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ANIMAL NUTRITION |
* Department of Animal and Poultry Science, University of Guelph, Guelph, ON, Canada N1G 2W1; and
and
Degussa AG, D-63403 Hanau, Germany
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Abstract |
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Key Words: Lysine • Nonstarch Polysaccharides • Pectin • Pigs • Protein Deposition • Threonine
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionLiterature Cited |
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). The use of ileal AA digestibility values in feed formulations assumes that the utilization of ileal digestible AA intake for the various body functions is not influenced by dietary AA source. Recent studies suggest that body protein deposition (PD) in pigs is influenced by dietary AA source, even when the apparent ileal digestible AA intake is kept constant across dietary AA sources (Batterham et al., 1990; Beech et al., 1991; Grala et al., 1998). These dietary effects may be attributed to specific nonstarch polysaccharides (NSP) or other antinutritional factors (Schulze et al., 1995).
It is well documented that feeding some types of NSP can increase endogenous N and AA losses at the terminal ileum of nonruminant animals (Mosenthin et al., 1994; Schulze et al., 1995). The type and source of NSP can influence the quantity and composition of endogenous gut protein secretion, as well as subsequent reabsorption, resulting in decreases in apparent ileal AA digestibility (Jansman et al., 2002). These antinutritional effects are more severe for water-soluble than for insoluble NSP (Larsen et al., 1994). However, little information is available on effects of dietary NSP on the utilization of apparent ileal digestible AA intake for the various body functions.
The objective of the present study was to determine the effect of feeding graded levels of pectin, a partially methoxylated hydrophilic polymer of galacturonic acid and a highly viscous, water-soluble NSP, on the utilization of apparent and standardized ileal digestible Thr and Lys intake for PD, and thus the dietary requirement for Thr and Lys.
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Materials and Methods |
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. Two groups of eight Yorkshire barrows of similar genetic background and growth potential were obtained from the University of Guelph Arkell Swine Research Center. The two groups of pigs had an average initial BW of 14.3 ± 1.4 kg (Lys study) and 17.2 ± 1.3 kg (Thr study), and were used to evaluate Lys and Thr utilization, respectively, in two separate N balance studies. Pigs were penned individually in floor pens (0.9 m x 1.5 m), with slatted plastic flooring (Möhn et al., 2000) and allowed a 7-d adaptation period. Within each N balance study, barrows were assigned to each of five dietary treatments during five subsequent experimental periods according to a crossover design; within each 14-d experimental period, each diet was fed to one or two pigs. Throughout the experiment, pigs had free access to water from nipple drinkers. At the conclusion, the mean BW were 43.0 ± 3.6 kg and 46.5 ± 4.2 kg for pigs in the Lys and Thr studies, respectively.
Diets and Feeding
Five soybean meal- and cornstarch-based, semisynthetic diets were formulated in which either Lys or Thr was the first-limiting AA. Diets contained (as-fed basis) 0 (control), 4, 8, or 12% pectin or 8% cellulose (as a source of insoluble NSP; another control treatment) as a substitute to cornstarch (Tables 1 and 2). In both N balance studies, 25% soybean meal was included as the only protein source. Dietary AA content was similar across all diets within the Lys and Thr study. In both studies, synthetic AA were added to the diets so that the ratios of standardized ileal digestible contents of essential AA to Lys exceeded the recommendations of Wang and Fuller (1989) by at least 20%, except for diets in the Thr study and when Thr was formulated to be the first-limiting AA (Table 2). Calculated dietary DE content was 16.5 MJ/kg for the control diet and 15.5 MJ/kg for diets containing pectin and cellulose (Tables 1 and 2). Titanium dioxide (0.1%; Sigma-Aldrich Canada Ltd., Oakville, Ontario, Canada) was included in all diets as an indigestible index for determining fecal N excretion. All diets were supplemented with vitamins and minerals to exceed requirements according to NRC (1998). The calculated Ca and P contents in all experimental diets were 0.85 and 0.60% (as-fed basis), respectively. In both studies, diets containing 4 and 12% pectin were prepared from ingredients, whereas diets with the intermediate pectin levels were prepared by blending the diets with the extreme pectin levels in the appropriate proportions.
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). In brief, AID of AA and ileal and fecal nutrient digestibility were determined in the five experimental diets using five grower pigs fitted with T-cannulas at the distal ileal and according to a Latin square design. Actual endogenous AA losses were quantified using the homo-arginine method. Experimental procedures were described previously by Nyachoti et al. (1997). The TID values were derived by correcting AID values for the actual endogenous ileal AA losses, and SID values were derived by correcting AID values for basal endogenous ileal AA losses only (Nyachoti et al., 1997; Zhu, 2003). In the digestibility study, the SEM for AID of Lys and Thr were 0.71 and 1.27%, respectively; these values were larger than the SEM for SID (0.70 and 1.10%, respectively) and TID (0.37 and 0.76%, respectively; Zhu, 2003).
Pigs were fed one of five experimental diets twice daily at 0830 and 1730, and feed allowances were adjusted for each period at 2.6 times maintenance energy requirements (NRC, 1998). Based on previous studies (Möhn et al., 2000; de Lange et al., 2001), energy intake did not limit PD.
Nitrogen Balance
In each experimental period, pigs were adapted to experimental diets for 7 d in floor pens, and then transferred into adjustable metabolism crates with Plexiglas siding (Möhn et al., 2000). Subsequent to a 2-d adaptation period in the metabolism crates, feces and urine were collected quantitatively over a 5-d period.
The urine was routed through the drainage point in the urine collection tray placed underneath the metabolism crates into containers via a funnel. To avoid contamination of urine with feces and hair losses, the funnels were lined with glass wool, supported by a plastic net. Urine was collected in tared bottles with 15 mL of 18 M sulfuric acid to lower the pH of urine to less than 3. For each successive 24-h collection period, a 5% aliquot was taken. Aliquots were pooled for each pig and N balance period, and stored at 4°C. At the completion of N balance periods, the pooled samples were sub-sampled for further analyses. Wasted feed was collected quantitatively using feed wastage trays placed underneath the feeders, pooled for each pig and N balance period, dried in an oven at 70°C to a constant weight, left over night to equilibrate moisture content, and weighed.
Feces were collected by a temporary fixation of polyethylene bags (2.27 kg; 15 cm x 30 cm), which were attached around the anus of the pigs. Bags were replaced at least twice daily, weighed, and stored frozen at –20°C. At the end of each N balance period, feces were pooled per pig, weighed, thawed for 24 h, and homogenized using a Hobart mixer (The Hobart Manufacturing Co. Ltd., Don Mills, Ontario, Canada), and water was added and reweighed. Two subsamples were taken from each homogenized sample. Samples were used for N-analysis in fresh material, and the other sample was weighed and freeze-dried for further analyses.
Chemical Analysis and Calculation of Body Protein Deposition
Representative feed samples were taken at each experimental period when the meals were prepared, and were pooled per dietary treatment at the completion of the experiment.
Nitrogen content in feed, feces, and urine were determined using the Kjeldahl method (AOAC, 1990). Amino acid content in feed was determined in the laboratories of Degussa (Degussa A.G., Hanau, Germany; Möhn et al., 2000). Because dietary N contents calculated from diet composition and analyzed N contents in diet ingredients were within 2.5% of analyzed values (Tables 1
and 2), calculated dietary N contents were used is subsequent calculations. In this manner unavoidable analytical error in determined N contents of feed ingredients and complete diets results in a systematic bias across all dietary treatments, rather than a random bias for each individual treatment.
Nitrogen retention (g/d) was calculated as N intake, considering feed allowance and feed wastage, minus N losses in feces and urine. Retained N values were converted to PD, assuming that retained body protein contained 16% N (NRC, 1998; Möhn et al., 2000). The Lys or Thr retention was calculated as PD x 7.08/100 (Möhn et al., 2000) or PD x 3.79/100 (de Lange et al., 2001), respectively.
Assessment of Lysine and Threonine Utilization
Average digestible Lys or Thr intakes (g/d) in the two N balance studies were calculated based on the average analyzed Lys or Thr contents across diets within the Lys and Thr study, respectively, and previously determined ileal digestibility of Lys and Thr in each of these diets (Zhu, 2003).
Disappearance of Lys (DISlys) or Thr (DISthr) was calculated to provide estimates of inevitable Lys and Thr catabolism (e.g., Möhn et al., 2000, de Lange et al., 2001). Values, expressed as fractions of TID Lys or Thr intake (%), were calculated as TID Lys or Thr intake minus Lys or Thr retained in PD and minus physical Lys or Thr losses. Physical Lys losses represented losses with skin and hair (4.0 mg/kg BW0.75; Moughan, 1999) and previously measured endogenous gut Lys losses, whereas physical Thr losses with skin and hair were 3.0 mg/kg BW0.75 (Moughan, 1999) plus previously measured endogenous gut Thr losses (Zhu, 2003). These disappearance values were identical to those calculated from apparent digestible AA intake minus AA retained in body protein and minus skin and hair AA losses.
The efficiency of utilizing SID Lys or Thr intake above maintenance requirements for PD (Klys or Kthr) were calculated to be consistent with estimates of efficiency suggested by NRC (1998). These values were calculated from Lys or Thr retained in PD, divided by SID Lys or Thr intake above Lys or Thr maintenance requirements. It was assumed that the maintenance Lys and Thr requirements were 36 and 54 mg/kg BW0.75, respectively (NRC, 1998).
Statistical Analyses
Statistical analysis was performed using the GLM procedures of SAS (SAS Inst., Inc., Cary, NC) according to the model Y = µ + Trt + Per + Anim + b x Lys (or Thr) intake + 
, where µ represents the overall mean, Trt represents treatment effects (n = 5), Per represents period effects (n = 5), and Anim represents pigs effects (n = 7 for Lys study; n = 8 for Thr study). The value b is a regression coefficient to adjust for slight differences in Lys or Thr intake among observations, and is the residual error. Using the Bartlett’s and Levene’s tests, it was confirmed that variances were homogenous across treatments. Regression analyses and orthogonal contrast analyses were used to evaluate effects of dietary pectin level and of added dietary cellulose on the various response criteria.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionLiterature Cited |
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). Two additional observations were missing due to incomplete collection of urine or feces (Tables 3 and 4).
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and 2). Because the inclusion level of N sources was the same across all experimental diets, it was assumed that the observed differences in analyzed CP content between diets reflected analytical or sampling errors and the same dietary CP content (12.93%; calculated value) was assumed for all diets for calculating N balance. All Lys and Thr in the Lys- and Thr-limiting diets, respectively, were supplied by soybean meal. Because CP analyzes confirmed that the inclusion level of soybean meal was the same in all diets, differences in analyzed Lys content between the diets within the Lys study (Table 1) and in analyzed Thr content between diets within the Thr study (Table 2), were assumed to reflect sampling or analytical errors. Based on Lys-limiting diets, the analyzed Lys and Thr contents seemed to decrease with increase dietary pectin inclusion level; however, this relationship was not observed in the Thr-limiting diets and the diets evaluated in the digestibility study (Zhu, 2003), suggesting that differences in analyzed AA contents across diets resulted from random effects rather than systematic effects of dietary pectin level. Therefore, the average dietary contents of 0.77% Lys in the Lys study and 0.50% Thr in the Thr study were used to calculate the various aspects of AA utilization for each of the dietary treatments.
In the Lys study, mean intakes of CP and total Lys were 129 g/d (SE = 1.9) and 7.9 g/d (SE = 0.12), respectively, whereas mean pig BW was 28 kg (SE = 0.2; Table 3). In the Thr study, mean intakes of CP and total Thr were 131 g/d (SE = 0.9) and 5.04 g/d (SE = 0.04), respectively, whereas mean pig BW was 32 kg (SE = 0.1; Table 4). There were no differences (P > 0.10) in initial BW, or of CP or AA intake, among treatments within each of the two N balance studies (Tables 3 and 4).
When Lys intake was included as a covariable, the efficiency of Lys utilization for PD was not influenced by period (P > 0.10). The efficiency of Thr utilization increased with period (P < 0.05). This effect was observed even when Thr intake was used as covariable. In the Lys study, there were no animal effects on PD and Lys utilization efficiency. In the Thr study, PD and Thr utilization efficiency differed among animals (P < 0.05). In the two N balance studies, and when pig effects were excluded from the statistical models, no interaction was observed between experimental period and dietary treatment, suggesting that the animals’ changing nutrient requirements with increasing BW did not influence responses to dietary treatments.
Utilization of Ileal Digestible Lysine for Whole-Body Protein Deposition
With increasing dietary pectin levels, daily AID and SID Lys intake were estimated to decrease linearly (P < 0.01), whereas estimated ileal endogenous gut Lys loss increased linearly (P < 0.01) from 0.37 to 0.77 g/d (Table 3). Daily intake of TID Lys was similar across treatments (Table 3). Adding 8% cellulose to the diet did not influence estimated AID, SID, and TID Lys intakes or endogenous gut Lys losses (P > 0.10) (Table 3).
Fecal protein excretion increased linearly (P < 0.01) with dietary pectin level, ranging from 8.8 to 14.6 g/d (Table 3). Including 8% cellulose in the diet increased (P < 0.05) fecal CP excretion as well, to 13.7 g/d (Table 3). Urinary CP excretion was not influenced (P > 0.10) by dietary pectin and cellulose levels. Across treatments, mean urinary CP excretion was 29.8 ± 1.03 g/d (Table 3). Consequently, PD decreased linearly (P < 0.01) with increasing pectin levels from 90.7 g/d to 85.3 g/d, whereas adding 8% cellulose to the diet did not influence PD (P > 0.10) in pigs fed a Lys-limiting diet (Table 3).
Estimated daily DISlys was not influenced (P > 0.10) by dietary pectin level (overall mean 0.84 ± 0.09 g/d). Estimated DISlys, expressed as a daily amount or fractions of AID Lys intake or of TID Lys intake, was not influenced (P > 0.10) by dietary pectin level either, with overall mean values of 11.7 ± 1.25 and 10.8 ± 1.15%, respectively (Table 3). Including 8% cellulose in the diet did not influence DISlys, and DISlys expressed as daily amount on a fraction of AID or TID intake, with 0.91 g/d, 12.4%, and 11.5%, respectively (Table 3; Figure 1). Estimated Lys utilization efficiency (Klys) was not influenced (P > 0.10) by dietary pectin level or by including 8% cellulose in the diets (overall mean 89.2 ± 3.4%; Table 3; Figure 2).
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). The quadratic effects (P < 0.05) indicate that these values reached a plateau at the highest dietary pectin levels. Estimated total ileal endogenous gut Thr loss increased linearly (P < 0.01) from 0.52 g/d to 0.98 g/d with dietary pectin level. Adding 8% cellulose to the diet did not influence estimated AID and SID Thr intake (P > 0.10), whereas TID Thr intake for the cellulose diet was higher than for the control diet (Table 4). An increased endogenous ileal Thr loss (P < 0.01) also was observed with the addition of 8% cellulose to the diet (Table 4).
Fecal CP excretion increased linearly (P < 0.01) with dietary pectin level, ranging from 10.4 to 17.5 g/d (Table 4). Including 8% cellulose in the diet also increased fecal CP excretion (P < 0.01) to 14.0 g/d (Table 4). Urinary CP excretion increased linearly (P < 0.01) with dietary pectin level ranging from 29.8 g/d to 35.1 g/d, whereas including 8% cellulose in the diet did not influence urinary CP excretion (P > 0.10; Table 4). Consequently, PD decreased linearly (P < 0.01) with increasing pectin levels from 93.4 to 76.7 g/d; PD also was decreased (P < 0.05) when 8% cellulose was added to the diet (Table 4; Figure 1).
Estimated DISthr, expressed as a daily amount or fractions of AID or TID Thr intake, were increased linearly (P < 0.01) with increasing dietary pectin level, from 0.58 to 0.93 g/d, 16.2 to 25.6%, and 14.2 to 20.4%, respectively. Including 8% cellulose in the diet increased DISthr, even though effects of cellulose were smaller than effects of pectin (P < 0.05; Table 4).
Estimated Thr utilization efficiency (Kthr) decreased linearly (P < 0.01) with dietary pectin level from 89.3% to 80.3%, Kthr decreased (P < 0.01) when 8% cellulose was added to the diet as well (Table 4; Figure 2). Across the five diets, Thr disappearance was correlated with ileal NDF plus pectin flow (r2 = 0.95) and fecal digestible NDF plus pectin intake (r2 = 0.90).
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionLiterature Cited |
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; Mosenthin et al., 1994; Zhu, 2003). Such negative effects are likely related to endogenous N loss and microbial fermentation in the gut (Schulze et al., 1995; McCullogh et al., 1998). However, to our knowledge the effect of dietary NSP on the utilization of ileal digestible AA intake for PD has not been evaluated. The dietary soluble NSP levels that were evaluated in the current study are rather extreme compared with levels in commercial pig diets. However, in diets containing large amounts of co-products from the food industry, such as wheat shorts and beet pulp, dietary soluble NSP level may approach 10% (Bach-Knudsen, 1997).
Among essential AA, metabolism and utilization of Thr are likely most severely influenced by dietary NSP effects on endogenous gut protein secretion and microbial activity in the intestinal lumen due to its high content in endogenous gut protein, and mucus in particular (de Lange et al., 1989; Lien et al., 1997). However, utilization of other AA that are present in endogenous secretions, such as cysteine and branch-chained AA (de Lange et al., 1989), may be influenced as well.
Pectin induces microbial fermentation in the upper and lower gut in growing pigs (Zhu, 2003). This can be attributed to pectin effects on digesta viscosity and passage rate, as well as pectin’s water-holding capacity and fermentability (Johansen et al., 1996). Dietary pectin intake, either directly or indirectly via microbial fermentation, induces intestinal morphology change, including hypertrophy of the small intestine (McCullogh et al., 1998), and increasing muscularis layer thickness and mucosal mass (Stark et al., 1996). Moreover, feeding NSP stimulates PD in visceral organs, especially in the upper and lower gut (Larsen et al., 1994) and endogenous protein secretion into the gut (de Lange et al., 1989; Schulze et al., 1995).
Threonine and Lysine Utilization for Body Protein Deposition
In the growing pig, PD is determined by the animal operational upper limit to PD, energy intake, or intake of the first-limiting essential nutrient (Moughan, 1999). In the two N balance studies, calculated daily intake of DE ranged from15.5 to 16.5 MJ across diets. Based on this level of DE intake, the potential PD, calculated according to Möhn et al. (2000), is 110 to 120 g/d, which is 10 to 20% greater than the observed PD in the current experiments. This suggests that Thr or Lys intake limited PD. The source of dietary energy varied slightly with diet NSP levels, which is likely to influence the animal’s endocrinology (Vaugelade et al., 2000). Apparently, those potential changes in endocrinology did not influence Lys utilization for PD. This suggests that the observed dietary effects on Thr utilization for PD are unlikely to be influenced directly by changes in the animal’s endocrinology as a result of NSP intake.
The observed period effect on Thr utilization for PD was consistent with a previous study (de Lange et al., 2001) and suggests that time or BW effects on Thr utilization for PD need to be explored further. De Lange et al. (2001) speculated that BW effects on maintenance Thr requirements are overestimated. In particular, the endogenous gut threonine losses need to be quantified more accurately and when careful consideration is given to experimental methodology (e.g., Nyachoti et al., 1997).
Estimated AA utilization efficiencies (Klys 89.2 %; Kthr 89.3 to 80.3%) in the current experiments were higher than the values obtained previously in our laboratory in serial slaughter studies (Möhn et al., 2000, Klys = 77%; de Lange et al., 2001, Kthr = 73.4%). Moreover, the values obtained in the current experiments were higher than those obtained by others in serial slaughter studies (Batterham et al., 1990, Klys = 73 to 75%; Beech et al., 1991, Kthr = 64%). These differences can be attributed to methodology and dietary protein sources. The N balance technique systematically overestimates N retention and, consequently, utilization of N and AA, compared with serial slaughter studies (Möhn et al., 2000; de Lange et al., 2001). This has been attributed to an underestimation of N losses with wasted feed and urinary and fecal N excretion (de Lange et al., 2001); however, the relative changes in PD and AA utilization are similar between N balances and serial slaughter observations (Möhn et al., 2000; de Lange et al., 2001). Across studies, Thr utilization seems influenced by dietary factors as well (Beech et al., 1991).
With increasing dietary pectin level, PD (Figure 1), dietary daily AID and SID intakes of Lys and Thr (Tables 3 and 4) were decreased linearly in both experiments, even though diets were equal in protein and AA contents and feed intake was constant across treatments. The decreased efficiencies of utilizing dietary protein and AA for PD reflected an increase in fecal N excretion in pigs fed Lys limiting diets, and in both urinary and fecal N excretion in pigs fed Thr-limiting diets. Fecal N excretion arises from the intake of truly undigested dietary protein, endogenous gut N losses, and excretion of bacterial protein (Varel et al., 1997; Moughan, 1999). Urinary N excretion, largely in the form of urea, arises primarily from minimum plus inevitable AA catabolism, catabolism of absorbed dietary AA that are in excess of requirements for PD, and N (NH3) generated during microbial fermentation in the intestinal lumen (Moughan, 1999).
As indicated by Zhu (2003), feeding pectin had little or no effect on true ileal N and AA digestibility, whereas it increased ileal endogenous gut N losses (Tables 3 and 4). However, these increases in ileal endogenous gut N losses do not explain the observed decrease in Kthr with increasing dietary pectin level as increases in ileal endogenous gut N losses are reflected in decreases in SID AA intake. Dietary pectin also might increase endogenous gut protein turnover because of increased losses of epithelial cells and increased ileal endogenous N secretions into the gut lumen. As a result, the amount of endogenous N that is reabsorbed is likely increased as well. This recycling of ileal endogenous N may increase first-pass catabolism of AA in the liver and possibly in intestinal tissue (Nyachoti et al., 1997; Fuller and Reeds, 1998). Moreover, endogenous N secretions into the hindgut represent a loss to the animal, and feeding pectin may increase these secretions. As a consequence, the net availability of AID AA intake for body PD may be decreased when ileal endogenous gut N losses or endogenous N secretions into the hindgut are increased (Grala et al., 1998). Because more of the first-limiting AA is catabolized, more of the other AA will be catabolized as well, resulting in increased urinary N excretion. This increase in AA catabolism associated with endogenous gut N losses is likely larger for Thr than for Lys. The Thr content in endogenous gut protein secretions is relatively large, due primarily to the high Thr content in mucus (Lien et al., 1997).
Microbial Fermentation in the Gut
It is recognized that the microflora are not confined to the large intestine, and that large populations of bacteria are present in the stomach, and in the lower part of the small intestine (Fuller and Reeds, 1998). Increased microbial mass and activity were observed at the distal ileum when the dietary pectin level was increased (Zhu, 2003), which is consistent with previous observations in pigs (Conway, 1994; Fuller and Reeds, 1998). Therefore, ileal AA digestibility reflects both enzymatic digestion and microbial fermentation in the gut lumen. A net increase in the degradation of dietary AA by microbes in upper gut will be reflected in increases in AID, SID, and TID of AA. Alternatively, microbial fermentation in the upper gut can result in a net yield of AA, which can decrease ileal AA digestibility or increase the net uptake of AA from the gut (Fuller and Reeds, 1998).
Microbes can use dietary ingested N and endogenous N, including urea, secreted into the gut as substrate (Mosenthin et al., 1992). Whether microbial fermentation in the gut results in a net yield or loss of AA to the animal will depend on the AA composition of N substrate, the AA composition of bacterial protein, and the net efficiency of microbial protein production (Fuller and Reeds, 1998). Moreover, the site of microbial fermentation should be considered. Microbial protein that is produced in the upper gut may be enzymatically digested and absorbed and used to provide AA to the host animal. Microbial protein that is produced in the hindgut will be of no benefit to the host. Based on these considerations, microbial fermentation in the upper gut can either increase or decrease available AA uptake by the host. Microbial fermentation in the lower gut represents a net loss of AA when microbes in the hind-gut use endogenous AA secreted into the hindgut as an N source.
The high correlation between Thr disappearance and ileal NDF plus pectin flow or fecal digestible NDF plus pectin intake suggests that feeding pectin stimulates endogenous AA losses from the hindgut, possibly via stimulation of microbial fermentation. Relationships between the various aspects of digestion and Thr utilization need to be evaluated in pigs fed diets that have a wide range of fermentation characteristics and varying effects on endogenous gut N losses.
For Lys-limiting diets, pectin level did not influence Klys, suggesting that microbial net synthesis of Lys, before the distal ileum, was compensating for potential increased Lys losses. Potential Lys losses can be the result of catabolism associated with endogenous N recycling and the use of endogenous Lys secreted into the gut as N substrate by microbes.
In pigs fed Thr-limiting diets and at similar AID and SID threonine intake, PD decreased with increasing dietary pectin level. This finding illustrates that the ileal AA digestibility assay does not always provide a good estimate of the available AA supply in pig diets. In particular, diet effects on the catabolism of AA associated with endogenous gut N losses and microbial fermentation in the upper and lower gut are not reflected in AID and SID of AA, or the combination of measured true ileal AA digestibility and endogenous ileal AA losses.
Diet effects on these aspects of AA metabolism and AA utilization for PD can be quite substantial for Thr and seem to be small for Lys. In addition, other effects of feeding ingredients on utilization of ileal digestible AA intake for PD should be considered, such as diet effects on the distribution of PD over the main body protein pools. When dietary fiber effects on Thr utilization are not considered, pork production efficiency may be compromised when pigs are fed high-fiber diets.
This study showed that ileal AA digestibility values are not always an accurate indicator of diet effects on AA utilization for PD in growing pigs. Dietary NSP effects on the utilization of ileal digestible AA intake for PD are substantial, and are larger for Thr than for Lys. These effects should be considered when evaluating the nutritional value of feedstuffs, and they imply that there are substantial dietary effects on the optimal balance among available AA in the diet, which should be considered in feed formulation. The underlying mechanisms need to be explored further.
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2 Correspondence—phone: 519-824-4120, ext. 56477; fax 519-836-9873; e-mail: cdelange{at}uoguelph.ca.
Received for publication February 10, 2004. Accepted for publication February 9, 2005.
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) or threonine (Thr;
) limiting diets and as influenced by added dietary pectin level (n = 6, 7, or 8 per data point; Tables 3