Pair-fed Pigs Research Articles

Effects of supplemental citrulline on thermal and intestinal morphology parameters during heat stress and feed restriction in growing pigs.

Study objectives were to characterize the effects of citrulline (CIT) on physiological and intestinal morphology metrics during heat stress (HS) and feed restriction. Forty crossbred gilts (30 ± 2kg body weight [BW]) were assigned to one of five treatments: (1) thermoneutral (TN) fed ad libitum (AL) with control (CON) supplement (TNAL; n = 8), (2) TN pair-fed (PF) with CON (PF-CON; n = 8), (3) TN PF with CIT (PF-CIT; n = 8), (4) HS AL with CON (HS-CON; n = 8), and (5) HS AL with CIT (HS-CIT; n = 8). During the period (P) 1 (7 d), pigs were in TN conditions (23.6 °C) and fed AL their respective supplemental treatments. During P2 (2.5 d), HS-CON and HS-CIT pigs were fed AL and exposed to cyclical HS (33.6 to 38.3 °C), while TNAL, PF-CON, and PF-CIT remained in TN and were fed either AL or PF to their HS counterparts. Citrulline (0.13g/kg BW) was orally administered twice daily during P1 and P2. HS increased rectal temperature (Tr), skin temperature (Ts), and respiration rate (RR) relative to TN pigs (0.8 °C, 4.7 °C, and 47 breaths/min, respectively; P < 0.01). However, HS-CIT had decreased RR (7 breaths/min, P = 0.04) and a tendency for decreased Tr (0.1 °C, P = 0.07) relative to HS-CON pigs. During P2, HS pigs had decreased feed intake (22%; P < 0.01) and a tendency for decreased average daily gain (P = 0.08) relative to TNAL pigs, and by experimental design, PF pigs followed this same pattern. Circulating lipopolysaccharide-binding protein tended to be decreased (29%; P = 0.08) in PF relative to TNAL pigs and was increased (41%; P = 0.03) in HS compared to PF pigs. Jejunum villus height was decreased in PF relative to TNAL pigs (15%; P = 0.03); however, CIT supplementation improved this metric during feed restriction (16%; P = 0.10). Jejunum mucosal surface area decreased in PF (16%; P = 0.02) and tended to decrease in HS (11%; P = 0.10) compared to TNAL pigs. Ileum villus height and mucosal surface area decreased in HS compared to TNAL pigs (10 and 14%, respectively; P ≤ 0.04), but both parameters were rescued by CIT supplementation (P ≤ 0.08). Intestinal myeloperoxidase and goblet cell area remained similar among treatments and intestinal segments (P > 0.24). In summary, CIT supplementation slightly improved RR and Tr during HS. Feed restriction and HS differentially affected jejunum and ileum morphology and while CIT ameliorated some of these effects, the benefit appeared dependent on intestinal section and stressor type.

Effects of dietary live yeast supplementation on growth performance and biomarkers of metabolism and inflammation in heat-stressed and nutrient-restricted pigs.

Study objectives were to determine the effects of dietary live yeast (Saccharomyces cerevisiae strain CNCM I-4407; ActisafHR+; 0.25g/kg of feed; Phileo by Lesaffre, Milwaukee, WI) on growth performance and biomarkers of metabolism and inflammation in heat-stressed and nutrient-restricted pigs. Crossbred barrows (n = 96; 79 ± 1 kg body weight [BW]) were blocked by initial BW and randomly assigned to one of six dietary-environmental treatments: 1) thermoneutral (TN) and fed ad libitum the control diet (TNCon), 2) TN and fed ad libitum a yeast containing diet (TNYeast), 3) TN and pair-fed (PF) the control diet (PFCon), 4) TN and PF the yeast containing diet (PFYeast), 5) heat stress (HS) and fed ad libitum the control diet (HSCon), or 6) HS and fed ad libitum the yeast diet (HSYeast). Following 5 d of acclimation to individual pens, pigs were enrolled in two experimental periods (P). During P1 (7 d), pigs were housed in TN conditions (20 °C) and fed their respective dietary treatments ad libitum. During P2 (28 d), HSCon and HSYeast pigs were fed ad libitum and exposed to progressive cyclical HS (28–33 °C) while TN and PF pigs remained in TN conditions and were fed ad libitum or PF to their HSCon and HSYeast counterparts. Pigs exposed to HS had an overall increase in rectal temperature, skin temperature, and respiration rate compared to TN pigs (0.3 °C, 5.5 °C, and 23 breaths per minute, respectively; P < 0.01). During P2, average daily feed intake (ADFI) decreased in HS compared to TN pigs (30%; P < 0.01). Average daily gain and final BW decreased in HS relative to TN pigs (P < 0.01); however, no differences in feed efficiency (G:F) were observed between HS and TN treatments (P > 0.16). A tendency for decreased ADFI and increased G:F was observed in TNYeast relative to TNCon pigs (P < 0.10). Circulating insulin was similar between HS and TN pigs (P > 0.42). Triiodothyronine and thyroxine levels decreased in HS compared to TN treatments (~19% and 20%, respectively; P < 0.05). Plasma tumor necrosis factor-alpha (TNF-α) did not differ across treatments (P > 0.57) but tended to decrease in HSYeast relative to HSCon pigs (P = 0.09). In summary, dietary live yeast did not affect body temperature indices or growth performance and had minimal effects on biomarkers of metabolism; however, it tended to improve G:F under TN conditions and tended to reduce the proinflammatory mediator TNF-α during HS. Further research on the potential role of dietary live yeast in pigs during HS or nutrient restriction scenarios is warranted.

Impact of a dietary challenge with peroxidized oil on the glutathione redox status and integrity of the small intestine in weaned piglets

Glutathione (GSH) is considered to play an important role in maintaining the integrity of the small intestine. In piglets, altered mucosal GSH levels might therefore be involved in weaning-induced changes of the small intestinal morphology and barrier function. To test this hypothesis, we aimed to challenge the mucosal GSH redox status during the first 28 days after weaning, by feeding diets containing 5% fresh linseed oil (CON), or 2.5% (OF1) or 5% (OF2) peroxidized linseed oil (peroxide value 225 mEq O2/kg oil) and exploring the effects on gut integrity. Piglets were pair-fed and had a total daily feed allowance of 32 g/kg BW. A fourth treatment included animals that were fed the control diet ad libitum (ACON). Animals were sampled at days 5 and 28 post-weaning. The malondialdehyde (MDA) concentration and GSH redox status (GSH/GSSG Eh) were determined in blood, liver and small intestinal mucosa. Histomorphology of the duodenal and jejunal mucosa was determined, and Ussing chambers were used to assess fluorescein isothiocyanate dextran (FD4) and horseradish peroxidase (HRP) fluxes across the mucosa. Results show that peroxidized linseed oil imposed an oxidative challenge at day 28, but not at day 5 post-weaning. At day 28, increasing levels of dietary peroxides to pair-fed pigs linearly increased MDA levels in duodenal and jejunal mucosa. Moreover, FD4 fluxes were significantly increased in OF1 (+75%) and OF2 (+64%) in the duodenum, and HRP fluxes tended (P=0.099) to show similar differences, as compared to CON. This co-occurred with a significant 11 mV increase of the hepatic GSH/GSSG Eh, potentiated by a significantly increased GSH peroxidase activity for treatments OF1 (+47%) and OF2 (+63%) in liver as compared to CON. Furthermore; duodenal HRP flux significantly correlated with the hepatic glutathione disulphide (GSSG) level (r=0.650), as also observed in the jejunum for hepatic GSSG (r=0.627) and GSH/GSSG Eh (r=0.547). The jejunal permeability was not affected, but FD4 and HRP fluxes significantly correlated with the local GSH (r=0.619; r=0.733) and GSSG (r=0.635; r=0586) levels. Small intestinal histomorphology was not affected by dietary lipid peroxides, nor were there any correlations found with the GSH redox system. To conclude, under oxidative stress conditions, jejunal barrier function is related to the local and hepatic GSH redox system. It is suggested that the hepatic GSH system participates in the elimination of luminal peroxides, and thereby impacts on duodenal barrier function.

Impact of PRRS Challenge on Calpain and Calpastatin Activity in Skeletal Muscle of Young Pigs

ObjectivesPorcine Reproductive and Respiratory Syndrome (PRRS) virus challenges in growing pigs are known to negatively affect growth performance. One hypothesis to explain this observation is that an increase in calpain system initiated protein degradation in muscle contributes to the reduction of muscle protein accretion. Calpain-1 and –2 are calcium dependent cysteine proteinases that are regulated by an endogenous inhibitor, calpastatin. The objective of this experiment was to define the extent to which PRRS challenge influences skeletal muscle calpain and calpastatin activity at 2 stages of infection (viremia and seroconversion).Materials and MethodsThirty-three pigs (11.3 ± 1.54 kg body weight (BW), approximately 6 wk of age) were assigned to a contemporary group (3 pigs per group) based on age and weight. Pigs were housed in individual pens in separate rooms depending on treatment. One pig per group was assigned to 1 of 3 treatments, 1)PRRS [PRRS challenged with ORF5 RFLP1–3-4 isolate (n = 11)], 2)Pair-fed [Non-challenged, daily feed intake matched to challenged pigs (n = 11)], and 3)Ad-lib [Non-challenged, Ad libitum fed (n = 11)]. Weekly BW, feed disappearance, and feed efficiency were assessed over each period. At days post inoculation (dpi) 9–10 (7 groups; viremia period) and 16 to 17 (4 groups; seroconversion period), pigs were euthanized and a 50-g sample of longissimus muscle was collected and homogenized in pre-rigor extraction buffer (100 mM Tris-HCl pH 8.3, 10 mM EDTA, 100 mg/L trypsin inhibitor, 2 μM E-64, and 0.1% 2-mercaptoethanol). Calpains and calpastatins were separated using anion exchange chromatography and quantified using casein as a substrate. Data from each time period were analyzed as a separate experiment. Data were analyzed using the mixed procedure in JMP Pro version 13.1 with fixed effects of treatment and a random effect of contemporary group. Means separations were conducted via Student t test with P < 0.05 considered significantly different.ResultsAt both time points, PRRS pigs had reduced ADG and G:F compared with Ad-lib and Pair-fed pigs (P < 0.01). Additionally, ADFI was reduced in PRRS and Pair-fed pigs compared with Ad-lib pigs (P < 0.001). At dpi 9–10, PRRS challenge resulted in greater calpastatin-2 (1.04) and total calpastatin (1.70) activity compared with the Pair-fed pigs (0.58, 1.06 respectively; P < 0.05). By contrast, at dpi 16 to 17, PRRS challenge resulted in greater calpastatin-1 (1.08) and total calpastatin activity (1.98) compared with Pair-fed controls (0.54, 0.89, respectively; P < 0.05). Calpain-1 and –2 were not significantly altered by treatment at either time point. The ratio of calpain-2 to total calpastatin activity was significantly (P < 0.05) less in muscle from PRRS challenged pigs (1.16) compared with muscle from the Pair-fed (2.47), but not the Ad-lib pigs (1.58).ConclusionThe results demonstrate that a decline in voluntary feed intake was not singularly responsible for the observed response to PRRS challenge. These results are counter to the hypothesis that PRRS challenge would decrease calpastatin activity. Moreover, the results of this study indicate a difference in calpastatin response to PRRS challenge, notably that PRRS challenge increased calpastatin-2 activity at dpi 9 to 10 and calpastatin-1 activity at dpi 16 to 17. The switch indicates a temporal response in skeletal muscle proteolysis due to PRRS virus challenge.

Impact of PRRS Challenge on Calpain and Calpastatin Activity in Skeletal Muscle of Young Pigs

ObjectivesPorcine Reproductive and Respiratory Syndrome (PRRS) virus challenges in growing pigs are known to negatively affect growth performance. One hypothesis to explain this observation is that an increase in calpain system initiated protein degradation in muscle contributes to the reduction of muscle protein accretion. Calpain-1 and –2 are calcium dependent cysteine proteinases that are regulated by an endogenous inhibitor, calpastatin. The objective of this experiment was to define the extent to which PRRS challenge influences skeletal muscle calpain and calpastatin activity at 2 stages of infection (viremia and seroconversion).Materials and MethodsThirty-three pigs (11.3 ± 1.54 kg body weight (BW), approximately 6 wk of age) were assigned to a contemporary group (3 pigs per group) based on age and weight. Pigs were housed in individual pens in separate rooms depending on treatment. One pig per group was assigned to 1 of 3 treatments, 1)PRRS [PRRS challenged with ORF5 RFLP1–3-4 isolate (n = 11)], 2)Pair-fed [Non-challenged, daily feed intake matched to challenged pigs (n = 11)], and 3)Ad-lib [Non-challenged, Ad libitum fed (n = 11)]. Weekly BW, feed disappearance, and feed efficiency were assessed over each period. At days post inoculation (dpi) 9–10 (7 groups; viremia period) and 16 to 17 (4 groups; seroconversion period), pigs were euthanized and a 50-g sample of longissimus muscle was collected and homogenized in pre-rigor extraction buffer (100 mM Tris-HCl pH 8.3, 10 mM EDTA, 100 mg/L trypsin inhibitor, 2 μM E-64, and 0.1% 2-mercaptoethanol). Calpains and calpastatins were separated using anion exchange chromatography and quantified using casein as a substrate. Data from each time period were analyzed as a separate experiment. Data were analyzed using the mixed procedure in JMP Pro version 13.1 with fixed effects of treatment and a random effect of contemporary group. Means separations were conducted via Student t test with P < 0.05 considered significantly different.ResultsAt both time points, PRRS pigs had reduced ADG and G:F compared with Ad-lib and Pair-fed pigs (P < 0.01). Additionally, ADFI was reduced in PRRS and Pair-fed pigs compared with Ad-lib pigs (P < 0.001). At dpi 9–10, PRRS challenge resulted in greater calpastatin-2 (1.04) and total calpastatin (1.70) activity compared with the Pair-fed pigs (0.58, 1.06 respectively; P < 0.05). By contrast, at dpi 16 to 17, PRRS challenge resulted in greater calpastatin-1 (1.08) and total calpastatin activity (1.98) compared with Pair-fed controls (0.54, 0.89, respectively; P < 0.05). Calpain-1 and –2 were not significantly altered by treatment at either time point. The ratio of calpain-2 to total calpastatin activity was significantly (P < 0.05) less in muscle from PRRS challenged pigs (1.16) compared with muscle from the Pair-fed (2.47), but not the Ad-lib pigs (1.58).ConclusionThe results demonstrate that a decline in voluntary feed intake was not singularly responsible for the observed response to PRRS challenge. These results are counter to the hypothesis that PRRS challenge would decrease calpastatin activity. Moreover, the results of this study indicate a difference in calpastatin response to PRRS challenge, notably that PRRS challenge increased calpastatin-2 activity at dpi 9 to 10 and calpastatin-1 activity at dpi 16 to 17. The switch indicates a temporal response in skeletal muscle proteolysis due to PRRS virus challenge.

The impact of Roux-en-Y gastric bypass surgery on normal metabolism in a porcine model.

BackgroundA growing body of literature on Roux-en-Y gastric bypass surgery (RYGB) has generated inconclusive results on the mechanism underlying the beneficial effects on weight loss and glycaemia, partially due to the problems of designing clinical studies with the appropriate controls. Moreover, RYGB is only performed in obese individuals, in whom metabolism is perturbed and not completely understood.MethodsIn an attempt to isolate the effects of RYGB and its effects on normal metabolism, we investigated the effect of RYGB in lean pigs, using sham-operated pair-fed pigs as controls. Two weeks post-surgery, pigs were subjected to an intravenous glucose tolerance test (IVGTT) and circulating metabolites, hormones and lipids measured. Bile acid composition was profiled after extraction from blood, faeces and the gallbladder.ResultsA similar weight development in both groups of pigs validated our experimental model. Despite similar changes in fasting insulin, RYGB-pigs had lower fasting glucose levels. During an IVGTT RYGB-pigs had higher insulin and lower glucose levels. VLDL and IDL were lower in RYGB- than in sham-pigs. RYGB-pigs had increased levels of most amino acids, including branched-chain amino acids, but these were more efficiently suppressed by glucose. Levels of bile acids in the gallbladder were higher, whereas plasma and faecal bile acid levels were lower in RYGB- than in sham-pigs.ConclusionIn a lean model RYGB caused lower plasma lipid and bile acid levels, which were compensated for by increased plasma amino acids, suggesting a switch from lipid to protein metabolism during fasting in the immediate postoperative period.

Gastric bypass in the pig increases GIP levels and decreases active GLP-1 levels

Gastric bypass surgery results in remission of type 2 diabetes in the majority of patients. The incretin hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) have been implicated in the observed remission. Most knowledge so far has been generated in obese subjects. To isolate the surgical effects of gastric bypass on metabolism and hormone responses from the confounding influence of obesity, T2D, or food intake, we performed gastric bypass in lean pigs, using sham-operated and pair-fed pigs as controls. Thus, pigs were subjected to Roux-en-Y gastric bypass (RYGB) or sham surgery and oral glucose tolerance tests (OGTT). RYGB pigs and sham pigs exhibited similar basal and 120-min glucose levels in response to the OGTT. However, RYGB pigs had approximately 1.6-fold higher 30-min glucose (p<0.01). Early insulin release (EIR) was enhanced approximately 3.5-fold in the RYGB pigs (p<0.01). Furthermore, GIP release, both acute and sustained release (p<0.001 and p<0.01, respectively), was increased approximately 2.5-fold and 1.4-fold, respectively, in RYGB pigs. Although total GLP-1 release increased approximately 2.1-fold after RYGB (p<0.001), active GLP-1 was 33% lower (p<0.01). Interestingly basal DPP4-activity was approximately 3.2-fold higher in RYGB pigs (p<0.001). In conclusion, RYGB in lean pigs increases the response of GIP, total GLP-1, and insulin, but reduces levels of active GLP-1 in response to an oral glucose load. These data challenge the role of active GLP-1 as a contributor to remission from diabetes after RYGB.

Effects of high ambient temperature on lipid metabolism in finishing pigs

AbstractIn this study, we investigated the effects of high ambient temperature on lipid metabolism in finishing pigs. Sixteen pigs ((79.6±1.2) kg) were randomly assigned to two groups: (1) ambient temperature of 30°C with ad libitum access to feed (HT; n=8) and (2) ambient temperature of 22°C and fed the average amount consumed by eight pigs in HT group on the previous day (PF; n=8). After 21 days of constant exposure to different environmental conditions, all the pigs were euthanized, and blood and tissue samples were obtained. High ambient temperature increased the proportion of backfat (P=0.04, +21.6%) and flare fat (P<0.01, +43.3%). Compared with pair-fed pigs, the activities of fatty acid synthase (FAS) and malic enzyme in backfat and flare fat were lower (P<0.05) in heat-stressed pigs, as were the amounts of acetyl-CoA-carboxylase and FAS in the longissimus muscle (LM), the amount of FAS in backfat (P<0.01), and FAS activity in the liver (P<0.01). Ambient temperature did not affect the amount of hormone-sensitive lipase in different tissues. The amount of lipoprotein lipase in flare fat tended to be higher (P=0.09, +28.3%), and the activities of β-hydroxyacyl coenzyme A dehydrogenase in front and back of LM were lower (P<0.01, −48.3 and −49.8%, respectively) at 30°C than at 22°C. The plasma concentration of high-density lipoprotein tended to be lower (P=0.08), but the plasma concentrations of very low-density lipoprotein (VLDL) (P=0.09, +50.0%) and nonestesterified fatty acid (NEFA) (P=0.04, +44.2%) were higher in heat-stressed pigs. We concluded that high ambient temperature depressed de novo fatty acid synthesis in both adipose tissues and the liver. However, β-oxidation of fatty acid in skeletal muscles was also inhibited in the high-temperature environment. As a result, more plasma NEFAs were used to synthesize VLDLs in the liver and were absorbed by adipose tissues. This may be one reason that high ambient temperature enhances the accumulation of backfat and flare fat in finishing pigs.

Gastric Bypass Surgery Induces Changes in Gut Hormone-Producing Cell Populations in a Porcine Model

Background: In most patients gastric bypass (GBP) causes remission of type 2 diabetes. It is established that plasma levels of gut hormones are affected by GBP, but it is not well understood how the enteroendocrine cells producing these gut hormones are affected by GBP. Objectives: We set out to investigate the effect of GBP on enteroendocrine cells in the stomach and intestine of pigs. Methods: Lean non-diabetic pigs were subjected to either GBP or sham-surgery and immunocytochemistry and morphometry for all major gut hormones in all parts of the GI-tract was performed. Sham-operated, pair-fed pigs were used as controls. Results: Postoperatively in the antrum, the density of gastrin-cells was lower (GBP 12.8±2.1 cells/μm2 versus sham 21.3±2.6 cells/μm2 ) while density of serotonin-cells was higher in GBP-pigs (GBP 21.6±2.3 cells/μm2 versus sham 10.6±0.7 cells/μm2). In the fundus, no effect of GBP was observed on any cell population. In the duodenum, densities of CCK- (GBP 5.1±1.0 cells/μm2 versus sham 2.6±0.4 cells/μm2), ghrelin- (GBP 3.4±0.5 cells/μm2 versus sham 1.4±0.2 cells/μm2), GIP- (GBP 5.5±0.3 cells/μm2 versus sham 2.3±0.3 cells/μm2) and neurotensin-cells (GBP 3.5±0.7 cells/μm2 versus sham 0.5±0.2 cells/μm2) were higher in the GBP-pigs. In the distal jejunum, density of ghrelin-cells was lower (GBP 0.7±0.2 cells/μm2 versus sham 2.3±0.4 cells/μm2) while densities of GIP- (GBP 3.5±0.3 cells/μm2 versus sham 2.4±0.2 cells/μm2) and secretin-cells (GBP 3.4±0.7 cells/μm2 versus sham 1.6±0.3 cells/ μm2) were higher in GBP-pigs compared to sham-pigs. In the ileum, densities of GIP-cells (GBP 5.4±0.4 cells/ μm2 versus sham 3.9±0.4 cells/μm2) and somatostatin-cells (GBP 3.3±0.4 cells/μm2 versus sham 2.1±0.3 cells/μm2) were higher, while densities of GLP-1-cells (GBP 5.0±0.5 cells/μm2 versus sham 8.8±1.4 cells/μm2) and PYYimmunoreactive cells (GBP 3.8±0.1 cells/μm2 versus sham 5.9±0.8 cells/μm2) were lower in the GBP-pigs. In the colon, densities of GIP- (GBP 2.8±0.3 cells/μm2 versus sham 1.4±0.2 cells/μm2), serotonin- (GBP 6.7±0.3 cells/μm2 versus sham 4.8±0.5 cells/μm2) and somatostatin-cells (GBP 1.9±0.2 cells/μm2 versus sham 1.3±0.1 cells/μm2) were higher in the GBP-pigs. GBP had no effect on villi length or total mucosa height in any of the intestinal segments analyzed, whereas duodenum (GBP 37.6±3.4 cells/μm2 versus sham 26.5±2.8 cells/μm2) and ileum (GBP 127±1.2 cells/μm2 versus sham 84.7±9.9 cells/μm2) of the GBP-pigs displayed higher proliferation, as assessed by Ki67 immunoreactivity. Conclusions: We conclude that GBP induces rapid and profound changes in the densities of gut hormoneproducing cells throughout the GI-tract in pigs. These changes seem to be the result of GBP per se and not a result of body weight or food intake. Also, GIP was increased in the GBP-pigs in all the intestinal segments analyzed.

Performance, serum amino acid concentrations and expression of selected genes in pair‐fed growing pigs exposed to high ambient temperatures

Heat stress (HS) depresses pig performance mainly because of appetite reduction, although other factors involved in the cellular availability of nutrients may also contribute to that depression. An experiment was conducted with twelve pair-fed pigs (30.3±2.7kg BW) to examine the effect of severe HS (up to 45°C) on the expression of genes coding for two cationic amino acid (AA) transporters (b(0,+) AT and CAT-1), leptin, heat-shock protein (Hsp-90) and myosin in several tissues; serum concentrations (SC) of AA; and performance. There were two treatments: Comfort, pigs housed at an average temperature of 22 (±2)°C; and HS, pigs housed in a similar room with no climate control, where temperature was raised up to 45°C. All pigs received the same wheat-soybean meal diet and had similar daily feed intake. Comfort pigs had a higher daily gain and better gain/feed ratio than HS pigs (p<0.05). The expression of b(0,+) AT in jejunum and liver, that of myosin in the Semitendinosus muscle, and leptin in adipose tissue was lower, but CAT-1 in jejunum and liver, and Hsp-90 in liver was higher in HS pigs. The SC of Lys and Met in HS pigs were around 55% and 20%, respectively, of that in Comfort pigs (p<0.05). In conclusion, HS affects the expression of cationic AA transporters, myosin, Hsp-90, leptin; the SC of Lys and Met; and the performance of pair-fed pigs. These results suggest that HS-related changes in gene expression affect the performance of pigs beyond the effect caused by the reduction in voluntary feed intake.

Influences of lipopolysaccharide-induced immune challenge on performance and whole-body protein turnover in weanling pigs

The objective of this study is to characterize the influence of immune stress induced by lipopolysaccharide (LPS) on protein utilization and turnover for early-weaned pigs. A total of 15, crossbred weanling pigs (initial body weight 10.15 ± 0.39 kg) were assigned to one of three treatments. Pigs were injected with LPS and fed ad libitum (LPS-challenge), or injected with endotoxin-free physiological salt solution (PSS) and fed ad libitum (control), or injected with PSS and fed the same amount of feed as LPS-challenged pigs (pair-feed). All pigs received a 4-d nitrogen balance trial. On d 1 and 3 of the trial, LPS-challenged pigs were injected intramuscularly with 200 μg/kg BW of LPS dissolved in 1 ml PSS. Pigs in other treatments were injected with 1 ml PSS. 15 N-Glycine (5 mg/kg BW) was gastrically infused after the second injection. Feces and urine were collected daily to determine the N output throughout the duration of the trial. Lymphocyte blastogenesis (LB) and serum immunoglobulins (IgA, IgG, IgM) were also detected to illustrate the LPS-induced immune responses. Results indicated that the injection of LPS significantly ( P < 0.01) elevated the LB and resulted in lower average daily gain (ADG), feed intake (ADFI) and efficiency of feed utilization than control pigs. Pair-fed pigs had higher performance than LPS-challenged pig but poorer than control pigs. Injection of LPS also resulted in significantly ( P < 0.01) lower nitrogen intake and efficiency of utilization than controls, and more fecal N excretion than Pair-fed pigs (3.19 ± 0.85 vs. 2.19 ± 0.67 g/d, P < 0.05). The whole-body nitrogen flux (4.34 ± 0.19 vs. 11.35 ± 0.12 g N/kg BW 0.75/d) and N accretion (5.57 ± 0.59 vs. 10.17 ± 1.12 g Pr/kg BW 0.75/d) were acutely ( P < 0.01) reduced as the feed intake decreased, but there was no significant difference between LPS-challenged and pair-fed pigs. Injection of LPS markedly ( P < 0.05) increased the protein degradation (16.76 ± 1.09 vs. 14.53 ± 1.24 g N/kg BW 0.75/d). It is concluded that LPS-induced immune challenge depresses growth performance and feed utilization efficiency by enhancing protein degradation rate and decreasing protein utilization for body protein retention.

Effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on growth and immunological measurements of starter pigs, and the efficacy of a polymeric glucomannan mycotoxin adsorbent.

An experiment was conducted to investigate the effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on growth and immunological parameters of starter pigs. A polymeric glucomannan mycotoxin adsorbent (GM polymer, Alltech Inc., Nicholasville, KY) was also tested for its efficacy in preventing Fusarium mycotoxicoses. A total of 150 starter pigs (initial weight of 9.3 +/- 1.1 kg) were fed one of five treatment diets (six pens of five pigs per diet) for 21 d. Diets included control, low level of contaminated grains, high level of contaminated grains, high level of contaminated grains + 0.20% GM polymer, and pair-fed control for comparison with pigs receiving the high level of contaminated grains. Feed intake and cumulative weight gain of pigs decreased linearly with the inclusion of contaminated grains in the diet throughout the experiment (P < 0.0001). Weight gains recovered, however, during wk 3 (P > 0.05). There was no difference between the pair-fed group and the pigs fed the diet containing the high level of contaminated grains in terms of weight gain or feed efficiency (P > 0.05). Feeding contaminated grains linearly increased the serum albumin:globulin ratio (P = 0.01), whereas serum urea concentrations and gamma-glutamyltransferase activities responded in a quadratic fashion (P = 0.02). When compared with the pair-fed pigs, serum concentrations of total protein (P = 0.01) and globulin (P = 0.02) were decreased in pigs fed the diet containing the high level of contaminated grains. The feeding of contaminated diets did not significantly alter organ weights expressed as a percentage of BW, serum immunoglobulin concentrations, percentages of peripheral blood lymphocyte subsets, contact hypersensitivity to dinitrochlorobenzene, or primary antibody response to sheep red blood cells (P > 0.05). It was concluded that most of the adverse effects of feeding Fusarium mycotoxin-contaminated grains to starter pigs were caused by reduced feed intake. Although supplementation of GM polymer to the contaminated diet prevented some toxin-induced changes in metabolism, it did not prevent the mycotoxin-induced growth depression under the current experimental conditions.

Radiographic manifestations of experimental aluminum toxicity in growing bone.

To evaluate the effect of aluminum on growing bone in the presence of normal renal function, the following experiment was performed. Eight littermate pair-fed pigs (5 weeks old) were randomly assigned to one of two study groups: control C, n = 4, or aluminum treated Al, n = 4. Daily intravenous injections of either aluminum 1.5 mg/kg/day (Al group) or vehicle only (C group) were given during the 8-week duration of the study. The radiographic findings which appeared in the aluminum-treated group and not in the controls consisted of areas of sclerosis in the submetaphyseal regions and the periphery of epiphyses. In addition there was separation of the anterior tibial tubercle. The growth plates did not increase in width despite the presence of osteomalacia and histologic evidence of extensive deposition of aluminum in bone. The area of sclerosis visualized in the radiographs correlated histologically with thickened bony trabeculae. The increased width of these trabeculae is attributable to an increase in primary spongiosum and broadened seams of osteoid.

Transhepatic hormone levels in the portacaval shunted pig—the effects of arginine upon gastrin and glucagon release

Hypergastrinemia and hyperglucagonemia follow portacaval shunt (PCS) or cirrhosis in man and experimental animals. The cause is unknown although portal diversion and hepatic dysfunction are suggested. In these studies transhepatic techniques were used to define the hepatic handling of basal and arginine-stimulated gastrin and glucagon levels in sham-operated and portacaval-shunted pigs and in a group of pair-fed sham-operated pigs. After PCS, basal gastrin levels were lower than those in sham-operated animals but were also lower in the pair-fed group, suggesting that the change resulted from partial starvation. Arginine-stimulation caused a rise in hepatic venous levels in PCS and in pair-fed pigs and in portal venous levels in shamoperated pigs. These data also suggested a response to diminished intake in PCS pigs. There was an immediate transitory rise in portal immunoreactive glucagon (Unger 30K) after PCS and a subsequent rise from the 4th postoperative day in all circulations. Arginine stimulation caused in sham-operated and PCS pigs a biphasic rise in the portal circulation and a later rise in the arterial circulation in PCS pigs. These data suggest that the effect of PCS upon gastrin levels is associated with the impaired appetite while the effect upon glucagon is the result of diversion past the liver.