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Biomedical subjects

R L Prior

Publications and source records attributed to R L Prior.

At least 55 records · Page 3Linked to original sources

Nitrogen and lipid metabolism in heifers fed at increasing levels of intake.

The relationship between N and lipid metabolism was investigated in heifers fed five different levels of feed intake (five heifers per treatment group). Targeted ME intakes were 84, 123, 157, 191, and 225 kcal per kt.75 per day, which were .76x, 1.12x, 1.43x, 1.74x, and 2.05x (times) the estimated ME requirement for maintenance. After 120 d on trial, the heifers were moved to a confinement building for 7 d, and feces and urine were collected over a 3-d period. On the 1st d of confinement, blood samples were collected every 15 min for a total of 15 samples. Because the group fed at 1.43x maintenance was fed improperly during the period in confinement, this group was omitted from the study. Adipose tissue samples were obtained at slaughter to obtain in vitro measures of lipid metabolism. As feed intake increased, N retention increased (P less than .05) from 1.7 to 24.3 g/d. Daily urinary N tau-methylhistidine excretion was significantly different between the .76x and 1.74x treatments (769 vs 1,575 mumol/d, respectively). The fractional breakdown rate of myofibrillar proteins also was significantly different between these two groups of heifers (1.49 vs 2.44%/d, respectively). Plasma glucose and insulin were lowest (P less than .05) at the lowest level of feed intake. Conversely, plasma nonesterified fatty acids were lowest (P less than .05) in those animals receiving the highest level of feed intake. Subcutaneous adipocytes were smallest (93 microns) in the heifers fed at 33% ad libitum intake and largest in heifers fed at 76 or 90% ad libitum intake (115 and 110 microns, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

Amber mutation creates a diagnostic MaeI site in the androgen receptor gene of a family with complete androgen insensitivity.

We have discovered in the X-linked androgen receptor gene a single nucleotide substitution that is the putative cause of complete androgen insensitivity (resistance) in a family with affected individuals in 2 generations. Earlier studies on the family indicated co-segregation of mutant phenotype and the RFLPs at the loci DXS1 and DXYS1. The mutation is an adenine-to-thymine transversion in exon 8 that changes the sense of codon 882 from lysine to an amber (UAG) translation termination signal. The substitution creates a recognition sequence for the restriction endonuclease MaeI: this permits ready recognition of hemizygotes and heterozygotes after amplification of genomic exon 8 by the polymerase chain reaction. The mutation predicts the synthesis of a truncated receptor that lacks 36 amino acids at the carboxy terminus of its 252-amino acid androgen-binding domain. The cultured genital skin fibroblasts of the one affected patient examined have normal levels of androgen receptor mRNA, but negligible androgen-receptor binding activity. These results accord with a variety of data from spontaneous and artificial mutations indicating that all portions of the steroid binding domain contribute to normal steroid binding by a steroid receptor.

Amino Acid Sequence↗

Arginine-deficient diets alter plasma and tissue amino acids in young and aged rats.

Blood and urine metabolites were measured in two experiments for young (2-mo-old) and aged (20-mo-old) male Sprague-Dawley rats fed arginine-devoid diets made isonitrogenous to a control 1.12% arginine diet by adding alanine or glycine. Diet, fed for 7 or 13 d, had little effect on urinary or plasma ammonia and urea. Urinary orotate excretion was more than 40-fold higher in rats fed the arginine-deficient diets (P less than 0.01) in both experiments. Source of nonessential N (alanine or glycine) in the arginine-deficient diets did not alter orotic acid excretion or plasma or urine ammonia or urea. Changes in plasma arginine, alanine and glycine concentrations reflected the levels of these amino acids in the diet. Tissue ornithine levels reflected dietary arginine level, but tissue citrulline was unaffected by dietary arginine. Glutamate and glutamine were greater in the plasma and liver of rats fed arginine-deficient diets. Plasma concentrations of glutamate and glutamine were positively correlated with urinary orotic acid excretion (P less than 0.05) and ornithine and arginine were negatively correlated with orotic acid excretion (P less than 0.01). Increased tissue glutamine may be related to the greater orotate excretion in rats fed arginine-devoid diets. The metabolic responses to dietary arginine deficiency were similar in young and aged rats. In general, concentrations of amino acids in plasma, liver and spleen were higher in aged rats.

Aging↗

Dietary arginine supplementation does not enhance lymphocyte proliferation or interleukin-2 production in young and aged rats.

Recent studies indicate that supplemental arginine may enhance in vitro lymphocyte mitogenesis. To determine whether dietary arginine could reverse age-associated losses in immune functions, we fed purified amino acid diets to young (2-mo-old) and aged (24-mo-old) Fischer 344 rats. Rats receiving control (1.12% arginine) or supplemented (3% arginine) diets were pair fed to intakes of deficient (0% arginine) rats. Another group was fed the supplemented diet ad libitum. On d 15, responses of splenocytes to phytohemagglutinin (PHA), concanavalin A (Con A), and pokeweed mitogen (PWM) were lower (P less than 0.01), but interleukin-2 (IL-2) production was higher (P less than 0.05) in aged rats than in young rats. At mitogen doses producing maximal stimulation, supplemental arginine did not enhance PHA-, Con A- or PWM-stimulated lymphocyte proliferation; PWM responses at sub-maximal doses were higher in pair-fed supplemented rats than in control or ad libitum supplemented rats (P less than 0.05). Arginine supplements did not increase thymus weights or IL-2 production above controls. In another experiment, weanling rats received control and supplemented diets in amounts equal to the intake of deficient rats for an average of 37 d. Splenocytes were cultured with mitogens at various arginine levels. No diet effect was observed. Mitogenesis was maximal when media arginine approximated normal plasma levels. Our results suggest that supplemental arginine has little effect on lymphocyte proliferation or IL-2 production in healthy young and aged rats.

Aging↗

Carcass composition and adipose tissue metabolism in growing sheep.

Experiments were conducted to investigate biological variables that influence fat accretion in growing ram lambs. Carcass composition and adipose tissue development were measured in Columbia-sired ram lambs from 32.0 to 73.9 kg body weight. Five or six ram lambs were slaughtered every 2 mo, from 4 to 10 mo of age. The percentage of carcass fat-free dry matter decreased with age from 30.9 to 27.5% (P less than .05), while the percentage of carcass fat increased from 17.7 to 33.4%. Similarly, offal fat-free dry matter decreased with age (from 24.5 to 21.5), and there was nearly a threefold increase in the percentage of offal fat (P less than .05 for both measures). Subcutaneous adipocyte diameter and lipogenesis in vitro increased from 4 to 6 mo of age, and did not increase further with age. A bimodal distribution of adipocytes was apparent in the 4-mo-old lambs, but was not observed in any other age group. The presence of glucose in incubation media stimulated acetate incorporation into fatty acids in vitro in adipose tissue from 8- and 10-mo-old lambs. However, glucose did not affect the rate of lipogenesis from lactate. The data indicate early, rapid increases in carcass fat accretion, which corresponded to similar increases in lipogenesis and lipogenic enzyme activities.

Adipose Tissue↗

Comparisons of lipogenesis and glucose metabolism between ovine and bovine adipose tissues.

Studies were initiated to compare glucose and lipid metabolism in vitro in subcutaneous adipose tissue of mature sheep and cattle. Mean adipocyte volume was significantly less in subcutaneous adipose tissue of sheep than in adipose tissue from cattle. The presence of acetate and lactate in the incubation medium increased total glucose utilization two- to three-fold in ovine adipose tissue, but had no effect on total glucose utilization in adipose tissue from cattle. Acetate provided 72-82% of the acetyl units to lipogenesis, depending on species and substrate concentration. There were no significant (P greater than 0.05) differences in the contribution of the pentose cycle to the provision of reducing equivalents to fatty acid biosynthesis, based on the incorporation of label from [3-3H]glucose into fatty acids. In ovine adipose tissue, acetyl-CoA carboxylase appeared to be rate-limiting to lipogenesis, while in bovine subcutaneous adipose tissue, the activity of fatty acid synthetase may have been the limiting step in lipogenesis. In addition, the low activity of ATP-citrate lyase, especially relative to aconitate hydratase, probably limited the conversion of lactate to fatty acids in ovine adipose tissue. It is unlikely that ATP-citrate lyase activity was rate-limiting to lipogenesis from lactate in bovine adipose tissue. The data indicate that extending the results obtained from adipose tissue from one species to lipid metabolism in ruminants in general may not be valid.

Acetates↗

Net portal absorption of lactate and volatile fatty acids in steers experiencing glucose-induced acidosis or fed a 70% concentrate diet ad libitum.

Five crossbred steers (347 kg) were surgically fitted with rumen fistulae, hepatic portal, abdominal aorta and mesenteric catheters to measure organic acid absorption from the gut during acute [intraruminal glucose, 12 g/kg body weight (G)] or subacute [ad libitum 70% concentrate diet (C)] acidosis. Samples were taken at time 0, then every 2 h for 48 h after a switch from an alfalfa diet to C, or dosing with G. Steers receiving C received G 1 wk later so that five steers provided four observations/treatment. Blood flow rates were determined by infusion of para-amino hippuric acid (PAH) and averaged 767.8 and 712.5 liters/h for C and G, respectively. Animals consuming C averaged 13.6 kg dry matter from 0 to 24 h and 1.5 kg from 24 to 48 h. Rumen pH declined to 4.2 for G compared with 6.0 for C. Blood pH and HCO3 showed only slight depressions for G from 16 to 26 h, the period of lowest rumen pH. Rumen L-lactate concentration averaged 53.4 mM (peak 77 mM) and 2.1 mM for G and C, respectively. Rumen D-lactate concentration averaged 30.2 mM (peak 47 mM) for G and 1.2 mM for C. Net portal absorption of L-lactate averaged 96.6 and 164.4 mmol/h, whereas that of D-lactate averaged 10.5 and 71.8 mmol/h for C and G, respectively. Mean net portal volatile fatty acid absorptions were 442.8, 192.1, 53.8, 5.3 and 10.4 mmol/h (C) and 100.0, 47.2, 9.4, .98 and .78 mmol/h (G) for acetate, propionate, butyrate, isobutyrate and isovalerate, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗

Net absorption of amino acids by portal-drained viscera and hind half of beef cattle fed a high concentrate diet.

Two experiments were conducted to measure the effect of level of feed intake on net amino acid absorption by portal-drained viscera of six beef heifers with catheters in a mesenteric vein, portal vein and iliac artery (Exp. 1) and to evaluate intrajugular infusion of insulin or glucose on amino acid uptake by hind half of four beef steers with catheters in posterior aorta and vena cava (Exp. 2). Experiment 1 was a replicated 3 X 3 Latin square design. Treatments were calculated intakes of 84, 157 or 225 kcal metabolizable energy (ME)/kg.75 live weight. Treatments in Exp. 2 were control (no infusion), insulin infusion (1.4 IU/min for 90 min) and glucose infusion (2.5 mmol/min for 90 min) in that order. Mean live weight of animals +/- SE was 295 +/- 4 kg (Exp. 1) and 345 +/- 15 kg (Exp. 2). The diet used in both experiments was pelleted, 85% concentrate (2.9 Mcal ME/kg dry matter). Blood flow (BF) was measured by dilution of a primed, continuous infusion of para-aminohippuric acid into the mesenteric vein (Exp. 1) or the posterior aorta (Exp. 2). Net uptake or absorption was the product of BF times portal-arterial (Exp. 1) or arteriovenous (Exp. 2) differences in amino acid concentrations in blood. Increased feed intake caused linear (P less than .05) increases in net absorption of several amino acids, including lysine, methionine, leucine and valine (Exp. 1). Feed intake did not affect (P greater than .05) net absorption of glutamate or glutamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗

In vitro rates of oxidation and gluconeogenesis from L(+)- and D(-)lactate in bovine tissues.

Slices of bovine kidney cortex, liver, heart and sternomandibularis muscle actively metabolized D- and L-lactate. Rates of D-lactate oxidation were greatest in kidney cortex followed by heart and liver with muscle exhibiting the lowest rates. L-lactate oxidation was greatest in kidney cortex followed by heart with liver and muscle exhibiting similar rates. Rates of oxidation of gluconeogenesis were similar for D- and L-lactate at 0.1 mm lactate but D utilization, as a percent of L, decreased as substrate concentrations increased to 50 mM. Bovine tissues appear to possess significant potential for D(-)lactate utilization. Estimates of this and possible interactions are discussed.

Animals↗

Interrelationships among diet, age, fat deposition and lipid metabolism in growing steers.

Subcutaneous adipose tissue samples were obtained by biopsy technique and at slaughter from steers fed either a corn concentrate or pelleted alfalfa (roughage) diet. Steers fed the roughage diet had slightly greater metabolizable energy intakes than the concentrate-fed steers due to greater rates of feed intake; however, steers fed the concentrate diet had faster rates of gain, primarily in the fat depots. Diet had no effect on the incorporation of 14C-labeled acetate and lactate into fatty acids, although 3H2O incorporation into fatty acids was greater in the concentrate-fed steers. Although backfat thickness was 60% greater in the concentrate-fed steers, the number of adipocytes per gram adipose tissue was unaffected by diet, suggesting adipose cell hyperplasia. The activities of acetyl-CoA carboxylase, fatty acid synthetase, ATP citrate lyase, NADP+ malate dehydrogenase, and hexokinase were greater in the steers fed the concentrate diet; pyruvate kinase activity was unaffected by diet. Fatty acid synthesis and several lipogenic enzyme activities increased with age and then declined markedly by the time of the terminal biopsy. Basal and net rates of lipolysis generally were unaffected by diet but increased with age of the animal. As the animals gained weight, the ratio of net fatty acids released to glycerol released decreased, suggesting more extensive reesterification of fatty acids released during lipolysis.

Adipose Tissue↗

Role of insulin and glucose on metabolite uptake by the hind half of beef steers.

Arterial and venous concentrations, extraction ratios and uptake of glucose, L-lactate and volatile fatty acids were measured in the hind half of four beef steers (340 to 360 kg) fitted with indwelling catheters in the posterior aorta and vena cava. The steers were fed hourly a pelleted, 85% concentrate diet. Treatments were control, iv infusion of insulin (1.4 IU/min) and iv infusion of glucose (149.4 mmol/h). Arterial blood concentration of glucose decreased from 3.23 mM (control) to 1.51 mM (insulin), then increased to 4.29 mM (glucose). Extraction ratio of glucose increased about threefold from 2.6 and of L-lactate decreased about fourfold from 9.2 during insulin infusion, then returned toward control values during glucose infusion. Extraction ratios of acetate (39), propionate (45) and butyrate (28) were similar among treatments. Uptake (two steers) of glucose from blood (mmol/h) increased from 38 (control) to 76 (insulin) and 99 (glucose). Uptake of acetate, propionate and butyrate from plasma (mmol/h) was, respectively, 105, 6.5, .93 (control); 170, 11.9, 3.53 (insulin) and 134, 10.9, 3.12 (glucose). Rates of uptake of glucose and propionate during control were slower (P less than .05) than rates during insulin or glucose infusion; nonsignificant changes in uptake of butyrate followed a similar pattern. Uptake of L-lactate tended to be inversely related to uptake of glucose. Treatments did not affect uptake of acetate or valerate. Uptake of all metabolites except valerate was positive, indicating net use by the hind half.

Animals↗

Bovine muscle glycogen as affected by fasting and refeeding.

Twelve bulls about 12 mo of age were used to study the effects of dietary stress and realimentation on muscle glycogen depletion and repletion over time. Needle biopsy techniques were used to obtain longissimus muscle samples 11 d before fasting, at the end of fasting, and 3, 7, 10 and 14 d postfasting. Fasting reduced (P less than .05) muscle glycogen from 77 to 50 mumol glycogen-glucose/g. Depressed muscle glycogen content persisted through d 3 while animals were reestablishing normal feed consumption. A glycogen repletion rate of 3 mumol glycogen-glucose X g-1 X d-1 was observed from d 3 to 7.

Animals↗

Pentose cycle flux and fatty acid synthesis in bovine adipose tissue slices incubated with 6-aminonicotinamide.

The effects of the purported inhibitor of 6-phosphogluconate dehydrogenase, 6-aminonicotinamide, on lipogenesis from acetate and the metabolism of glucose were investigated in bovine adipose tissue. The incorporation of [U-14C]acetate and tritium from [3-3H]glucose into fatty acids was stimulated by 6-aminonicotinamide proportionately, indicating that the pentose cycle provided the same percentage of NADPH required for fat synthesis in the absence and presence of 6-aminonicotinamide. Tissue samples incubated with 6-aminonicotinamide displayed higher maximal activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase than control samples. The cellular content of 6-phosphogluconate was increased by 6-aminonicotinamide by 40% in samples incubated with 2 mM glucose (plus 33 mU/ml insulin) and 10 mM acetate; 6-aminonicotinamide stimulated the production of L-lactate in either the absence or presence of acetate. Studies with 1-, 6-, and U-14C-labeled glucose indicated that 6-aminonicotinamide increased the proportion of utilized glucose metabolized by the pentose cycle in the absence, but not in the presence of acetate. Unlike results observed in rat adipose tissue, the primary effect of 6-aminonicotinamide was to increase the proportion of NADPH produced by the pentose cycle that was utilized for fat synthesis secondarily to the stimulation of lipogenesis by an unknown mechanism.

6-Aminonicotinamide↗

Metabolic responses to fasting and alloxan-induced diabetes mellitus in steers.

To induce diabetes mellitus in 8 steers, they were fasted for 96 hours and given 110 mg of alloxan/kg of body weight (IV, in 1 dose) immediately before refeeding. Subsequently, 4 of the steers were treated with insulin (0.1 to 3 U/kg) to control hyperglycemia and 4 were not given insulin. Four control steers were fasted and refed. Fasting increased serum phosphorus, total protein, and bilirubin and decreased serum magnesium and potassium. Refeeding returned serum values of magnesium, potassium, total protein, and bilirubin toward base-line values, regardless of treatment group. However, serum phosphorus remained increased in steers with alloxan-induced diabetes and was not lowered by insulin injections. Sodium and chloride values were depressed in steers with alloxan-induced diabetes; these values remained significantly (P less than 0.05) lower than base-line values, even in steers given insulin. Fat infiltration was evident in the pancreas, liver, and to some extent, kidneys of steers with alloxan-induced diabetes, but was occasionally present in tissues of steers given insulin.

Animals↗

Digestion and absorption of nutrients by beef heifers fed a high concentrate diet.

A replicated, 3 X 3 Latin square design was used to evaluate effects of calculated metabolizable energy (ME) intake by beef heifers on apparent digestibility (AD), retention and net absorption (portal-arterial plasma concentration times portal plasma flow measured by dye dilution) of various nutrients. Six Hereford X Angus heifers (295 +/- 4 kg) with catheters in portal and mesenteric veins and iliac artery were fed once daily a high concentrate, pelleted diet to provide 84, 157 or 225 kcal ME/kg0.75. Linear (P less than 0.05) responses to increased ME intake included AD of dry matter (84.9-76.7%); AD of digestible energy (DE) (83.4-74.3%); AD of nitrogen (N) (70.5-62.1%); N retained (-6.3 to 25.6 g/day); portal blood flow (444-782 liters/hour); and net absorption of volatile fatty acids (VFA) (311-795 mmol/hour), L-lactate (62.5-118.4 mmol/hour), and urea-N (-19.9 to -51.4 mmol/hour). Net ammonia-N absorption increased linearly (P less than 0.10) from 35.6 to 43.8 mmol/hour as ME intake increased. Net glucose absorption was negative at low intake, but tended to increase to positive values as intake increased. Moles of acetate (46.3), propionate (29.3) or 4-carbon VFA (6.3) per 100 mol of net organic acid (VFA plus L-lactate) absorbed were similar among intake levels. Intake level did not affect proportions of DE intake (0.43) or calculated ME intake (0.46) accounted for by net organic acid absorption.

Absorption↗

Interrelationships between insulin and lipid metabolism in normal and alloxan-diabetic cattle.

Three experiments were performed to elucidate the role of insulin in regulating adipose tissue lipogenesis and lipolysis in the bovine. First, 4-day fasted steers were injected with 110 mg/kg alloxan on the day of refeeding; half the group received sufficient insulin to maintain near-normal blood glucose levels. Biopsy samples of subcutaneous adipose tissue were obtained throughout this and subsequent experiments. Insulin therapy increased the incorporation of 14C-labeled substrates into fatty acids, but was not necessary to increase lipogenic enzyme activities to control values. Steers in the second experiment were not fasted prior to alloxan injection (60 mg/kg). Seven days after alloxan treatment, the animals were injected with insulin, while a control group was pair-fed to the level of intake observed for the alloxan-treated steers during the first 7-day period. Whereas alloxan treatment decreased, and insulin therapy increased substrate incorporation and lipogenic enzyme activities, these effects were more closely correlated with levels of feed intake than with insulin levels. Alloxan treatment increased the basal but not the stimulated lipolytic rate in adipose tissue, and insulin treatment depressed the increased rate of lipolysis, as reflected in the plasma levels of free fatty acids and triglycerides. In the third experiment, one group of steers was injected with 1-6 U/kg of insulin, while a second group received insulin injections plus glucose infusions (125.3 mmol/hour). Increases in substrate incorporation and the activity of acetyl CoA carboxylase were observed in the insulin plus glucose-infused steers, but not in those animals receiving insulin alone. There were no effects of insulin or glucose plus insulin treatment on basal or stimulated lipolytic rates. The results of this study suggest that circulating insulin levels do not influence in vivo rates of lipogenesis in the bovine animal to the degree observed in the laboratory rat.

ATP Citrate (pro-S)-Lyase↗

Role of insulin in regulating amino acid metabolism in normal and alloxan-diabetic cattle.

Experimental diabetes was induced in the bovine in two experiments by intravenous injection of alloxan (110 mg/kg or 60 mg/kg) in order to determine the role of insulin on nitrogen and amino acid metabolism. In experiment 1, insulin was injected to control hyperglycemia in one group of steers immediately after alloxan treatment (110 mg/kg). In experiment 2, insulin was injected beginning 6 days following alloxan treatment (60 mg/kg) to control hyperglycemia. Plasma glucose increased to 800-1400 mg/100 ml within 5-6 days following alloxan administration (experiment 1). A large surge of insulin release occurred immediately after alloxan administration, which was followed by a decrease in insulin concentrations to subnormal levels in those animals not treated with insulin. Alloxan-treated steers became acidotic by day 2 as indicated by a drop in blood pH, bicarbonate and base excess. Acid-base status improved in steers treated with alloxan plus insulin but did not return to normal. Alloxan treatment caused a marked increase in serum urea-N and creatinine concentrations and insulin treatment of the alloxanized animal decreased both serum urea-N and creatinine concentrations. Treatment with alloxan caused a two- to threefold increase in the plasma concentrations of valine, isoleucine, leucine, lysine and 3-methylhistidine and a decrease in alanine, threonine, citrulline and arginine. Insulin treatment of the alloxanized bovine maintained normal plasma concentrations of valine, isoleucine and leucine. In a third experiment, the injection of insulin (6 U/kg) into normal cattle caused a transient decline in plasma concentrations of branched-chain amino acids (BCAA); however, if glucose was continuously infused (125 mmol/hour) in addition to insulin injection, a sustained decrease in plasma BCAA concentrations was observed. These data support the concept that insulin promotes decreased plasma concentrations of BCAA either by promoting tissue anabolism by stimulating tissue uptake and protein synthesis or decreasing proteolysis and BCAA release.

Amino Acids↗

Influence of diet on glucose turnover and rates of gluconeogenesis, oxidation and turnover of D-(-)-lactate in the bovine.

D-(-)-Lactate metabolism as influenced by the level of roughage in the diet was examined in eight Hereford heifers (306 kg) fed ad libitum as alfalfa hay diet (R) (2.02 Mcal ME/kg) (ME, metabolizable energy) or a 90% concentrate diet (C) (2.95 Mcal ME/kg) for 18 days. Animals were adjusted to negative pressure hoods (188 liter/minute airflow) and fitted with jugular and urinary catheters. Animals received 32.2 and 71.4 microCi of D-[U-14C]lactate and 435.7 and 233.3 microCi of 2-[3H]glucose for the primer dose and hourly infusion rates, respectively. Blood, expired CO2 and urine samples were taken at 30-minute intervals for 6 hours with CO2 and urine samples taken for an additional 24 and 42 hours, respectively. ME intakes were not different between diets (P greater than 0.05) for the day of infusion. Glucose turnover rates were 143.3 and 154.3 mmol/hour, whereas, D-(-)-lactate turnover was 0.67 and 0.57 mmol/hour for R anc C, respectively. Rates of oxidation and gluconeogenesis were 0.61 and 0.22 mmol/hour for R and 0.55 and 0.16 mmol/hour for C. Recovery of 14C in urine and expired air accounted for 3.73 and 44.3% of the infused dose for R and 2.13 and 43.5% of the infused dose for C. Oxidation was the major route of D-(-)-lactate elimination but the potential for D-(-)-lactate elimination from the bovine under high D-(-)-lactate loads is as yet undetermined.

Animal Nutritional Physiological Phenomena↗