomly divided into nine treatments, with six replications of 16 birds per replication, including a control treatment and four patterns with different element sources (inorganic or organic): (1) Control treatment (basic diet without added extra trace minerals, CT); pattern 1, NRC (1994) recommended level (NRC-L): (2) inorganic minerals of NRC-L pattern (IN), (3) organic minerals of NRC-L pattern (ON); pattern 2, NY/T 33-2004 recommended level (NY/T-L): (4) inorganic minerals of NY/T-L pattern (IY), (5) organic minerals of NY/T-L pattern (OY); pattern 3, 50% NRC (1994) recommended level (50% NRC-L): (6) inorganic minerals of 50% NRC-L pattern (IHN), (7) organic minerals of 50% NRC-L pattern (OHN); pattern 4, the ratio of minerals in blood of laying hens was taken as the supplement proportion of trace elements, and Zn was supplemented depended on NRC recommended level (TLB): (8) inorganic minerals of TLB pattern (IB), (9) organic minerals of TLB pattern (OB). Two weeks were allowed for adjustment to the conditions and then measurements were made over eight weeks. Supplementation of trace elements led to increased daily egg weight (p < 0.05). Patterns of minerals in diets affected the content of liver Mn, pancreas Mn, tibia Mn, and the tissues Se (p < 0.05). Sources of minerals had positive effects on daily egg weight (p < 0.05), the concentrations of liver Fe, kidney Cu, tissues Se (except spleen), and fecal Se (p < 0.05). In conclusion, diet supplemented with the organic trace minerals of 50% NRC-L pattern (OHN) in laying hens promoted optimum laying performance, mineral deposition, and reduced mineral excretion.

To determine the effect of heat stress (HS) on adipose tissue metabolome, a combination of liquid chromatography-mass spectrometry-based metabolomics profiling approaches was applied to characterize changes of metabolite classes in adipocytes differentiated in culture (in vitro) and mesenteric adipose tissue of pigs exposed to HS (in vivo). Effect of HS on the composition of individual fatty acids in cultured adipocytes, mesenteric adipose tissue, and serum of animals was also investigated using gas chromatography analysis. In vitro, preadipocytes were differentiated either under control (37 °C) or HS (41.5 °C) temperature for 9 d. For the animal experiment, pigs were kept either in control (Con) environment (20 °C) with ad libitum feed intake, HS (35 °C) temperature with ad libitum feed intake (HS), or at 20 °C with pair feeding to the HS pigs. In cultured cells, HS increased triglyceride and decreased monoacylglycerol (P < 0.05) species accumulation compared with control. Phosphatidylinositol and phosphatidylserine were increased by HS, whereas phosphatidylcholine, phosphatidylethanolamine, and phosphatidylglycerol were decreased relative to control (P < 0.05). Heat-stressed adipocytes in culture also had higher concentrations of saturated (SFA) and monounsaturated fatty acids (P < 0.05) relative to control. Pathways of proline and biotin metabolism were elevated (P < 0.05) by HS in adipocytes. The metabolomics signatures in adipocytes cultured under HS indicates that pathways centered around diacylglycerol metabolism are impacted by HS. In adipose tissue from animals in the HS treatment, there was increased (P < 0.05) abundance of 4,8 dimethylnonanoyl carnitine (P < 0.05). Heat-stressed animals also had higher (P < 005) serum linoleic, total polyunsaturated fatty acids, and decreased total SFA than PF (P < 0.05). These results indicate that HS elevates lipogenic pathways while suppressing fatty acid oxidation and demonstrate the usefulness of metabolomics analysis as a tool for determining the impact of HS in pig tissues.

This study investigated the effects of dietary live yeast (LY) supplementation to sows during late gestation and lactation on sow and litter performance indices and colostrum and milk proteome profiles. On Day 77 of gestation, 20 sows were allotted to each of 2 dietary treatments: without (control) or with LY (Saccharomyces cerevisiae) supplementation at 0.05% of diet during gestation and 0.1% during lactation. Sow performance was recorded on Days 77 and 112 of gestation and Day 19 of lactation. Litter characteristics were recorded at birth and weaning. Colostrum and milk samples were collected on Days 0, 10 and 18 of lactation for shotgun proteomic analysis. Results showed that there was a higher abundance of immune‐associated proteins such as Ig‐like domain‐containing protein and complement proteins (Complement C8 alpha chain and C1q domain‐containing proteins) in the colostrum and IgG heavy chain in Day 10 milk of LY sows than control sows (p < 0.05), whereas the abundance of prostaglandin D synthase was greater in D10 milk of control sows than LY sows (p < 0.05). Additionally, milk fat globule EGF and factor V/VIII domain‐containing protein and Niemann–Pick C2 were found to be more abundant in both Days 10 and 18 milk samples from LY sows (p < 0.05). Overall, these results showed that dietary gestational and lactational LY supplementation increased the abundance of immune‐associated proteins in colostrum and proteins involved in lipid uptake and processing in mature milk. Maternal dietary live yeast supplementation during late gestation and lactation increased the abundance of immune‐associated proteins in colostrum and proteins involved in lipid uptake and processing in mature milk.