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R L Prior

Publications and source records attributed to R L Prior.

At least 19 recordsLinked to original sources

Dietary arginine deficiency alters flux of glutamine and urea cycle intermediates across the portal-drained viscera and liver of rats.

The effect of an arginine-deficient diet on net flux of amino acids across the portal-drained viscera and across the liver was studied in rats. Blood was obtained after food deprivation and 1 and 2 h after a meal of a 1.0% arginine control diet or an arginine-deficient diet containing 3.4% glutamate. The arginine-deficient diet decreased net portal-drained viscera flux of arginine and increased net portal-drained viscera flux of ornithine and proline. However, net portal-drained viscera flux of citrulline (0.35 +/- 0.05 mumol/min) was not influenced by diet; of this rate, 46% (0.16 mumol/min) bypassed the liver and was available for extrahepatic arginine synthesis. However, rats continued to exhibit signs of arginine deficiency such as decreased blood arginine concentrations (by 28%) and increased orotic acid excretion (90-fold). Arterial blood glutamine concentration was 25% higher in rats fed the arginine-deficient diet. In the fed state, net hepatic flux of glutamine was elevated from 0.15 (control) to 1.39 mumol/min, indicating that the liver was a major source of the increased blood glutamine concentrations. Increased production of hepatic glutamine and orotic acid may help rats compensate for dietary arginine deficiency, whereas splanchnic output of citrulline was not increased with dietary arginine deficiency even with a substantial dietary supply of glutamate.

Amino Acids

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

Xylazine-induced hyperglycemia in beef cattle.

Intravenous administration of xylazine to beef cattle (10 animals, 0.2 mg/kg of body weight) resulted in rapid onset (less than 15 minutes) of hyperglycemia. Plasma glucose values increased to 195 +/- 15 mg/dl and 305 +/- 10 mg/dl at 15 minutes and 3 hours, respectively. Concomitantly, plasma insulin concentrations dropped from 23 +/- 2 microU/ml before xylazine to 5.8 +/- 0.7 microU/ml and 2.4 +/- 0.3 microU/ml at 15 minutes and 3 hours, respectively. Parallel decreases (20%) were observed for percentage of hemoglobin, red blood cell number, and packed cell volume. Plasma urea nitrogen was significantly (P less than 0.01) incrased within 3 hours of xylazine administration (6.7 +/- 0.9 mg/dl vs 11.4 +/- 0.7 mg/dl). Marked changes in concentrations of plasma-free fatty acids were not observed. Alternative means of anesthesia must be considered in those instances in which biopsy material is to be used for studies of carbohydrate metabolism in vitro.

Animals