Mechanisms underlying distinct subcellular localization and regulation of epithelial long myosin light-chain kinase splice variants.

Intestinal epithelia express two long myosin light-chain kinase (MLCK) splice variants, MLCK1 and MLCK2, which differ by the absence of a complete immunoglobulin (Ig)-like domain 3 within MLCK2. MLCK1 is preferentially associated with the perijunctional actomyosin ring at steady state, and this localization is enhanced by inflammatory stimuli including tumor necrosis factor (TNF). Here, we sought to identify MLCK1 domains that direct perijunctional MLCK1 localization and their relevance to disease. Ileal biopsies from Crohn's disease patients demonstrated preferential increases in MLCK1 expression and perijunctional localization relative to healthy controls. In contrast to MLCK1, MLCK2 expressed in intestinal epithelia is predominantly associated with basal stress fibers, and the two isoforms have distinct effects on epithelial migration and barrier regulation. MLCK1(Ig1-4) and MLCK1(Ig1-3), but not MLCK2(Ig1-4) or MLCK1(Ig3), directly bind to F-actin in vitro and direct perijunctional recruitment in intestinal epithelial cells. Further study showed that Ig1 is unnecessary, but that, like Ig3, the unstructured linker between Ig1 and Ig2 (Ig1/2us) is essential for recruitment. Despite being unable to bind F-actin or direct recruitment independently, Ig3 does have dominant negative functions that allow it to displace perijunctional MLCK1, increase steady-state barrier function, prevent TNF-induced MLCK1 recruitment, and attenuate TNF-induced barrier loss. These data define the minimal domain required for MLCK1 localization and provide mechanistic insight into the MLCK1 recruitment process. Overall, the results create a foundation for development of molecularly targeted therapies that target key domains to prevent MLCK1 recruitment, restore barrier function, and limit inflammatory bowel disease progression.

Inulin supplementation induces expression of hypothalamic antioxidant defence genes in weaned piglets.

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 1ß, 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.

Mechanism of endocytic regulation of intestinal tight junction remodeling during nutrient starvation in jejunal IPEC-J2 cells.

Intestinal epithelial cells are tightly bound by tight junction proteins (TJP) which are dynamic and sensitive to environmental stress. However, the role of the endocytic pathway in the regulation of TJP abundance and tight junction integrity during nutrient stress is poorly understood. Therefore, this study was conducted to investigate the regulation of TJP abundance during nutrient starvation and the role of the endocytic mechanism in this process. IPEC-J2 cells were subjected to nutrient starvation in Krebs-Ringer bicarbonate buffer (KRB) and abundance of TJP, an indication of tight junction remodeling, was characterized with RT-PCR, western blotting and immunofluorescence. Abundance of TJP was dynamically regulated by nutrient starvation. The protein levels of claudin-1, 3, and 4 were initially downregulated within the first 6 hours of starvation, and then, increased thereafter (P < .01). However, there was no change in occludin and ZO-1. Lysosome and proteasome inhibitors were used to determine the contribution of these protein degradation pathways to the TJP remodeling. Short-term starvation-induced degradation of claudin-1, 3, and 4 was found to be lysosome dependent. Specifically, the downregulation of claudin-3 and 4 was via a dynamin-dependent, but clathrin and caveolae independent, endocytic pathway and this downregulation was partly reversed by amino acids supplementation. Interestingly, the re-synthesis of TJP with prolonged starvation partly depended on proteasome function. Collectively, this study, for the first time, elucidated a major role for dynamin-dependent endocytosis of claudin-3 and 4 during nutrient stress in intestinal epithelial cells. Therefore, transient endocytosis inhibition may be a potential mechanism for preserving tight junction integrity and function in metabolic or pathological states such as inflammatory bowel disease that involves destruction of intestinal epithelial TJP.

Mechanisms of deoxynivalenol-induced endocytosis and degradation of tight junction proteins in jejunal IPEC-J2 cells involve selective activation of the MAPK pathways.

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.

Impact of maternal live yeast supplementation to sows on intestinal inflammatory cytokine expression and tight junction proteins in suckling and weanling piglets.

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-1ß 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.

Increasing evidence supports the benefits of improving sow nutrition during gestation and lactation to promote gastrointestinal development and overall health of piglets. The objective of this research was to investigate the effects of maternal live yeast (LY) supplementation to sows during late gestation and lactation periods on the intestinal health of suckling and weaned piglets. Sows were fed LY during gestation and lactation and piglets were killed for sampling at different time points to track the temporal effect of maternal LY supplementation on changes in markers of intestinal health and development on postnatal days 0, 10, and 18, and postweaning days 7 and 14. Results showed that maternal LY supplementation affected several markers of health and development in the offspring, especially the expression of tight junction proteins, inflammatory cytokines, and antioxidant enzymes. These results indicate that nutritional intervention during gestation and lactation could serve as an effective strategy for raising piglets with better health and growth performance.

PPARγ activation inhibits endocytosis of claudin-4 and protects against deoxynivalenol-induced intestinal barrier dysfunction in IPEC-J2 cells and weaned piglets.

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.

Quercetin attenuates deoxynivalenol-induced intestinal barrier dysfunction by activation of Nrf2 signaling pathway in IPEC-J2 cells and weaned piglets.

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.

EPA and DHA inhibit endocytosis of claudin-4 and protect against deoxynivalenol-induced intestinal barrier dysfunction through PPARγ dependent and independent pathways in jejunal IPEC-J2 cells.

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.

Effects of Reduced Dietary Protein at High Temperature in Summer on Growth Performance and Carcass Quality of Finishing Pigs.

The objective of this experiment was to investigate the effects of reduced dietary protein at natural high temperature in summer on the growth performance and carcass quality of finishing pigs. A total of 72 crossbreed pigs (Duroc × Landrace × Yorkshire) at an average body weight (BW) of 77 ± 5.7 kg were randomly assigned to two treatments, based on BW and sex, in six replicates per treatment, with six pigs per pen, using a randomized complete block design. The dietary crude protein (CP) level of the normal protein diet (NP) and the reduced protein diet (LP) were 12% and 10%, respectively. The growth performance and serum biochemical parameters of the pigs were analyzed for a 28-day experimental period. At the end of the experiment, 12 pigs were harvested to measure carcass characteristics and pork quality. The average highest ambient temperature during the experiment period was about 32.4 °C. There was a trend for the average daily feed intake (ADFI) to be lower in the pigs on the reduced protein diet compared to the control (p < 0.10) in the 0−28 day period. The serum urea nitrogen was lower (p < 0.05) for pigs fed the reduced protein diets only on day 14. The carcass characteristics and pork quality were not affected by dietary treatments. In conclusion, decreasing dietary crude protein percentage from 12% to 10% in finishing pigs in summer may have no negative effects on growth performance and carcass quality.

Effect of a carbohydrase admixture in growing pigs fed wheat-based diets in thermoneutral and heat stress conditions.

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-ß-1,4-xylanase, 4,600 units α-l-arabinofuranosidase and 860 visco-units endo-1,3(4)-ß-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 IL1ß 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.

Effects of brown rice particle size on energy and nutrient digestibility in diets for young pigs and adult sows.

The objective of this study was to evaluate the effects of brown rice particle size on the apparent total tract digestibility (ATTD) of energy and nutrients in diets fed to pigs at four different stages and determine the optimal particle size (OPS) of brown rice for young pigs and adult sows. Eighteen weanling piglets (initial body weight (BW): 10.2 ± 0.4 kg), 18 growing barrows (initial BW: 35.6 ± 1.5 kg), 24 gestating sows (initial BW: 220 ± 2.8 kg), and 24 lactating sows (initial BW: 208 ± 3.8 kg) were allotted to 1 of 3 or 4 diets based on completely randomized design with six replicates per diet. Within each stage, brown rice-soybean meal diets were formulated, and the only difference among diets was the brown rice used was ground to the specified particle size. Each stage lasted 19 days, including 7 days for cage adaptation, 7 days for diet adaptation, and 5 days for total feces and urine collection. For weanling and growing pigs, the results showed that pigs fed brown rice milled to 600 µm had a greater ATTD of dry matter (DM), gross energy (GE), and crude protein (CP) than pigs fed brown rice ground to 800 µm. However, there was no improvement in the ATTD of energy and nutrients for pigs fed brown rice milled to 600 µm versus 400 µm. The concentration of nitrogen (N) in feces significantly reduced (p < 0.01) as brown rice particle size decreased from 800 to 400 µm. However, there were no differences in phosphorus (P) output and absorbed P among diets. For gestating and lactating sows, a reduction in particle size from 1,000 to 800 µm significantly improved (p < 0.01) the ATTD of DM, GE, and CP in diets. However, there was also no improvement in the ATTD of energy and nutrients for pigs fed brown rice milled from 800 to 400 µm. In conclusion, considering the energy required for milling and nutrient digestibility, milling brown rice to 600 and 800 µm are recommended in diets for young pigs and adult sows, respectively. The OPS of brown rice for pigs at different physiological stages should be considered to economically and accurately formulate diets.

Digestible energy and metabolizable energy contents of konjac flour residues and ramie in growing pigs.

The objectives of this study were to determine: 1) the effects of konjac flour residues and ramie on digestible energy (DE), metabolizable energy (ME) and apparent total tract digestibility (ATTD) of nutrients in diets fed to growing pigs, 2) the DE and ME contents of konjac flour residues and ramie. Thirty barrows were allotted to 1 of 5 treatments with 6 replicates per treatment. The 5 diets include a corn-soybean meal basal diet (CTL), konjac flour residues diets containing 15% konjac flour residues (LK) or 30% konjac flour residues (HK), and ramie diets containing 15% ramie (LR) or 30% ramie (HR). The experiment lasted 19 days, including 7 days for cage adaptation, 7 days for diet adaptation, and 5 days for total feces and urine collection. The energy values and ATTD of nutrients in each diet were determined, and DE and ME contents of konjac flour residues and ramie were calculated. The results showed that consumption of konjac flour residues significantly increased (P < 0.01) the fecal moisture content compared with the ramie treatment. The LK, HK and HR diets had lower (P < 0.01) DE values compared with the CTL diet. The HR diet had greater (P < 0.01) DE value compared with the HK diet. The LK and LR diets showed greater (P < 0.01) ATTD of DM, OM, GE and CP compared with the HK and HR diets. The HK diet had the lowest (P < 0.01) ATTD of ether extract (EE) among the 5 diets. No differences were observed for the ATTD of NDF and ADF among the 5 diets. Moreover, the DE and ME values of konjac flour residues under 2 inclusion levels (15% and 30%) were 11.66, 11.87 MJ/kg and 10.41, 10.03 MJ/kg, respectively. The corresponding values for ramie were 13.27, 13.16 MJ/kg and 13.07, 12.82 MJ/kg, respectively. In conclusion, the differences in fecal moisture content and the ATTD of EE among the 5 diets were mainly due to the different chemical compositions of konjac flour residues and ramie. Compared with konjac flour residues, ramie has greater DE and ME values under the same inclusion level.

Determination of net energy content of soybean oil fed to growing pigs using indirect calorimetry.

The objectives of this experiment were: (i) to determine the net energy (NE) of soybean oil (SBO) fed to growing pigs using indirect calorimetry (IC); and (ii) to evaluate the effects of inclusion rate of SBO on heat production, oxidative status and nutrient digestibility in growing pigs. Eighteen growing barrows were allotted to three diets based on completely randomized design with six replicate pigs (period) per diet. Diets included a corn-soybean meal basal diet and two test diets containing 5% or 10% SBO at the expense of corn and soybean meal. During each period, pigs were individually housed in metabolism crates for 14 days, including 7 days to adapt to feed, metabolism crate and environmental conditions. On day 8, pigs were transferred to the open-circuit respiration chambers for measurement of daily O2 consumption and CO2 and CH4 production. During this time, pigs were fed one of the three diets at 2.4 MJ metabolizable energy/kg body weight (BW)0.6 /day. Total feces and urine were collected and daily total heat production (THP) was measured from days 9 to 13 and fasted on day 14 to evaluate their fasting heat production (FHP). The results show that trends of decreased apparent total tract digestibility of neutral detergent fiber (linear, P = 0.09) and acid detergent fiber (linear, P = 0.07) were observed as the content of dietary lipids increased. The average THP for the three diets were 1326, 1208 and 1193 kJ/kg BW0.6 /day, respectively. The FHP of pigs averaged 843 kJ/kg BW0.6 /day and was not affected by diet characteristics. A reduction of the respiratory quotients in the fed state as the inclusion level of SBO increased was observed. In conclusion, the NE values of SBO we determined by indirect calorimetry were 33.45 and 34.05 MJ/kg dry matter under two inclusion levels. THP could be largely reduced when SBO is added in the feed, but the THP of SBO included at 5% in a corn-soybean meal diet is not different from the THP of SBO included at 10%.

Determination of net energy content of dietary lipids fed to growing pigs using indirect calorimetry.

The objective of this experiment was to determine the NE content of different dietary lipids fed to growing pigs using indirect calorimetry. Thirty-six growing (initial BW: 41.1 ± 3.1 kg) barrows were allotted to 6 diets based on completely randomized design with 6 replicate pigs per diet. Diets included a corn-soybean meal basal diet and 5 test diets each containing 10% palm oil, poultry fat, fish oil, corn oil, or flaxseed oil at the expense of corn and soybean meal. During each period, pigs were individually housed in metabolism crates for 14 d, which included 7 d for adaptation to feed, metabolism crates, and environmental conditions. On day 8, pigs were transferred to the open-circuit respiration chambers and fed 1 of the 6 diets at 2.3 MJ ME/kg BW0.6/day. Total feces and urine were collected and daily heat production (HP) was also calculated from day 9 to day 13. On the last day of each period (day 14), pigs were fasted and the fasting heat production (FHP) was measured. The results show that the FHP of pigs averaged 809 kJ/kg BW0.6·day-1 and was not affected by diet characteristics. The DE values were 35.98, 36.84, 37.11, 38.95, and 38.38 MJ/kg DM, the ME values were 35.79, 36.56, 36.92, 37.73, and 38.11 MJ/kg DM, and the NE values were 32.42, 33.21, 33.77, 34.00, and 34.12 MJ/kg DM, for the palm oil, poultry fat, fish oil, corn oil, and flaxseed oil, respectively. Based on our result, we concluded that the DE content of dietary lipid varied from 91% to 98% of its GE content, the ME content of dietary lipid was approximately 99% of its DE content, and the NE content of dietary lipid was approximately 90% of its ME content in growing pigs.

Net energy content of rice bran, defatted rice bran, corn gluten feed, and corn germ meal fed to growing pigs using indirect calorimetry.

The objective of this experiment was to determine the effects of increased fiber content in diets on heat production (HP) and NE:ME ratio and to determine the NE content and NE:ME ratio of full-fat rice bran (FFRB), defatted rice bran (DFRB), corn gluten feed (CGF), and corn germ meal (CGM) fed to growing barrows using indirect calorimetry (IC). Thirty growing barrows (28.5 ± 2.4 kg BW) were allotted in a completely randomized design to 5 dietary treatments that included a corn-soybean meal basal diet and 4 experimental diets with a constant ratio of corn and soybean meal (difference method) containing 30% FFRB, DFRB, CGF, and CGF. Pigs were housed in individual metabolism crates for 20 d including 14-d adaptation to the diet and 6 d to determine the HP and total collection of feces and urine in respiration chambers. Pigs were fed their respective diets at 550 kcal ME·kg BW0.60-1·d-1 on the basis of BW measured on days 0, 7, and 14. The apparent total tract digestibility (ATTD) of DM, GE, and OM were greater (P < 0.01) in pigs fed the basal diet. The ATTD of DM, GE, and OM in pigs fed the DFRB diet were lesser (P < 0.01) when compared with those fed the basal and FFRB diets. The ATTD of ether extract (EE) in pigs fed the FFRB diet was greater (P < 0.01) compared with those fed basal, DFRB, CGF, and CGM diets. The HP adjusted for the same ME intake was greater (P < 0.01) in pigs fed the DFRB, CGF, and CGM diets compared with those fed basal and FFRB diets. The NE:ME ratio in pigs fed the FFRB diet was greater (P < 0.01) when compared with those fed the DFRB, CGF, and CGM diets. The NE content of FFRB, DFRB, CGF, and CGM determined using the IC method were 2,952, 1,100, 1,747, and 2,079 kcal/kg DM, respectively. The NE content of FFRB, CGF, and CGM determined using the IC method were 3.5%, 3.8%, and 1.8% greater, respectively, than the predicted values, whereas NE content of DFRB determined using the IC method was 2.1% lower than the predicted values. In conclusion, pigs fed the fiber-rich ingredients had greater HP and lower nutrient digestibility. However, pigs fed FFRB diets containing greater fat content had a lower heat increment and, therefore, higher utilization efficiency. The NE:ME ratio ranged from 71.6% to 82.4%. The NE of FFRB, DFRB, CGF, and CGM determined using the IC method were 2,952, 1,100, 1,747, and 2,079 kcal/kg DM, respectively.