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Biomedical subjects

D L Harmon

Publications and source records attributed to D L Harmon.

At least 37 records · Page 2Linked to original sources
PubMed2001

Molecular identification of high-affinity glutamate transporters in sheep and cattle forestomach, intestine, liver, kidney, and pancreas.

Glutamate metabolism is essential to support many facets of metabolism. The objective of this study was to determine the tissue distribution of glutamate transporters known to support the tissue metabolism of glutamate. The expression of proteins capable of high-affinity glutamate transport (system X-(AG)) by epithelia isolated from the rumen, omasum, duodenum, jejunum, ileum, cecum, and colon and homogenates of liver, kidney, and pancreatic tissues from wethers (n = 4; BW = 28.4 +/- 8.4 kg) and steers (n = 3; BW = 426 +/- 32.3 kg) fed forage-based diets was evaluated by immunoblot analysis. Proteins EAAC1 (62, 93 kDa) and GLT-1 (142, 188, >202 kDa) were expressed by every tissue examined. In contrast, GLAST1 (140 kDa) was expressed only by the pancreas, and EAAT4 (67 kDa) was detected only in sheep brain. To corroborate protein expression data, the presence and size of transporter mRNA in ileal, liver, and pancreatic homogenates were evaluated by Northern analysis. GLAST1 mRNA (2.4, 4.3 kb) was detected only in the pancreas, whereas EAAC1 (2.2, 2.8 kb) and GLT-1 (12.1 kb) mRNA transcripts were detected in all three tissues. The expression of EAAT4 and GLT-1 mRNA was confirmed by reverse transcriptase-polymerase chain reaction analyses. Sequencing of the resulting partial-length ovine GLT-1 cDNA revealed 100% identity with the rat homolog. Overall, these data demonstrate that sheep and cattle share the same pattern of system X-(AG) transporter expression, which differed among tissues and transporter isoforms. Accordingly, these data provide the fundamental knowledge to initiate research that determines whether the expression of high-affinity glutamate transporters by ruminants is sensitive to ontogenic and(or) dietary regulation.

ATP-Binding Cassette Transporters↗
PubMed2001

Influence of alpha-linked glucose on sodium-glucose cotransport activity along the small intestine in cattle.

Thirteen steers (378+/-23 kg) were used in a split-plot experimental design to evaluate the effect of small intestinal carbohydrate on sodium-glucose cotransport in brush border membrane vesicles prepared from five equidistant sites along the small intestine. The steers consumed 7.2+/-0.4 kg/d ground fescue hay and soybean meal-based supplement and were infused ruminally or postruminally with a partial alpha-amylase starch hydrolysate (914.5+/-8.3 g/d) for 7 d. On d 7, five equidistant 1-m small intestinal sections were harvested and frozen in liquid N for later preparation of brush-border membrane vesicles. Maltase activity of the homogenate and vesicle preparations changed (P < 0.001; lowest in the duodenum, highest in the jejunum) and alkaline phosphatase decreased (P < 0.001) along the small intestine. With respect to the original homogenates, the vesicle preparations were enriched 9.80+/-0.83- and 7.64+/-0.67-fold for alkaline phosphatase and maltase, respectively; enrichments were not different between treatments (P = 0.76 and 0.39, respectively). However, alkaline phosphatase and maltase enrichment changed (P < 0.001) along the small intestine. Recoveries of alkaline phosphatase and maltase activities (25.0+/-0.2% and 19.5+/-0.2%, respectively) in the vesicle preparation were not affected (P = 0.29 and 0.21, respectively) by treatment but changed (P < 0.001) along the intestine. Recovery of protein in the vesicle preparation was 2.60+/-0.01% and was not affected by treatment or intestinal site. Sodium-glucose cotransport activity (220+/-44 pmol x mg(-1) x s(-1)) was not affected (P = 0.34) by treatment but did change (P < 0.001; lowest in the ileum, highest in the proximal and mid-jejunum) along the small intestine. Apparent Km of the sodium-glucose cotransporter for glucose was 62.8+/-5.8 microM. The specific activity of maltase was highest in the jejunum, and sodium-glucose cotransport was highest in the first two jejunal sites. However, duodenal maltase activity was lowest and ileal sodium-glucose cotransport activity was lowest. Sodium-glucose cotransport activity may limit small intestinal starch assimilation in the distal small intestine. It does not seem that glucose arising from carbohydrate hydrolysis regulates activity of sodium-dependent glucose transport in cattle.

Alkaline Phosphatase↗
PubMed2000

Community-living nonagenarians in northern ireland have lower plasma homocysteine but similar methylenetetrahydrofolate reductase thermolabile genotype prevalence compared to 70-89-year-old subjects.

This cross-sectional study assessed relationships between plasma homocysteine, 'thermolabile' methylenetetrahydrofolatereductase (MTHFR) genotype, B vitamin status and measures of renal function in elderly (70-89 years) and nonagenarian (90+ years) subjects, with the hypothesis that octo/nonagenarian subjects who remain healthy into old age as defined by 'Senieur' status might show reduced genetic or environmental risk factors usually associated with hyperhomocysteinaemia. Plasma homocysteine was 9.1 micromol/l (geometric mean [GM]) for all elderly subjects. Intriguingly, homocysteine was significantly lower in 90+ (GM; 8.2 micromol/l) compared to 70-89-year-old subjects (GM; 9.8 micromol/l) despite significantly lower glomerular filtration rate (GFR) and serum B12 in nonagenarian subjects and comparable MTHFR thermolabile (TT) genotype frequency, folate and B6 status to 70-89-year-olds. For all elderly subjects, the odds ratio and 95% confidence intervals for plasma homocysteine being in the highest versus lowest quartile was 4.27 (2.04-8.92) for age <90 compared >90 years, 3.4 (1.5-7.8) for serum folate <10.7 compared >10.7nmol/l, 3.0 (0.9-10.2) for creatinine >140 compared <140 umol/l and 2.1 (1.0-4.4) for male sex. This study shows that plasma homocysteine does not invariably increase with age. Compared to similarly enlisted 70-89-year-olds, apparently well, mentally alert, community-living 90+ year olds approximating 'Senieur' status, show lower homocysteine, which is unexplained by renal function, TT genotype and B vitamin status, suggesting that lower homocysteine may be associated with survival.

Age Distribution↗
PubMed2000

Influence of fiber fermentability on nutrient digestion in the dog.

Eight mature dogs (17.2 +/- 0.2 kg) surgically fitted with ileal T-cannulas were used in a replicated 4-x-4 Latin-square-design experiment to evaluate nutrient disappearance at the terminal ileum and through the digestive tract. Two fiber types, cellulose, a crystalline, slowly fermented fiber, and pectin, a soluble, rapidly fermented fiber, were fed in different increments, and the effects on nutrient availability were assessed. Treatments included 1) 100% cellulose, 2) 66% cellulose and 33% pectin, 3) 66% pectin and 33% cellulose, and 4) 100% pectin. Fiber was added at 10% of diet dry matter (DM). Diets were fed at 100% of ME for maintenance and offered at 0730 and 1730 h. All periods were 21 d, which included 3 d of diet transition and 7 d of adaptation. Daily DM intake was 210 +/- 5 g. Total tract and large-intestine DM digestibility increased linearly (P < 0.01) with increased pectin. These changes in DM digestion were largely the result of changes in fiber digestion. Fermentation of total dietary fiber in the large intestine went from less than zero to 39% of ileal flow (linear, P < 0.01). Total-tract crude-protein digestibility decreased linearly (P < 0.01) with increased pectin. This study demonstrated that fiber fermentability significantly affects digestion in the dog. Increasing fermentable fiber increased the digestion of DM and energy. However, increased fiber fermentability inversely affects crude protein digestibility. The lower crude-protein digestibility could be attributed to larger microbial protein excretion as a result of greater fermentation of pectin versus cellulose.

Ammonia↗
PubMed2000

Dietary carbohydrate source and energy intake influence the expression of pancreatic alpha-amylase in lambs.

In ruminants, pancreatic alpha-amylase is the primary enzyme responsible for the initial hydrolysis of alpha-linked glucose in the small intestinal lumen. The objective of this experiment was to examine the effects of altered dietary starch and energy supply on the expression of pancreatic alpha-amylase mRNA, protein and activity in lambs. Wether lambs (n = 24; 28 +/- 0.5 kg body weight) were fed low or high starch diets at 1.2 or 1.8 x net energy of maintenance for at least 28 d before tissue collection. Lambs fed the high energy/high starch diet tended to have more pancreatic alpha-amylase protein (54.5 kDa; P: = 0.08) and had greater activity (P: = 0.03), but alpha-amylase mRNA (1.6 kb) tended to be lower (P: = 0.17). Additionally, rumen fluid total short-chain fatty acid concentration was greater (P: = 0.04) and plasma glucose concentration tended to be greater (P: = 0.07) in lambs fed the high energy/high starch diet. However, pancreatic trypsinogen protein (25. 5 kDa) and jejunal maltase activity were not influenced by dietary treatment, suggesting that different regulatory systems are involved in regulating the tissue protein or activity levels of these two enzymes compared with alpha-amylase. These data suggest that dietary regulation of pancreatic alpha-amylase expression in ruminants is complex and probably regulated by transcriptional and post-transcriptional events.

Animals↗
PubMed2000

Efficacy of laidlomycin propionate in low-protein diets fed to growing beef steers: effects on steer performance and ruminal nitrogen metabolism.

We conducted two experiments to evaluate the effect of the ionophore laidlomycin propionate (LP) on steer performance and ruminal N metabolism. Experiment 1 was a 91-d growth study evaluating the growth and ruminal characteristics of steer calves consuming supplemental LP. Steers (n = 96; 255 +/- 3 kg; four steers/pen; six pens/treatment) were used in a randomized complete block design with a 2 x 2 factorial arrangement of treatments consisting of two levels of dietary CP (formulated to be 10.5 and 12.5% of DM) with and without LP (11 mg/kg diet DM). Ruminal fluid was collected via stomach tube on d 91 from one steer randomly selected from each pen. No CP x LP interactions were observed with performance data (P > .64). Final weight and total gain were greater (P < .07) for 12.5% CP and LP compared with 10.5% CP and control steers, respectively. Also, DMI was increased (P = .08) with 12.5% CP but not with LP supplementation (P = .36). In addition, ADG and gain:feed ratio were greater (P < .03) for both 12.5% CP and supplemental LP. Ruminal NH3 N concentration was greater (P < .09) with 12.5% CP and LP. Total VFA concentration and molar proportion of acetate were not affected by treatment (P > .11). However, propionate concentration was increased (P < .09) with 12.5% CP and LP, and acetate:propionate was lower (P = .02) with LP supplementation. In Exp. 2, six steers were used in a replicated 3 x 3 Latin square design to compare ruminal fermentation and protein degradation in steers without ionophore feeding or adapted to LP or monensin. In vitro deamination of amino acids by adapted ruminal microbes was also assessed. Ionophore supplementation decreased (P = .07) ruminal NH3 N concentration compared with control steers, and LP increased (P = .02) ruminal NH3 N compared with monensin. Molar proportion of acetate was decreased (P = .02) and propionate increased (P = .01) with ionophore treatment. Consequently, ionophore supplementation depressed the acetate:propionate ratio (P = .01). In situ degradation rate of soybean meal (SBM) CP was greater (P = .09) with ionophore treatment, but estimates of SBM undegradable intake protein were not altered by treatment (P > .25). Microbial specific activity of net NH3 N release and alpha-amino N degradation were decreased (P < .04) with ionophores. Based on this study, LP and monensin did not affect the extent of ruminal degradation of SBM CP but decreased amino acid deamination.

Animal Feed↗
PubMed2000

Influence of the novel urease inhibitor N-(n-butyl) thiophosphoric triamide on ruminant nitrogen metabolism: I. In vitro urea kinetics and substrate digestion.

Two in vitro digestion experiments were conducted to evaluate the influence of the novel urease inhibitor N-(n-butyl) thiophosphoric triamide (NBPT) on in vitro urea kinetics, substrate digestion, and fermentation characteristics. In Exp. 1, in vitro incubations were conducted in 50-mL test tubes containing .25 g of ground fescue hay to which 0, 6.5, 13, 26, or 52 mg of NBPT in a buffered ruminal fluid innoculum was added. Tubes were incubated in triplicate at 39 degrees C and replicated on consecutive days, with NH3 N and urea concentrations measured at 0, 10, 30, 60, 120, 240, and 360 min. Samples for VFA analysis were collected at 6 h, and incubations were continued through 48 h to estimate true digestibility (based on NDF analysis). Increasing the dose of NBPT tended (P < .12) to linearly depress the rate of urea hydrolysis and decreased (P < .0004) subsequent NH3 N formation. Although total VFA concentration at 6 h increased linearly (P < .03), acetate:propionate and estimated true digestibility decreased (P < .01) with increasing NBPT concentration. In Exp. 2, we compared in vitro urea kinetics and digestion of forage-only or mixed forage-grain substrates in response to addition of NBPT. In vitro incubations were conducted in 50-mL test tubes containing either .5 g of ground fescue hay or .5 g of a ground fescue hay and ground corn mixture (50:50, DM basis) to which 0, 6.5, 13, 26, or 52 mg of NBPT in a buffered ruminal fluid innoculum was added. Tubes were incubated in triplicate at 39 degrees C and replicated on consecutive days, with NH3 N and urea concentrations measured at 0, .5, 1, 2, 4, 8, 12, 24, and 48 h. At 48 h, samples for VFA analysis were collected and true digestibility (based on NDF analysis) was estimated. No (P > .10) NBPT dose x substrate interactions were detected. Increasing the dose of NBPT depressed (P < .003) the rate of urea hydrolysis and subsequent NH3 N formation, regardless of substrate. Although total VFA concentration was unaffected (P > .10), the acetate:propionate and estimated true digestibility decreased (P < .002) with higher NBPT addition. In both experiments, the rate of urea degradation was not different (P > .20) from zero for the 26 and 52 mg NBPT treatments, indicating that nearly complete inhibition of urease had been achieved. We conclude that NBPT can be used to reduce the rate of NH3 N release from dietary urea and, thereby, offers the potential to improve nonprotein nitrogen utilization in ruminants.

Animal Feed↗
PubMed2000

Influence of the novel urease inhibitor N-(n-butyl) thiophosphoric triamide on ruminant nitrogen metabolism: II. Ruminal nitrogen metabolism, diet digestibility, and nitrogen balance in lambs.

Three lamb metabolism experiments were conducted to investigate the effects of chronic administration of the novel urease inhibitor N (n-butyl) thiophosphoric triamide (NBPT) on ruminal N metabolism, fermentation, and N balance. In Exp. 1, ruminally cannulated wethers (n = 28; 45.0 +/- .9 kg) were administered one of seven doses of NBPT (0 [control], .125, .25, .5, 1, 2, or 4 g of NBPT daily) and fed a common cracked corn/cottonseed hull-based diet twice daily containing 2% urea at 2.5% of initial BW for the duration of the 15-d experiment. Overall, NBPT decreased (linear P < .0001; quadratic P < .001) ruminal urease activity, resulting in linear increases (P < .0001) in ruminal urea and decreases in ruminal NH3 N concentrations. However, the detection of an NBPT x day interaction (d 2 vs 15; P < .01) indicated that this depression in urea degradation diminished as the experiment progressed. Increasing NBPT linearly decreased (P < .01) total VFA concentrations on d 2 of the experiment, but it had no effect (P > .10) on d 15. Increasing NBPT had no effect (P > .10) on DM or ADF digestibilities, but it linearly decreased (P < .01) N digestibility. Supplementing NBPT produced a linear increase (P < .05) in urinary N excretion and a linear decrease (P < .01) in N retention. In Exp. 2, ruminally cannulated wethers (n = 30; 46.8 +/- .6 kg) were fed one of two basal diets (2.0 vs 1.1% dietary urea) at 2.5% of initial BW and dosed with either 0 (control), .25, or 2 g of NBPT daily for the duration of the 15-d experiment. There were no NBPT x dietary urea interactions (P > .10) for Exp. 2. Increasing NBPT depressed (linear and quadratic P < .0001) ruminal urease activity, producing linear (P < .0001) increases in urea N and linear decreases in NH3 N in the rumen. As in Exp. 1, an NBPT x day interaction (P < .05) was noted for urea, NH3 N, and total VFA concentrations; the maximum response to NBPT occurred on d 2 but diminished by d 15 of the experiment. Administration of NBPT did not influence (P > .10) DM, ADF, or N digestibilities in Exp. 2. In Exp. 3, wether lambs (n = 30; 26.4 +/- .7 kg) were subjected to the same treatment regimen as in Exp. 2 for a 14-d N balance experiment. Although several NBPT x dietary urea interactions (P < .05) were noted, increasing NBPT did not affect (P > .10) N digestibility. Administration of NBPT quadratically increased (P < .10) urinary N excretion, producing a linear decrease (P < .05) in N retention. These results suggest that although NBPT is capable of inhibiting ruminal urease short-term, the ruminal microflora may be capable of adapting to chronic NBPT administration, thereby limiting its practical use in improving the utilization of dietary urea.

Ammonia↗
PubMed1999

Localization of the gene for autosomal recessive congenital hereditary endothelial dystrophy (CHED2) to chromosome 20 by homozygosity mapping.

Congenital hereditary endothelial dystrophy (CHED) is a corneal disorder that presents with diffuse bilateral corneal clouding. Vision may be severely impaired, and many patients require corneal transplantation. Both autosomal dominant (AD) and autosomal recessive (AR) forms of the disorder have been described. The gene responsible for AD CHED (HGMW-approved symbol CHED1) has been mapped to the pericentromeric region of chromosome 20. Investigating a large, consanguineous Irish pedigree with autosomal recessive CHED, we have previously excluded linkage to this AD CHED locus. We now describe a genome-wide search using homozygosity mapping and DNA pooling. Evidence of linkage to chromosome 20p was demonstrated with a maximum lod score of 9.30 at a recombination fraction of 0.0 using microsatellite marker D20S482. A region of homozygosity in all affected individuals was identified, narrowing the disease gene locus to an 8-cM region flanked by markers D20S113 and D20S882. This AR CHED (HGMW-approved symbol CHED2) disease gene locus is physically and genetically distinct from the AD CHED locus.

Chromosome Mapping↗
PubMed1999

Methionine synthase D919G polymorphism is a significant but modest determinant of circulating homocysteine concentrations.

Elevation in plasma homocysteine concentration has been associated with vascular disease and neural tube defects. Methionine synthase is a vitamin B(12)-dependent enzyme that catalyses the remethylation of homocysteine to methionine. Therefore, defects in this enzyme may result in elevated homocysteine levels. One relatively common polymorphism in the methionine synthase gene (D919G) is an A to G transition at bp 2,756, which converts an aspartic acid residue believed to be part of a helix involved in co-factor binding to a glycine. We have investigated the effect of this polymorphism on plasma homocysteine levels in a working male population (n = 607) in which we previously described the relationship of the C677T "thermolabile" methylenetetrahydrofolate reductase (MTHFR) polymorphism with homocysteine levels. We found that the methionine synthase D919G polymorphism is significantly (P = 0.03) associated with homocysteine concentration, and the DD genotype contributes to a moderate increase in homocysteine levels across the homocysteine distribution (OR = 1.58, DD genotype in the upper half of the homocysteine distribution, P = 0.006). Unlike thermolabile MTHFR, the homocysteine-elevating effects of the methionine synthase polymorphism are independent of folate and B(12) levels; however, the DD genotype has a larger homocysteine-elevating effect in individuals with low B(6) levels. This polymorphism may, therefore, make a moderate, but significant, contribution to clinical conditions that are associated with elevated homocysteine.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1999

Genetic analysis of the thermolabile variant of 5, 10-methylenetetrahydrofolate reductase as a risk factor for ischemic stroke.

Mild hyperhomocysteinemia is a risk factor for atherosclerotic vascular disease. Homozygosity for the C677T mutation in the gene for 5,10-methylenetetrahydrofolate reductase (MTHFR) is frequently associated with hyperhomocysteinemia, particularly in individuals with low levels of serum folate, and has been directly associated with cardiovascular disease in certain populations. The purpose of this study was to establish whether the C677T mutation, which causes thermolabile MTHFR, is a risk factor for ischemic stroke in the Irish population. The homozygous C677T genotype has previously been associated with coronary heart disease in Ireland. We collected blood from 174 individuals (minimum age 60 years) who had suffered an ischemic stroke that was confirmed by computed tomography brain scan. Control subjects (n=183) aged >/=60 years, who had never suffered a stroke or transient ischemic attack, were recruited from hospitals and active retirement groups in the same geographical area. MTHFR genotypes were determined and other known risk factors for stroke were documented. In the control group, the frequency of subjects with the homozygous C677T genotype was 10.4%. In patients who had suffered ischemic stroke, the frequency was 15.5%. This difference was not statistically significant. The odds ratio of stroke for C677T homozygotes, with other genotypes as a reference group, was 1.59, 95% CI=0.85, 2.97. The data indicate that the homozygous C677T MTHFR genotype is at most a moderate risk factor for ischemic stroke.

Aged↗
PubMed1999

Nutritional evaluation of poultry by-product meal as a protein source for ruminants: small intestinal amino acid flow and disappearance in steers.

Six Angus steers (260+/-4 kg initial BW) fitted with ruminal, duodenal, and ileal cannulas were used in a 6 x 6 Latin square design to evaluate the effect of feeding poultry by-product meal (PBM) on small intestinal flow and disappearance of amino acids. The diets were provided at 2% of BW on a DM basis, formulated to contain 11.5% CP, and consisted of 49% corn silage, 36% cottonseed hulls, and 15% supplement on a DM basis. Supplements were formulated to contain 37% CP with sources of supplemental N being soybean meal (100% SBM) and 0, 25, 50, 75, and 100% PBM, with urea used to balance for N. Duodenal flow of all amino acids increased linearly (P < .07) as PBM increased in the diet and, except for His, increased (P < .09) for 100% PBM compared with 100% SBM. Similar results were observed for duodenal flow of nonbacterial amino acids, which linearly increased (P < .05) with PBM and were greater (P < .05) for 100% PBM than for 100% SBM. Soybean meal increased (P < .09) the duodenal flow of nonbacterial Lys compared with 0% PBM, and 0% PBM increased (P < .04) flow of Val, Ala, and Pro compared with 100% SBM. Duodenal bacterial essential, nonessential, and total amino acid flows were not affected (P > .80) by PBM; however, they were greater (P < .02) for 100% SBM than for 100% PBM. In addition, nonessential and total bacterial amino acid flows were increased (P < .06) for 100% SBM compared with 0% PBM. Small intestinal disappearance of Lys and Pro increased linearly (P < .09) as PBM increased, and 100% PBM increased (P < .07) disappearance of Arg and Ala compared with 100% SBM. Supplemental N source had no effect (P > .31) on apparent small intestinal disappearance of essential, nonessential, and total amino acids. These data suggest that when PBM, SBM, and urea were used as sources of supplemental N, the daily disappearance of amino acids from the small intestine of steer calves consuming a corn silage- and cottonseed hull-based diet was similar.

Amino Acids↗
PubMed1999

Alkaloid binding and activation of D2 dopamine receptors in cell culture.

Ergot and pyrrolizidine alkaloids, either extracted from endophyte-infected tall fescue, synthesized, or purchased commercially, were evaluated in cultured cells to estimate their binding to the D2 dopamine receptor and subsequent effects on cyclic AMP production in GH4ZR7 cells, transfected with a rat D2 dopamine receptor. Ergopeptide alkaloid (alpha-ergocryptine, bromocryptine, ergotamine tartrate, and ergovaline) inhibition of the binding of the D2-specific radioligand, [3H]YM-09151-2, exhibited inhibition constants (K(I)) in the nanomolar range, whereas dopamine was less potent (micromolar). The lysergic acid amides (ergine and ergonovine) were 1/100th as potent as the ergopeptide alkaloids. Ergovaline and ergotamine tartrate were equally effective in inhibiting vasoactive intestinal peptide (VIP)-stimulated cyclic AMP production, with consistent nanomolar effective concentration (EC50) values. The remaining ergopeptide alkaloids (alpha-ergocryptine and bromocryptine), lysergic acid amides (ergonovine and ergine), and dopamine were 1/100th as potent. Two representative pyrrolizidines, N-formylloline and N-acetylloline, exhibited no binding activity at the D2 dopamine receptor or effects on the cyclic AMP system within the concentration ranges of nanomolar to millimolar. Our results indicate that the commercially available ergot alkaloids ergotamine tartrate and ergonovine may be used interchangeably in the D2 dopamine receptor system to simulate the effects of extracted ergovaline and ergine and to examine responses in receptor binding and the inhibition of cyclic AMP.

Animals↗
PubMed1999

Estimating true digestibility of nonstructural carbohydrates in the small intestine of steers.

Four Angus steers (318 +/- 16 kg) fitted with ruminal, duodenal, and ileal cannulas were used in a 4 x 4 Latin square design to determine carbohydrate disappearance from the small intestine (SI). Steers were fed fescue hay at 1.8% of BW and abomasally infused with starch hydrolysate (SH) at 10, 20, or 40 g/h or glucose (G) at 30 g/h. Starch hydrolysate was raw cornstarch digested by a heat-stable alpha-amylase. Experimental periods were 10 d with 6 d of adaptation, 3 d of digesta and feces collection, and 1 d of rest. Glucose (% of infused) had greater (P < .001) apparent small intestinal and postruminal disappearance (% of infused) compared with 20 and 40 g/h SH. Starch hydrolysate infusion linearly increased (P < .001) apparent SI, large intestinal (LI), and total intestinal starch disappearance (g/d) and quadratically increased (P < .003) apparent SI and total intestinal starch disappearance (% of infused). Ileal starch flow from infusion increased quadratically (P < .03) as SH infusion increased. True SI and total intestinal starch disappearance increased linearly (P < .001; g/d) with SH infusion. However, SH infusion quadratically decreased (P < .02) efficiency of true SI starch disappearance (% of infused). True LI starch disappearance (g/d and % of infused) quadratically increased (P < .03) as SH infusion increased. These data demonstrate that, even in animals fed all-forage diets, there is a significant flow of alpha-glucosides, and these need to be considered when evaluating intestinal carbohydrate digestion.

Animals↗
PubMed1999

Net nutrient flux in visceral tissues of lambs fed diets differing in supplemental nitrogen source.

Eight multicatheterized wethers (35.9 +/- .8 kg BW) were used in a replicated 4 x 4 Latin square design to measure N retention and net uptake and release of plasma metabolites across the portal-drained viscera (PDV), hepatic (HEP), and total splanchnic (TS) tissues in response to changes in supplemental N source. Treatments selected to provide different amounts of undegradable intake protein (UIP) were urea, soybean meal (SBM), poultry by-product meal (PBM), and bloodmeal:corn gluten meal (BMCGM; 50:50 CP basis). Diets (urea, SBM, PBM, and BMCGM) contained 12.9, 13.8, 13.6, and 13.2% CP, respectively. Periods were 10 d, with total feces and urine collected on d 7 to 10 and blood sampled on d 10. Wethers were fed at 2% of BW in 12 daily portions. Nitrogen retention was 2.2, 3.3, 4.1, and 4.4 g/d for urea, SBM, PBM, and BMCGM, respectively. Urea had less (P < .01) N retention than SBM, PBM, and BMCGM; SBM had less N retention (P < .01) than PBM and BMCGM. Arterial, portal, and hepatic plasma flows were greater (P < .09) for SBM than for PBM and BMCGM (21 vs 16, 17; 84 vs 72, 72; 105 vs 87, 88 L/h). Portal plasma flow was greater (P < .10) for urea than for SBM, PBM, and BMCGM (85 vs 84, 72, 72 L/h). Portal-drained viscera and TS alpha-amino N (AAN) fluxes were less (P < .05) for PBM than for BMCGM (20.5 vs 26.6 and 7.2 vs 15.1 mmol/h), but TS AAN flux was less (P < .05) for urea than for SBM, PBM, and BMCGM (6.9 vs 16.9, 7.2, 15.1 mmol/h). Portal-drained viscera flux and HEP removal of NH3 N were greater (P < .001) for SBM than for PBM and BMCGM (27.7 vs 19.4, 20.6; -28.1 vs -20.0, -21.4 mmol/h). Gut use was less (P = .07) and HEP and TS fluxes of urea N were greater (P < .01) for SBM than for PBM and BMCGM (-4.92 vs -8.32, -7.93; 25.87 vs 16.54, 20.00; 20.95 vs 8.22, 12.07 mmol/h). These data suggest that PBM and BMCGM improved efficiency of N use compared with urea and SBM by reducing urinary N loss.

Animal Feed↗
PubMed1998

Effect of B-group vitamins and antioxidant vitamins on hyperhomocysteinemia: a double-blind, randomized, factorial-design, controlled trial.

Mild hyperhomocysteinemia is accepted as a risk factor for premature cardiovascular disease. In a population with a high prevalence of cardiovascular disease, we screened a group of clinically healthy working men aged 30-49 y (n = 509) for plasma homocysteine and 5,10-methylene tetrahydrofolate reductase (MTHFR) genotype status. Those with mildly elevated homocysteine concentrations (> or = 8.34 micromol/L) were selected for intervention. In a randomized, factorial-design, controlled trial we assessed the effects of B-group vitamins and antioxidant vitamin supplementation on homocysteine concentrations. The 132 men were randomly assigned to one of four groups: supplementation with B-group vitamins alone (1 mg folic acid, 7.2 mg pyridoxine, and 0.02 mg cyanocobalamin), antioxidant vitamins alone (150 mg ascorbic acid, 67 mg RRR-alpha-tocopherol, and 9 mg beta-carotene), B-group vitamins with antioxidant vitamins, or placebo. Intervention was double-blind. A total of 101 men completed the 8-wk intervention. When homocysteine concentrations were analyzed by group, significant (P < 0.001) decreases (32.0% and 30.0%, respectively) were observed in both groups receiving B-group vitamins either with or without antioxidants. The effect of B-group vitamins alone over 8 wk was a reduction in homocysteine concentrations of 27.9% (95% CI: 22.0%, 33.3%; P < 0.001) whereas antioxidants alone produced a nonsignificant increase of 5.1% (95% CI: -2.8%, 13.6%; P = 0.21). There was no evidence of any interaction between the two groups of vitamins. The effect of B-group vitamin supplementation seemed to depend on MTHFR genotype. Supplementation with the B-group vitamins with or without antioxidants reduced homocysteine in the men with mildly elevated concentrations, and hence may be effective in reducing cardiovascular risk.

Adult↗
PubMed1998

Nutritional evaluation of poultry by-product meal as a protein source for ruminants: effects on performance and nutrient flow and disappearance in steers.

We conducted three studies with steers to evaluate poultry by-product meal (PBM) as a supplemental N source for ruminants. An in situ study compared the solubility, degradation rate, and ruminal escape of PBM N with blood meal (BM), corn gluten meal (CGM), and soybean meal (SBM) N. Additionally, an 84-d growth study (n = 95, 228+/-5 kg BW) and a digestion trial (6 x 6 Latin square) were conducted. The basal diet for the growth and digestion studies consisted of 49% corn silage, 36% cottonseed hulls, and 15% supplement (DM basis). Sources of supplemental N (% of total supplemental N) were 100% SBM and 0, 25, 50, 75, and 100% PBM, with urea used to balance for N. In situ ruminal escape N (25.2, 55.3, 86.7, and 98.9% for SBM, PBM, CGM, and BM, respectively) was greater (P < .05) for PBM than for SBM; however, a greater (P < .05) proportion of BM and CGM N escaped ruminal degradation compared with PBM. Dry matter intake, ADG and gain/ feed increased linearly (P < .003) as PBM increased; however, no differences (P > .48) were observed in these variables for 100% PBM compared with 100% SBM. Duodenal N flow and small intestinal N disappearance increased linearly (P < .05) as PBM increased in the diet. Bacterial N flow to the small intestine was not affected (P > .19) by treatment; however, 100% SBM decreased (P < .04) bacterial CP synthesis (g bacterial N/kg OM disappearance from the stomach) compared with 0 and 100% PBM. In vivo ruminal escape N of PBM and SBM was 40.6 and 13.7%, respectively. Ruminal NH3 N decreased linearly (P < .001) as PBM increased. These data suggest that PBM can replace SBM as a source of supplemental N for steer calves that consume a diet based on corn silage and cottonseed hulls.

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