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PubMed2002

Modelling mammary metabolism in the dairy cow to predict milk constituent yield, with emphasis on amino acid metabolism and milk protein production: model evaluation.

A model of mammary metabolism has been constructed and parameterized, with milk protein synthesis represented as a function of five essential amino acids (EAA) (Hanigan et al., 2001). Herein the model is evaluated using both the data used to construct the model (reference data) and an independent data set (literature data), and sensitivity to inputs and parameter estimates is assessed. The model predicted metabolite removal well for the reference data with exceptions for glutamate, glucose, and acetate. However, predictions of milk protein synthesis exhibited significant mean positive bias, which apparently was associated with the representation of milk protein synthesis. Adjustment of model parameters removed the mean bias, however, prediction accuracy was still inadequate. Simulation of the single reference experiment containing all critical inputs resulted in predictions of milk protein output that explained 53% of the observed variation, suggesting that the limited accuracy of the model when applied to the entire reference data set was due to assumptions regarding missing inputs. Mammary removal of glutamate, isoleucine, lysine, phenylalanine, tyrosine, valine, glycerol, beta -hydroxybutyrate (BHBA), and acetate were predicted less accurately when simulations of the independent data set were conducted. Twenty-five percent of the observed variation in milk protein yields for the independent data set was explained by the model. Refitting parameters for removal of isoleucine, lysine, phenylalanine, tyrosine, valine, glycerol, BHBA, and acetate raised the variation explained to 43%. Sensitivity analysis indicated that milk protein synthesis was responsive to only the five EAA used in its determination, with sensitivity to any single EAA falling to zero as supply of the EAA exceeded protein synthetic needs. Similarly, milk protein synthesis was readily affected by parameters associated with removal and metabolism of the five EAA. Milk lactose was found to be sensitive to glucose input as well as to similar parameters and inputs as milk protein. It is concluded that representation of the milk protein synthesis process as a function of a single limiting EAA may not be adequate and might be better represented by simultaneous consideration of multiple EAA. Additional work on the description of energy metabolism is also suggested.

Amino Acids↗
PubMed1992

Muscle protein turnover and amino acid metabolism in patients with chronic renal failure.

Muscle protein turnover and amino acid (AA) exchange were studied in 4 patients with chronic renal failure (CRF) and in 5 controls in the postabsorptive state by using the forearm perfusion method together with the systemic infusion of 3H-Phe. In CRF patients muscle protein breakdown is increased and is associated with a parallel increase in protein synthesis. Protein breakdown is inversely related to arterial bicarbonate. Net proteolysis is unchanged. The release of total AA, glutamine and alanine is not different from controls, whereas the release of valine and leucine is reduced and serine uptake tends to be decreased. In conclusion, in postabsorptive patients with CRF, well before the uremic stage, an increased protein breakdown associated with metabolic acidosis takes place; net proteolysis is unaffected. Alterations in BCAA metabolism suggest the occurrence of increased BCAA degradation proceeding beyond the transamination step.

Adult↗
PubMed1992

Branched-chain amino acid metabolism in isolated perfused liver of cirrhotic rats.

We examined the possible contribution of the liver to the alterations in branched-chain amino acid (BCAA) metabolism in cirrhosis. The livers of male Sprague-Dawley rats with CCl4-induced cirrhosis were removed and placed in a recirculating perfusion system. Net amino acid uptake and release were determined over 55 min. Results were compared with those obtained with control animals, which were either pair-fed or fed ad libitum. Intrahepatic amino acid concentrations were determined at the end of the perfusion. The release of isoleucine and leucine was significantly lower in the cirrhotic livers than in the controls fed ad libitum. There was no difference between the cirrhotic and pair-fed groups with regard to the fluxes of the three BCAA. Intrahepatic concentrations of BCAA were reduced only in pair-fed controls. These results suggest that both cirrhosis and a low protein/calorie diet alter hepatic BCAA flux, but via different mechanisms. In cirrhosis, alterations could be due both to low food intake and to BCAA metabolism in non-parenchymal cells.

Amino Acids, Branched-Chain↗
PubMed1983

Branched-chain amino acid metabolism in chronic renal failure.

Interorgan exchange of branched-chain amino acids (BCAA) in the postabsorptive state was evaluated in 16 patients with chronic renal failure (CRF) and in 20 subjects with normal renal function, by measuring arterial-venous differences of BCAAs across the leg, brain, hepato-splanchnic (HS) bed, and kidney. In CRF, arterial blood levels of valine are significantly reduced, whereas leucine and isoleucine levels are not different from controls; valine and leucine levels are directly related to GFR. In CRF, a significant decrease in the release of valine by the leg is observed; the leucine release tends to be lower; for both these amino acids, leg release is directly related to their arterial levels. Both ratios of valine and leucine release to total amino acid release by the leg are significantly reduced in CRF. Furthermore, in CRF cerebral uptake and fractional extraction of valine and isoleucine are decreased. In normal subjects, valine and leucine are significantly extracted by the HS bed, whereas in CRF the HS uptake of valine and its fractional extraction fall significantly and leucine uptake is unchanged. The kidney releases significant amounts of leucine both in CRF and in controls. In conclusion, in CRF in the postabsorptive state the exchange of BCAAs, mainly valine, is altered rather early at the major sites of production and utilization, and the flux of these amino acids among the organs is decreased. The primary defect is the decreased output by peripheral tissue, which reduces the supply of BCAAs to the brain and HS bed. Regional metabolic disturbances further impair BCAA utilization.

Adult↗
PubMed2006

A peroxisomal glutathione transferase of Saccharomyces cerevisiae is functionally related to sulfur amino acid metabolism.

Saccharomyces cerevisiae cells contain three omega-class glutathione transferases with glutaredoxin activity (Gto1, Gto2, and Gto3), in addition to two glutathione transferases (Gtt1 and Gtt2) not classifiable into standard classes. Gto1 is located at the peroxisomes, where it is targeted through a PTS1-type sequence, whereas Gto2 and Gto3 are in the cytosol. Among the GTO genes, GTO2 shows the strongest induction of expression by agents such as diamide, 1-chloro-2,4-dinitrobenzene, tert-butyl hydroperoxide or cadmium, in a manner that is dependent on transcriptional factors Yap1 and/or Msn2/4. Diamide and 1-chloro-2,4-dinitrobenzene (causing depletion of reduced glutathione) also induce expression of GTO1 over basal levels. Phenotypic analyses with single and multiple mutants in the S. cerevisiae glutathione transferase genes show that, in the absence of Gto1 and the two Gtt proteins, cells display increased sensitivity to cadmium. A gto1-null mutant also shows growth defects on oleic acid-based medium, which is indicative of abnormal peroxisomal functions, and altered expression of genes related to sulfur amino acid metabolism. As a consequence, growth of the gto1 mutant is delayed in growth medium without lysine, serine, or threonine, and the mutant cells have low levels of reduced glutathione. The role of Gto1 at the S. cerevisiae peroxisomes could be related to the redox regulation of the Str3 cystathionine beta-lyase protein. This protein is also located at the peroxisomes in S. cerevisiae, where it is involved in transulfuration of cysteine into homocysteine, and requires a conserved cysteine residue for its biological activity.

Amino Acid Sequence↗
PubMed1998

Sexual differences in branched chain amino acid metabolism into fatty acids and cholesterol in Harderian gland of golden hamster.

The Harderian gland of golden hamster (Mesocricetus auratus) secretes copious lipids, most of which is 1-alkyl-2,3-diacylglycerol (ADG). We previously reported that the composition of ADG shows marked sexual dimorphism [Seyama et al. (1995) J. Biochem. 117, 661-670]. Male ADG contains only straight chain alkyl and acyl groups, but female ADG contains a lot of branched chain ones too. In this study, we investigated the metabolism of branched chain amino acids (BCAAs) and analyzed the incorporation of the metabolites into lipids in the Harderian gland. Golden hamsters were injected intraperitoneally with [U-14C]BCAAs, and Harderian glands were obtained at 3, 6, 9, and 24 h after injection. Lipids were then extracted from the glands and analyzed. Thin layer chromatography revealed that the ADG was labeled in both sexes, but the profile depended on the sex. The cholesterol fraction was labeled only in the male gland. The alkyl and acyl groups of ADG were subjected to radio-gas liquid chromatography. As for the alkyl groups, radioactivity was detected in straight-C16 and -C18 chains in males, while branched-C17 and -C19 chains were labeled in females. As for the acyl groups, straight-C14, -C15, and -C16 chains were labeled in males, while in females, branched-C17 and -C19 chains were labeled as well as a straight-C16 chain. These results suggest that the BCAA metabolism should be regulated as to the sex at the step of branched chain acyl-CoA degradation in the Harderian gland of golden hamster, which causes the sexual dimorphism in the lipid composition in this gland.

Amino Acids↗
PubMed2001

Alternate cadmium exposure differentially affects amino acid metabolism within the hypothalamus, median eminence, striatum and prefrontal cortex of male rats.

This work was designed to analyze the possible changes in glutamate, aspartate and glutamine content induced by cadmium exposure in the hypothalamus, striatum and prefrontal cortex of rats, using an alternate schedule of metal administration. Pubertal-adult differences were also evaluated. In adult control rats, glutamate and aspartate contents in the anterior hypothalamus decreased as compared to pubertal controls. After cadmium administration from day 30 to 60 of life, the content of anterior hypothalamic glutamate and aspartate diminished. In adult control animals, the glutamine content increased in mediobasal hypothalamus as compared to pubertal controls. After cadmium exposure from day 30 to 60 of life, the mediobasal glutamine content increased, and after cadmium treatment from day 60 to 90 of life, the mediobasal aspartate content decreased. In adult control rats the content of glutamine, glutamate and aspartate of the posterior hypothalamus decreased significantly. After cadmium administration in pubertal animals, posterior hypothalamic contents of glutamine, glutamate and aspartate diminished. Cadmium treatment of adult animals caused a decrease in glutamine content, as compared to controls. In adult control rats, only glutamate and aspartate content increased in the prefrontal cortex as compared to the values found in pubertal controls. When cadmium was administered to adult animals, only the aspartate content decreased. In the striatum, cadmium decreased the glutamine and aspartate contents when administered from day 60 to 90 of life. These data suggest that cadmium differentially affects amino acid metabolism in the hypothalamus, striatum and prefrontal cortex. Age-dependent effects of cadmium on these brain areas appeared to have occurred.

Aging↗
PubMed1983

Relationship between central nervous system hydrogen ion regulation and amino acid metabolism in hypercapnia.

Resting level of ventilation is affected by change in hydrogen ion [H+] and by certain amino acid neurotransmitters in the brain and cerebral fluids. Hypercapnia alters both [H+] and amino acid content. Therefore, the effect of 90 min of hypercapnia on blood and cerebrospinal fluid (CSF) contents of selected amino acids and ammonia was studied in anesthetized mongrel dogs using 13N-labeled ammonia. Metabolic turnover of CSF ammonia was not significantly altered by hypercapnia, but CSF equilibrium concentration of metabolized ammonia, i.e., glutamine, a precursor of the neurotransmitters glutamic acid and gamma amino butyric acid, varied linearly with CSF bicarbonate and hydrogen ion concentration. The percentage of CSF glutamine derived from tracer-labeled ammonia metabolized in the central nervous system (CNS) rose from 30% at normocapnia to 60% after 90 min of hypercapnia, whereas at the same time, the CSF transfer rate of glutamine increased by a factor of 2. These observations show that there is a significant correlation between CNS transfer of glutamine and CNS hydrogen ion regulation during hypercapnia.

Acid-Base Equilibrium↗
PubMed2006

Lessons from genetic disorders of branched-chain amino acid metabolism.

Genetic disorders of BCAA metabolism produce amino acidopathies and various forms of organic aciduria with severe clinical consequences. A metabolic block in the oxidative decarboxylation of BCAA caused by mutations in the mitochondrial branched-chain alpha-keto acid dehydrogenase complex (BCKDC) results in Maple Syrup Urine Disease (MSUD) or branched-chain ketoaciduria. There are presently five known clinical phenotypes for MSUD, i.e., classic, intermediate, intermittent, thiamin-responsive, and dihydrolipoamide dehydrogenase (E3)-deficient, based on severity of the disease, response to thiamin therapy, and the gene locus affected. Reduced glutamate, glutamine, and gamma-aminobutyrate concentrations induced by the accumulation of branched-chain alpha-ketoacids in the brain cortex of affected children and neonatal polled Hereford calves are considered the cause of MSUD encephalopathies. The long-term restriction of BCAA intake in diets and orthotopic liver transplantation have proven effective in controlling plasma BCAA levels and mitigating some of the above neurological manifestations. To date, approximately 100 mutations have been identified in four (branched-chain alpha-ketoacid decarboxylase/dehydrogenasealpha [E1alpha], E1beta, dihydrolipoyl transacylase [E2], and E3) of the six genes that encode the human BCKDC catalytic machine. We have documented a strong correlation between the presence of mutant E2 proteins and the thiamin-responsive MSUD phenotype. We show that the normal E1 component possesses residual decarboxylase activity, which is augmented by the binding to a mutant E2 protein in the presence of the E1 cofactor thiamin diphosphate. Our results provide a biochemical model for the effectiveness of thiamin therapy to thiamin-responsive MSUD patients.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1999

Effects of ammonia on the anaplerotic pathway and amino acid metabolism in the brain: an ex vivo 13C NMR spectroscopic study of rats after administering [2-13C]] glucose with or without ammonium acetate.

The 13C-label incorporation into glutamate, glutamine, aspartate and gamma-aminobutyric acid (GABA) from [2-13C] glucose was measured by 13C nuclear magnetic resonance (NMR) spectroscopy to directly examine the effects of ammonia on the activity of pyruvate carboxylase (i.e., the anaplerotic pathway) and the amino acid metabolism in the rat brain in vivo. Rats were sacrificed by exposure to microwaves at 7.5, 15, 30, and 60 min after an i.v. injection of [2-13C] glucose with or without ammonium acetate. After the injection of ammonium acetate, the brain contents of glutamate, aspartate and GABA had decreased, however, the percentage of 13C enrichment of C3 of glutamine, glutamate and GABA, and C2 and C3 of aspartate had increased. The 13C entered the TCA cycle via pyruvate carboxylase from [2-13C] glucose, labeling the C2 or C3 positions of aspartate, the C2 or C3 positions of glutamate and glutamine, and the C3 or C4 positions of GABA first and second turns of the tricarboxylic acid (TCA) cycle. The C4/C3 labeling ratio in GABA was lower than the analogous ratio in glutamate (C2/C3) and higher than that of glutamine (C2/C3). The order of these ratios (glutamate > GABA > glutamine) was not altered by the injection of ammonium acetate. These findings directly indicate that ammonia increases the anaplerotic pathway and that the 13C-skeletons entered glial glutamine through the anaplerotic pathway flow from glia to neuron. A fraction of the glutamine is used in the direct synthesis of GABA via glutamate, whereas the remaining fraction of glutamine passed through the neuronal TCA cycle before synthesizing GABA.

Acetates↗