Synthesis and some biological properties of 4-valine-oxytocin and 1-deamino-4-valine-oxytocin.
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Animals↗
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5-Valine-oxytocin and 1-deamino-5-valine-oxytocin. Syntheses and some pharmacological properties.
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Biological Assay↗
Relationship of the pool of intracellular valine to protein synthesis and degradation in cultured cells.
To explore the role of the pool of intracellular free valine in the processes of protein synthesis and protein degradation, cultured hepatoma (HTC) cells were incubated in media containing varying concentrations of L-valine, under conditions of constant rates of protein synthesis and protein breakdown, and at steady state levels of intracellular valine specific radioactivities. Two types of experiments were compared: in the first (designated "incorporation experiment"), unlabeled cells were exposed to [3H]valine for a short period of time. In the second (termed "reincorporation experiment"), cells were prelabled with [3H]valine and then incubated for a brief period with media containing different concentrations of unlabeled valine; reincorporation of [3H]valine was calculated by the difference between the release of [3H]valine from labeled cellular proteins at low valine concentrations, and the maximal rate of the release at high valine concentrations. In both types of experiments, the rates of [3H]valine incorporation or reincorporation were compared with the respective specific radioactivities of free intracellular valine. In the incorporation experiment, the rates of [3H]valine incorporation into protein calculated by the intracellular specific radioactivities were not constant, but showed an upward deviation at low valine concentrations. This is in agreement with the results of Mortimore, G.E., Woodside, K.H., and Henry, J.E. ((1972) J. Biol. Chem. 247, 2776-2784) in the perfused rat liver. By contrast, in the reincorporation experiment, the calculated rates of [3H]valine reincorporation based on intracellular specific radioactivities were constant throughout the range of valine concentrations. The constant value of calculated valine reincorporation was lower by 30 to 50% than the calculated rate of valine incorporation at high valine concentrations. The following model is proposed to explain these results. There is one common pool of free intracellular valine, but there are two sites where valyl-tRNA can be formed. The first is an internal site that utilizes valine from the intracellular pool, and the second is an external (possibly membranous) system that converts extracellular valine directly to valyl-tRNA. Valine originating from protein degradation flows into the intracellular pool, from which it can be reutilized by the internal system. According to these assumptions, in the incorporation experiment and at low valine concentrations, the specific activity of valyl-tRNA is higher than that of the intracellular pool of free valine, due to the contribution of the external system. On the other hand, in the reincorporation experiment the specific activity of extracellular valine is negligible in comparison with that of the intracellular pool. Therefore, in this case the specific activity of valyl-tRNA is proportional to that of the intracellular pool, with a constant dilution by unlabeled valine of extracellular origin...
Cell Line↗
The role of valine in the biosynthesis of penicillin N and cephalosporin C by a Cephalosporium sp.
1. The production of penicillin N, but not that of cephalosporin C, was inhibited by the addition of d-valine to suspensions in water of washed mycelium of Cephalosporium sp. 8650. The production of cephalosporin C was selectively inhibited by gamma-hydroxyvaline. 2. l-[(14)C]Valine was taken up rapidly and virtually completely by suspensions of washed mycelium but d-[(14)C]valine and alpha-oxo[(14)C]-isovalerate were taken up relatively slowly. 3. Part of the l-valine was rapidly degraded in the mycelium and part was incorporated into protein. Turnover of the valine in the amino acid pool was estimated to occur in 10-17min. 4. No detectable amount of l-[(14)C]valine was converted into the d-isomer in the mycelium. alpha-Oxo[(14)C]isovalerate was rapidly converted into l-[(14)C]valine in mycelium and mycelial extracts. 5. d-[(14)C]Valine was partially converted into the l-isomer in the mycelium and (14)C from d-valine was incorporated into protein. 6. The labelling of penicillin N and cephalosporin C by (14)C from l-[(14)C]valine was consistent with the view that l-valine is a direct precursor of C(5) fragments of both antibiotics and that any intermediates involved are present in relatively small pools in rapid turnover. 7. Labelling of the antibiotics with (14)C from d-[1-(14)C]valine appeared to occur after the latter had been converted into the l-isomer. Unlabelled d-valine did not decrease the efficiency of incorporation of (14)C from l-[1-(14)C]valine. 8. Intracellular peptide material which contained, among others, residues of alpha-aminoadipic acid, cysteine and valine, was rapidly labelled by (14)C from l-[1-(14)C]valine in a manner consistent with it being an intermediate in the biosynthesis of one or both of the antibiotics. 9. Labelling of penicillin N from l-[1-(14)C]valine occurred more rapidly than that of cephalosporin C. However, the effects of d-valine and gamma-hydroxyvaline on antibiotic production and the course of labelling of the antibiotics from l-[(14)C]valine could not readily be explained on the assumption that penicillin N was a precursor of cephalosporin C.
Acremonium↗
Valine requirement of the lactating sow.
An experiment was conducted using production and metabolic criteria to estimate the valine requirement of the lactating sow. Ground corn, gelatin, corn sugar, vitamins, minerals and indispensable amino acids were used to formulate a diet containing all the essential nutrients except valine. L-valine was added to provide .23 (basal), .38, .53, .68 and .83% valine. Twenty-five mature Landrace x Yorkshire sows were randomly assigned to the five dietary treatments. Milk production and average pig weight gain increased quadratically (P less than .01) and were maximized at .68% dietary valine. Total solids production (p less than .05) and protein production (P less than .01) increased with increasing level of valine, and both were maximized at .68% dietary valine. Protein content also was maximized (P less than .01) at .68% dietary valine. Fecal (P less than .05) and urinary (P less than .01) nitrogen decreased with increasing valine, yielding greatest (P less than .01) nitrogen retention (excluding milk nitrogen) at .53% dietary valine. Because daily milk nitrogen production also increased (P less than .01) with increasing valine, there were no treatment differences (P greater than .05) in nitrogen balance (including milk nitrogen). Plasma valine concentration increased (P less than .01) gradually until .53% valine was fed, after which there was a rapid increase in concentration. Plasma isoleucine and leucine decreased (P less than .01) with increasing dietary valine. Plasma urea concentration was minimal (P less than .05) with .38% dietary valine. When all the criteria measured are considered, the lactating sow's requirement of valine is between .53 and .68%. The metabolic data support .53% dietary valine for the requirement, although the maximum response in production parameters at .68% dietary valine suggests that the requirement is above .53% dietary valine.
Amino Acids↗
Valine requirement of nursery pigs.
Six experiments were conducted to determine the true digestible valine requirement of 5- to 20-kg pigs. In Exp. 1, a valine-deficient diet for 5- to 10-kg pigs was developed and validated in terms of growth performance in response to supplemental L-valine. A different basal diet was validated for 10- to 20-kg pigs in Exp. 2. Both diets were demonstrated to be deficient in valine and to support performance equivalent to typical nursery diets when fortified with L-valine. In Exp. 3, true ileal digestibility of valine in the two basal diets was determined in eight pigs fitted with a simple T-cannula at the terminal ileum. Another four pigs received an enzymatically hydrolyzed casein-based diet to determine endogenous contributions to collected ileal digesta. The two diets were found to have true valine digestibilities of 82% (5- to 10-kg pigs) and 86% (10- to 20-kg pigs). In Exp. 4, 80 weaned pigs (5.8 kg) were offered the basal diet fortified with five incremental doses (0.08%) of L-valine. Weight gain increased quadratically (P < 0.05) with increasing levels of valine. Broken-line analysis revealed a true digestible valine requirement of 0.86 +/- 0.03%. In Exp. 5, the true digestible valine requirement of 10- to 20-kg pigs was estimated with 120 pigs (10.9 kg) using the second basal diet fortified with six incremental doses (0.05%) of L-valine. The data suggested a digestible valine requirement level of about 0.775%, which was reevaluated in Exp. 6, wherein pigs did not respond to levels of digestible valine higher than 0.775%. In conclusion, requirement estimates were 2.50 and 2.22 g of true digestible valine per megacalorie of ME for 5- to 10- and 10- to 20-kg pigs, respectively. These empirical estimates are in close agreement with recent estimates of the National Research Council Subcommittee on Swine Nutrition of 2.48 and 2.11 g of true digestible valine per megacalorie of ME, respectively.
Animal Nutritional Physiological Phenomena↗
Global expression profiling and physiological characterization of Corynebacterium glutamicum grown in the presence of L-valine.
Addition of L-valine (50 to 200 mM) to glucose minimal medium had no effect on the growth of wild-type Corynebacterium glutamicum ATCC 13032 but inhibited the growth of the derived valine production strain VAL1 [13032 DeltailvA DeltapanBC(pJC1ilvBNCD)] in a concentration-dependent manner. In order to explore this strain-specific valine effect, genomewide expression profiling was performed using DNA microarrays, which showed that valine caused an increased ilvBN mRNA level in VAL1 but not in the wild type. This unexpected result was confirmed by an increased cellular level of the ilvB protein product, i.e., the large subunit of acetohydroxyacid synthase (AHAS), and by an increased AHAS activity of valine-treated VAL1 cells. The conclusion that valine caused the limitation of another branched-chain amino acid was confirmed by showing that high concentrations of L-isoleucine could relieve the valine effect on VAL1 whereas L-leucine had the same effect as valine. The valine-caused isoleucine limitation was supported by the finding that the inhibitory valine effect was linked to the ilvA deletion that results in isoleucine auxotrophy. Taken together, these results implied that the valine effect is caused by competition for uptake of isoleucine by the carrier BrnQ, which transports all branched-chained amino acids. Indeed, valine inhibition could also be relieved by supplementing VAL1 with the dipeptide isoleucyl-isoleucine, which is taken up by a dipeptide transport system rather than by BrnQ. Interestingly, addition of external valine stimulated valine production by VAL1. This effect is most probably due to a reduced carbon usage for biomass production and to the increased expression of ilvBN, indicating that AHAS activity may still be a limiting factor for valine production in the VAL1 strain.
Acetolactate Synthase↗
Prevention of fatty liver and maintenance of systemic valine depletion using a newly developed dual infusion system.
BACKGROUND: Valine-depleted amino acid imbalance, while having a suppressive effect on tumor growth, may induce fatty liver. METHODS: We administered a valine-depleted total parenteral nutrition (TPN) solution by the central venous route to non-tumor-bearing rats and examined the time course of the development of fatty liver. In an attempt to prevent this condition, we administered a continuous infusion of low concentrations of valine via the portal vein simultaneously with administration of central venous valine-depleted nutrition for 4 days. RESULTS: A marked accumulation of triglyceride was observed in the liver on day 4 of the administration of valine-depleted nutrition. It is speculated that such accumulation is the cause of fatty liver. The level of valine in the peripheral blood began to decrease soon after administration was begun and resulted in a state of systemic valine deficiency. Rats given 25% or more of the valine concentration in the standard TPN solution via the portal vein simultaneously with the administration of central venous valine-depleted nutrition, had a triglyceride level similar to that of the control group. The group given 50% or less of the valine concentration had a level of valine in the peripheral blood as low as that of the valine-depleted group, indicating the maintenance of a valine-deficient state. CONCLUSION: Administration of low concentrations of valine via the portal vein simultaneous with central venous administration of valine-depleted TPN solution may prevent fatty liver.
Animals↗
Dose-response relationships for valine in the growing White Pekin duck.
The response of White Pekin ducks to supplements of L-valine was studied during 3 wk posthatching. The basal valine concentration was 6.8 g/kg in a diet containing 18% CP and 2,990 kcal ME/kg (12.5 MJ ME/ kg). L-valine was supplemented in eight graded levels up to 12.7 g/kg at the expense of L-glutamic acid. Three pens of 14 ducks were allocated to each valine level. Diets were offered ad libitum. Body weight gain and feed/gain ratio were studied. At the end of wk 3, ducks were killed, processed to a homogenous mass, and analyzed for total body CP and amino acid content. Accretion of protein and amino acids was calculated. Additionally, a 5-d N balance study was conducted with separate ducks of the same hatch beginning on d 11 (6 ducks per treatment). The response of ducks to increasing valine concentration was described by exponential functions. Ducks significantly responded to the increasing valine concentration in growth, feed/gain ratio, and protein accretion. Ninety-five percent of y(max) in BW gain and protein accretion were achieved with 8.0 and 7.9 g valine/kg, respectively. The content of protein in gained BW was, on average, 149 g/kg without a significant valine effect. The valine content in accreted body protein was also unaffected by dietary valine (4.1 g/16 g N on average), which suggested that a major shift in body protein fractions did not occur. The overall efficiency of valine utilization was affected by dietary valine concentration and showed a maximum of 49%. Data from the balance study showed basically the same response of ducks, but the estimated optimum in dietary valine concentration was lower (7.0 g/kg). A comparison with published broiler data indicated that ducks and broilers in this age period were similar with regard to the valine content in gained protein and the efficiency of utilization of supplemented valine.
Amino Acids↗
Valine requirement of the high-producing lactating sow.
Two hundred three (40 or 41/treatment, average parity 4.3) Large White x Landrace or Large White x Chester White x Landrace sows were used to determine the valine requirement of sows with a genetic capacity for high milk production. All diets were formulated to contain .90% total lysine, with all amino acids other than valine formulated to be at least 110% of their suggested estimates relative to lysine based on ratios derived from the National and Agricultural Research Councils. The control diet was formulated to .75% total valine, and crystalline valine replaced cornstarch to provide additional treatments containing .85, .95, 1.05, and 1.15% total dietary valine. Corresponding valine:lysine ratios were 83, 94, 106, 117, and 128%. Mean litter size after adjustment was 10.3 pigs across treatments, and average lactation length was 26 d. Number of pigs weaned was not affected by dietary valine (mean = 10.2 pigs), nor was daily sow feed (mean = 6.24 kg) or lysine (mean = 56 g) intake. Valine intake increased (linear, P < .001) as dietary valine increased. Litter weight at d 21 and at weaning (d 26) increased (linear, P < .02) with increasing dietary valine (62.4 to 65.5 kg and 76.1 to 79.9 kg, respectively). Litter weight gain increased from d 0 to 7 (linear, P < .06) and from d 0 to 21 and d 0 to weaning (linear, P < .02) as dietary valine increased. Dietary valine had no effect (P > .10) on sow weight change, 10th rib, or last lumbar backfat change from d 0 to 21 or d 0 to weaning or on days from weaning to estrus. These results demonstrate that increasing dietary valine for high-producing sows (21-d litter weights > 60 kg) results in improved litter weight gain. Based on the linear responses observed, the requirement is at least 1.15% of the diet (72 g/d of valine intake) to maximize litter weaning weight and litter weight gain, much greater than recommended currently by the National Research Council (100% of lysine, 36.5 g/d) or the Agricultural Research Council (70% of lysine, 25.5 g/d).
Amino Acids↗
REGULATORY MECHANISMS IN THE BIOSYNTHESIS OF ISOLEUCINE AND VALINE. I. GENETIC DEREPRESSION OF ENZYME FORMATION.
Ramakrishnan, T. (Yale University, New Haven, Conn.), and Edward A. Adelberg. Regulatory mechanisms in the biosynthesis of isoleucine and valine. I. Genetic derepression of enzyme formation. J. Bacteriol. 87:566-573. 1964.-A total of 60 mutants of Escherichia coli K-12 resistant to 10(-2)m valine were isolated from the valine-sensitive F' strain AB1206. Conjugation experiments showed that in five of these mutants the valine-resistance locus is closely linked to the structural genes governing isoleucine-valine biosynthesis. In these five valine-resistant mutants, three enzymes of the isoleucine-valine pathway were found to be coordinately derepressed: l-threonine deaminase, dihydroxy acid dehydrase, and transaminase B. Two other enzymes of this pathway, the condensing enzyme and the reductoisomerase, were unaffected. The mutation from valine-sensitivity to valine-resistance appears to have altered an operator locus, because the derepressed state is dominant over the repressed state in diploids heterozygous for the valine-resistance locus. The valine-resistant mutants excrete isoleucine into the medium. The significance of these findings with respect to the valine-sensitivity of E. coli K-12 and the regulation of the biosynthesis of isoleucine and valine by this organism are discussed.
Drug Resistance↗
The effect of valine deficiency on neutral amino acid patterns in plasma and brain of the rat.
Valine deficiency in rats produced motor incoordination attributable to selective damage to the red nuclei, midbrain structures that modulate motor activity. Neither incoordination nor red nuclei damage occurs in rats deprived of valine, isoleucine and leucine, thus suggesting that valine neurotoxicity results from amino acid imbalance rather than from lack of valine per se. To explore this possibility, we compared neutral amino acid patterns in plasma and brain of rats fed for 7 days a complete diet fed ad libitum or pair-fed, a valine-free diet or a diet lacking in all three essential branched-chain amino acids (BCAA). Statistical evaluation showed that plasma valine in valine-deprived rats was lower (P less than 0.01) than in pair-fed and ad libitum-fed controls but did not differ from rats lacking BCAA. Brain valine in valine-deprived rats did not differ from ad libitum-fed controls and actually was higher (P less than 0.01) than in pair-fed and BCAA-deprived rats. The most striking changes seen in the amino acid pattern of valine-deprived rats as compared to all other groups were in the increased leucine:valine ratio (P less than 0.01 for plasma and brain) and in the increased leucine + isoleucine:valine ratio (P less than 0.01 plasma; P less than 0.001, brain). These results are consistent with the view that amino acid imbalance is a critical factor in the development of the neurotoxicity of valine deficiency.
Amino Acids↗
Utilization of alpha-keto and alpha-hydroxy analogues of valine by the growing rat.
When 70-80-g male albino rats eat a diet furnishing daily requirement of valine for optimal growth (70 mumol/g) and all other nutrients ("complete diet"), they gain weight at an average rate of 3.0 g/100 g body wt/day. When valine is removed, they lose weight at an average 2.1 g/100 g body wt/day. The growth retardation is improved or corrected by adding valine to the diet, daily weight gain being proportional to dietary valine content over a range of 0-70 mumol/g. Addition of alpha-ketoisovaleric acid instead of valine to the valine-free diet also improves or corrects the growth failure. Percent efficiency of alpha-ketoisovaleric acid as a substitute for valine was calculated as: 100 x (micromole valine per gram diet required to produce specified growth response)/(micromole alpha-ketoisovaleric acid per gram diet required to produce the same response). Efficiency of the substitution is inversely related to dietary content of the keto analogue, being 80% when diet contains 17.5 mumol/g (molar equivalent of (1/4) the daily requirement of valine), and 37% when diet provides 140 mumol/g (molar equivalent of twice the daily requirement of valine).alpha-Hydroxyisovaleric acid also substitutes for valine. Efficiency of the substitution at the single ration tested, 70 mumol/g diet, is 45%, similar to that for the keto analogue under the same conditions. When [1-(14)C]alpha-ketoisovaleric acid is injected intravenously, 30-80% of the administered radioactivity is exhaled as (14)CO(2) within 24 h. This finding suggests that inefficiency of alpha-ketoisovaleric acid as a substitute for valine results in part from degradation of the keto acid to isobutyric acid by branched chain dehydrogenase-decarboxylase. Oral administration of neomycin, polymyxin, and bacitracin reduces efficiency of alpha-ketoisovaleric acid as a substitute for valine by (1/4)-(1/2). This effect suggests that transamination of the keto acid may be performed in part by gastrointestinal microbes.
Animals↗
Assessment of protein turnover in perfused rat liver. Evidence for amino acid compartmentation from differential labeling of free and tRNA-gound valine.
Total protein synthesis in perfused livers of fed rats was determined by measuring the rate of valine incorporation based on the specific activity of valine attached to tRNA. Rates were not significantly altered when perfusate valine was increased from 0.40 to 5 mM and were similar to values calculated earlier from the specific activity of extracellular valine at a concentration of 15 mM. Overall protein degradation, computed from the sum of the rates of synthesis and the total increase of free intra- and extracellular valine, corresponded closely to the increase of free valine that occurred between 5 and 15 min after the addition of cycloheximide. In the latter experiments advantage was taken of the fact that the previously established suppressive effect of cycloheximide on proteolysis does not begin initially with the inhibition of synthesis, but 15 min later. Thus, the release of valine from 5 to 15 min was assumed to represent rates of protein degradation in effect prior to the addition of cycloheximide. The close agreement found among these independent assessments of protein metabolism thus appears to eliminate much of the previous uncertainty in the quantitation of hepatic protein turnover. In the course of these studies we noted that the specific activity of valyl-tRNA attained steady state values that were intermediate between specific activities of the extracellular and intracellular pools, but appeared to reach a steady state sooner than that of intracellular valine. To evaluate these early events more precisely, the specific activity of valine in tRNA and the intracellular pool was measured in a series of single-pass perfusion experiments where extracellular valine concentration and specific activity were held constant. The intracellular valine specific activity rose with a half-life of 1.2 min. By contrast, the rise in the specific activity of valyl-tRNA was biphasic: the initial phase of the valyl-tRNA curve was rapid, while the second phase had a half-life equal to that of intracellular valine. These data show that at physiological concentrations of valine, valyl-tRNA derives its amino acids from both the extracellular and cytoplasmic pools, and that at least some tRNA is charged by extracellular amino acids before they mix with intracellular amino acid pools, possibly from a precursor pool at or near the cell membrane.
Amino Acids↗
Growth, carcass traits, and plasma amino acid concentrations of gilts fed low-protein diets supplemented with amino acids including histidine, isoleucine, and valine.
Three experiments were conducted to determine the fifth-limiting amino acid for growing pigs in an 11% CP, corn-soybean meal diet. In each experiment, 36 gilts (initial weight 19.5, 21.9, and 21.0 kg, respectively) were penned individually and fed one of six diets in a randomized block design for 35 d. Diets containing 16, 12, and 11% CP were fed in each experiment. All 12 and 11% CP diets were supplemented with lysine, tryptophan, threonine, and methionine to provide the same total concentrations as those in the 16% CP diet. In Exp. 1, the 11% CP diet was supplemented with isoleucine, valine, or isoleucine + valine to concentrations equal to those in the 16% CP diet. In Exp. 2, the 11% CP diet was supplemented with histidine, histidine + valine, or histidine + isoleucine + valine. In Exp. 3, the 11% CP diet was supplemented with valine, histidine + valine, or isoleucine + valine. Gilts were allowed free access to feed and water. In all experiments, ADG and feed efficiency (G/F) were reduced (P < or = 0.07) as dietary protein was reduced. Supplementation of isoleucine alone further reduced (P < 0.05) ADG, ADFI, G/F, and fat-free lean gain. In contrast, supplementation of valine alone resulted in numerical increases in ADG and ADFI in two experiments, although the differences were not significant (P > 0.05). Supplementation with histidine and valine together resulted in growth performance equal to or greater than that of pigs fed the 12% CP diet, but less than that of pigs fed the 16% CP diet. Supplementation of isoleucine and valine together resulted in better growth performance (P < 0.05) than supplementation of either amino acid alone. In two experiments (Exp. 1 and 3), supplementation of the 11% CP diet with isoleucine and valine together resulted in ADG that were not significantly different (P > 0.05) from those of pigs fed the 16% CP diet. Supplementation of all three amino acids (Exp. 2) did not improve performance over supplementations with histidine and valine. Plasma urea concentrations were reduced (P < 0.05) as dietary protein was lowered from 16 to 12%. Additions of crystalline amino acids did not affect plasma urea levels. Plasma amino acid concentrations reflected the dietary additions of crystalline amino acids, but did not assist in the identification of the sequence of limiting amino acids. These data suggest that valine is the fifth-limiting amino acid and that either histidine or isoleucine is the sixth-limiting amino acid in an 11% CP diet.
Amino Acids, Essential↗
Determination of low isotopic enrichment of L-[1-13C]valine by gas chromatography/combustion/isotope ratio mass spectrometry: a robust method for measuring protein fractional synthetic rates in vivo.
A method was developed for measuring protein fractional synthetic rates using the N-methoxycarbonylmethyl ester (MCM) derivative of L-[1-13C]valine and on-line gas chromatography/combustion/isotope ratio mass spectrometry (GC/C/IRMS). The derivatization procedure can be performed rapidly and GC separation of valine from the other branched-chain amino acids, leucine and isoleucine, is easily obtained. A good linear relationship was observed between the increment of the 13C/12C isotope ratio in CO2 gas derived from the combustion of derivatized valine and the tracer mole ratio of L-[1-13C]valine to unlabelled valine. The limit of quantitation was at an L-[1-13C]valine tracer mole ratio of 0.0002. The method was used to measure the isotopic enrichment of L-[1-13C]valine in standard mixtures and in skeletal muscle of six growing piglets infused with L-[1-13C]valine (2 mg kg-1 h-1 for 6 h). After infusion of L-[1-13C]valine the mean tracer mole ratio in plasma of L-[1-13C]valine at the isotopic steady state was 0.0740 +/- 0.0056 (GC/MS, mean +/- SEM) and the mean tracer mole ratio of valine in muscle protein fraction at 6 h was 0.000236 +/- 0.000038 (GC/C/IRMS). The resulting mean protein fractional synthetic rate in piglet skeletal muscle was 0.052 +/- 0.007% h-1, which is in good agreement with literature data obtained with alternative, more elaborate techniques. By this method protein fractional synthetic rates can be measured at low isotopic enrichment levels using L-[1-13C]valine, the MCM derivative and on-line GC/C/IRMS.
Animals↗
Alanine and aspartate formation during growth on valine-C14 by Pseudomonas aeruginosa.
Sokatch, J. R. (University of Oklahoma School of Medicine, Oklahoma City). Alanine and aspartate formation during growth on valine-C(14) by Pseudomonas aeruginosa. J. Bacteriol. 92:72-75. 1966.-Pseudomonas aeruginosa grown with dl-valine-4,4'-C(14) synthesized alanine labeled mainly in carbons 1 and 3, indicating that the isopropyl carbons of valine were the precursors of pyruvate for alanine formation by a pathway which did not involve randomization of isotope. Alanine from cells grown on valine-1-C(14) contained isotope only in the carboxyl carbon, suggesting another route to pyruvate from valine by carbon dioxide fixation. Oxidation of valine to propionyl-coenzyme A (CoA), as it occurs in animal tissues, followed by the oxidation of propionyl-CoA to acrylyl-CoA, lactyl-CoA, and pyruvate, would account for the isotope data. Cells grown on valine oxidized valine, isobutyrate, and propionate immediately, whereas cells grown on acetate did not oxidize valine or isobutyrate and required an induction period before propionate was oxidized. P. aeruginosa grown with propionate-1-C(14) or propionate-2-C(14) formed alanine-1-C(14) and alanine-2-C(14), respectively, which agrees with the contention that at least part of the propionate is oxidized via the acrylate pathway. Aspartate formed from valine-1-C(14) was labeled only in the carboxyl carbons, whereas that formed from valine-4,4'-C(14) was labeled in all four carbons, but most heavily in carbons 1 and 3. These data suggest that the main route for the formation of the carbon skeleton of aspartate was by a C(3) plus C(1) condensation, with the C(3) unit derived from the isopropyl carbons of valine and the C(1) unit probably from carbon dioxide.
Acetates↗
Increasing valine, isoleucine, and total branched-chain amino acids for lactating sows.
One hundred eighty-five (n = 24 to 27/group; average parity 1.3) sows (PIC, Line C-15) were used to evaluate effects of the interrelationship between isoleucine and valine on sow and litter performance. Diets were formulated to .90% total lysine with all amino acids other than isoleucine and valine at least 110% of their suggested requirement estimate relative to lysine using ratios derived from the National and Agricultural Research Councils. The control diet was formulated to .50% isoleucine and .72% valine. L-Valine and L-isoleucine replaced cornstarch to provide .72 or 1.07% dietary valine, and .50, .85, or 1.20% isoleucine. A seventh diet contained .50% isoleucine and 1.42% valine. Mean litter size after cross-fostering was 11.1 pigs, and average lactation length was 20.3 d. No valine x isoleucine interactions were observed (P > .10) for most response criteria. Number of pigs weaned (mean = 10.9), sow feed intake (mean = 6.13 kg), and lysine intake (mean = 55 g/d) were not affected by dietary isoleucine or valine. Litter weight and weight gain at weaning increased as dietary valine (P < .07), isoleucine (linear, P < .07), and total branched-chain amino acids (linear, P < .02) increased. Twelve sows per treatment (84 total) were milked manually on either d 17 or 18 of lactation. Increasing dietary valine increased milk DM and fat (linear, P < .01). Milk DM, CP, and fat increased (linear, P < .002) as dietary isoleucine increased. The casein fraction of milk protein increased (linear, P < .01) and whey and nonprotein N fractions decreased (linear, P < .06, P < .01, respectively) as dietary isoleucine increased. Based on these results, valine and isoleucine increased litter weights. The independent increases in litter weaning weights from adding valine and isoleucine suggest separate modes of action in lactating sows.
Amino Acids↗