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At least 19 recordsLinked to original sources

PubMed1976

[Characterisation of D(-)glyceric acid from Nocardia caviae (author's transl)].

A glycolipid was found in a strain of Nocardia caviae. It consists of glucose, myristic, palmitic and stearic acids and a polyhydroxylated acid. The structure of this hydroxyacid was demonstrated by the identification of the product glycerol after LiA1H4 reduction of the glycolipid methyl ester and subsequent hydrolysis, by comparison of the infrared spectra of the hydroxyacid and glyceric acid, by gas chromatography of acetylated methyl and ethyl esters of the polyhydroxylated acid and of standard glyceric acid and by mass spectrometry of the diacetylated methyl ester. The hydroxyacid from the glycolipid is D(-)glyceric acid, a compound rarely found amongst natural products.

Glucose↗

PubMed1977

Determination of the configurations of lactic and glyceric acids from human serum and urine by capillary gas-liquid chromatography.

The separation of the enantiomers of lactic and glyceric acids can be achieved by capillary gas chromatography on SP-1000 using the corresponding O-acetylated methyl esters. The structures of the derivatives were proved by proton magnetic resonance spectroscopy and mass spectrometry. The method has been used for the determination of the absolute configuration of lactic and glyceric acids isolated from serum and urine from different patients.

Capillary Action↗

PubMed1976

D-glyceric-acidaemia and non-ketotic hyperglycinaemia. Clinical and laboratory findings in a new syndrome.

The clinical and laboratory findings in a 2 1/2-year-old boy with non-ketotic hyperglycinaemia are reported. Except for a somewhat impaired liver function there was a picture similar to the cases previously reported in the literature. The patient deviated from the classical description, however, in the excretion of large amounts of D-glyceric acid in the urine. The same compound was also repeatedly found in the serum. It is suggested that the large amounts of glycine found in various body fluids are secondary to a hitherto undescribed enzymatic defect in the degradation of D-glyceric acid.

Amino Acid Metabolism, Inborn Errors↗

PubMed1975

The mechanism of end product inhibition of serine biosynthesis. V. Mechanism of serim inhibition of phosphoglycerate dehydrogenases.

The reduction of enzyme-bound DPN constitutes a half-reaction of phosphoglycerate dehydrogenase and has been investigated fluorometrically. Serine was found to inhibit the half-reaction to the same extent and with the same degree of cooperation as the steady state reaction. This finding identifies the ternary complex conversion as the point in the reaction sequence at which serine inhibition occurs. Delta H determinations for the half-reaction showed no difference whether serine was or was not present and led to the conclusion that the inhibitory effect of serine could only manifest itself through the delta S term in the expression for the formation of the activated transition state complex. DL-3-P[2-2H]glyceric acid showed no primary isotope effect in the half-reaction. This result excludes hydrogen transfer as the rate-limiting step in the half-reaction and confirms that an isomerization step, affected by serine, exists in the ternary complex conversion scheme. The deuterated 3-P-glyceric acid shows an isotope effect of 2 in the steady state reaction.

Alcohol Oxidoreductases↗

PubMed1977

Role of rat-liver alcohol dehydrogenase in the glycerol pathway to L-lactate in homogenates.

14C-Distribution in the C3-chain of L-lactate after incubation of various 14-C-labelled prescursors ([1-14C] and [3-14C] glycerol; [3-14C] glyceraldehyde and glycerid acid; D- and L-[3-14C] serine; [1-14C] fructose and [6-14C] glucose) with homogenate showed that (1) most of the glycerol is metabolized to L-lactate via D-glyceraldehyde; the remainder may possibly form L-lactate via dihydroxyacetone; (2) a part of D-glyceraldehyde and D-glyceric acid may produce glycerol before L-lactate is formed; (3) D and L-serine do not form measurable amounts of L-lactate via D-glyceric acid; (4) rat-liver alcohol dehydrogenase (E.N.1.1.1.1) does not contribute to conversion to L-lactate of dihydroxyacetone phosphate from fructose nor of D-glyceraldehyde phosphate from glucose.

Alcohol Oxidoreductases↗

PubMed1979

A compound representing the D-glycerate terminus of the methylglucose-containing polysaccharide of Mycobacterium smegmatis.

In order to study the structure of the methylglucose-containing polysaccharide (MGP) of Mycobacterium smegmatis by NMR spectroscopy, we have prepared the model compound O-alpha-D-glucopyranosyl-(1 leads to 2)-D-glyceric acid. This compound, which represents the aglycon-containing terminus of MGP, was made from leucorse [O-alpha-D-glucopyranosyl-(1 leads to 5)-D-fructopyranose] by successive treatment with sodium borohydride, lead tetraacetate, and hypobromite. The structure of O-alpha-D-glucopyranosy.-(1 leads to 2)-D-glyceric acid was confirmed by chemical and enzymic methods. 13C and 1H NMR spectra of this compound, together with spectra of several disaccharides, were obtained for future reference in the polysaccharide study. The nine resonances in the 13C spectrum were assigned by comparison with the spectrum of methyl alpha-D-glucopyranoside. Analysis of the 1H NMR spectrum showed that the two methylene protons on C-3 of the glycerate moiety were less equivalent in the sodium salt than in the acid. This may be attributable to hydrogen bonding between the carboxylate and the hydrogen atom of the glycerate 3-hydroxyl group.

Carbohydrate Conformation↗

PubMed1976

The synthesis of chiral glycerides starting from D- and L-serine.

A method for synthesizing chiral glycerides starting from L- or D-serine is described. Optically-active serine (both enantiomers are commerically available) was transformed into glyceric acid by stereospecific diazotization. The configuration at carbon atom 2 was maintained during the reaction. The glyceric acid was then converted into optically pure isopropylideneglycerol - which is an important intermediate in the synthesis of mono-, di- and triglyderides - by esterification followed by acetalization with acetone and reduction with lithium aluminium hydride. Reaction of this intermediate with triphenylphosphine in tetrachloromethane followed by acid-catalysed hydrolysis and dehydrohalogenation provided optically-active glycidol (2,3-epoxy-1-propanol). The epoxy ring of an ester of glycidol and a fatty acid was then opened stereospecifically with retention of configuration by heating the glycidol ester in the presence of a second fatty acid and a catalyst. This yielded a chiral 1,3-diglyceride which could be converted into a chiral triglyceride.

Diglycerides↗

PubMed1975

32P distribution into 2,3-bisphosphoglyceric acid from human erythrocytes following molybdate-catalyzed hydrolysis.

Normal human washed erythrocytes were incubated in autologous plasma with 32P for varying periods of time. 2,3-Bisphosphoglyceric acid the major organic phosphate ester of red cells, was first isolated and purified by anion-exchange chromatography; subsequently, the C-2Pi was selectively hydrolyzed by a molybdate-catalyzed reaction. The C-2-bound Pi of 2,3-P2-glyceric acid was found to have a significantly higher specific activity than C-3 Pi. Intramolecular equilibration was not reached until the 180-min incubation. No evidence of overhydrolysis or internal randomization by the molybdate reaction was noted which was confirmed following hydrolysis of double-label 2,3-P2-glyceric acid 32P C-2, 33P C-3.

Chromatography↗

PubMed1977

Properties of Escherichia coli mutants deficient in enzymes of glycolysis.

Physiological properties of mutants of Escherichia coli defective in glyceraldehyde 3-phosphate dehydrogenase, glycerate 3-phosphate kinase, or enolase are described. Introduction of a lesion in any one of the reversible steps catalyzed by these enzymes impaired both the glycolytic and gluconeogenic capabilities of the cell and generated an obligatory requirement for a source of carbon above the block (gluconeogenic) and one below (oxidative). A mixture of glycerol and succinate supported the growth of these mutants. Mutants lacking glyceraldehyde 3-phosphate dehydrogenase and glycerate 3-phosphate kinase could grow also on glycerol and glyceric acid, and enolase mutants could grow on glycerate and succinate, whereas double mutants lacking the kinase and enolase required l-serine in addition to glycerol and succinate. Titration of cell yield with limiting amounts of glycerol with Casamino Acids in excess, or vice versa, showed the gluconeogenic requirement of a growing culture of E. coli to be one-twentieth of its total catabolic and anabolic needs. Sugars and their derivatives inhibited growth of these mutants on otherwise permissive media. The mutants accumulated glycolytic intermediates above the blocked enzyme on addition of glucose or glycerol to resting cultures. Glucose inhibited growth and induced lysis. These effects could be substantially overcome by increasing the osmotic strength of the growth medium and, in addition, including 5 mM cyclic adenosine 3',5'-monophosphate therein. This substance countered to a large extent the severe repression of beta-galactosidase synthesis that glucose caused in these mutants.

Carbohydrate Metabolism↗

PubMed1976

D-Glyceric acidemia in a patient with chronic metabolic acidosis.

A patient is described with glyceric acidemia and glyceric aciduria. The main clinical problems in infancy were severe metabolic acidosis and failure to thrive. The patient needs permanent treatment with bicarbonate. Hyperglycinemia, as described in the first case discovered elsewhere, was not present. The glyceric acid was found to have the D-configuration, as analyzed by capillary gas chromatography of its di-O-acetyl-l-menthyl ester. The abnormality may result from a defect in serine metabolism.

Acidosis↗

PubMed1975

Carbohydrate metabolism and its response to catecholamines as modified in alkalotic rat.

Metabolic activities and their responses to catecholamines were studied in fasted rats exposed to simulated altitudes. Analysis of hepatic levels of gluconeogenic intermediates revealed the inhibition of gluconeogenesis between glyceric acid 3-P and fructose 6-P associated with a rise of the ratios of redox pairs such as lactate to pyruvate in livers of alkalotic rats. Inhibition of gluconeogenesis was indicated also by the suppressed incorporation of glutamate 14C into blood glucose. Since no activation was detected on glycolytic pathway of skeletal muscles, marked hyperlactacidemia during alkalosis appeared to result from the suppression of hepatic gluconeogenesis. Most of metabolic actions of epinephrine and isoproterenal known to be mediated via the beta receptor were significantly reduced but not completely abolished during alkalosis. Exceptionally, hyperinsulinemia induced by isoproterenol was completely reversed and replaced by hypoinsulinemia during alkalosis. Despite hypoinsulinemia, hyperglycemia induced by glucose load decreased more rapidly in alkalotic than in normal rats. In view of the fact that the adrenergic alpha receptor is involved in theinhibition of insulin secretion, the observed irregular modifications of catecholamine actions could be explained on the basis of a postulate that the adrenergic alpha-receptor functions are potentiated in alkalosis.

Alkalosis, Respiratory↗

PubMed1976

D-glyceric acidemia: biohcemical studies of a new syndrome.

Studies of a mentally retarded boy, clinically suffering from nonketotic hyperglycinemia, are reported. Using combined gas chromatography-mass spectrometry, enzyme specificity studies, and spectropolariometry D-glyceric acid in extremely elevated concentrations was demonstrated in both serum and urine (serum: 1.0-1.3 mmol/liter, urine: 33-187 mmol/liter). Hydroxypyruvic acid was not detectable in urine from this boy using a gas chromatographic method with a limit of detection of 0.3 mmol/liter. Enzyme assays of D-glyceric dehydrogenase on blood leukocytes demonstrated significantly lower activity in the patient compared with five normal children.

Alcohol Oxidoreductases↗

PubMed1977

Gas chromatographic and mass spectrometric studies on urinary organic acids in a patient with congenital lactic acidosis due to pyruvate decarboxylase deficiency.

Detailed studies, using gas chromatography and mass spectrometric methods, of the urinary organic acids excreted by a patient with proven pyruvate decarboxylase deficiency are reported. In addition to the greatly-increased levels of lactate and pyruvate, marked elevation in the levels of 2-oxoglutaric, malic, and isocitric acids were observed, with associated increases 2-hydroxyglutaric, fumaric, succinic, and glyceric acids, and reduced citric acid excretion. The levels of excretion during clinically static and acute periods are compared to those in a normal neonate and normal infants. The metabolites observed indicate a probable defect in the oxidation of pyruvate by pyruvate dehydrogenase and suggest the presence of secondary defects in the tricarboxylic acid cycle. Studies of this type may enable the relatively rapid identification of the probable underlying enzyme deficiency in cases of congenital lactic acidosis, prior to confirmatory enzyme studies.

Acidosis↗

PubMed1978

Glycolic acid in urine. A colorimetric method with values in normal adult controls and in patients with primary hyperoxaluria.

An improved Chromotropic acid-sulfuric acid assay for urinary glycolic acid is described. The sample (0.5 ml or less) is precleaned by filtering through strongly acidic and strongly basic ion-exchangers and compared with a standard made up in normal urine. From the many compounds tested, only glyceric acid in pathologically high concentrations interfers partially; this interference can be recognized at 776 nm and eliminated by a second determination. Per man-day, 8--12 samples can be analyzed. Recovery of 0.8 mmol/l glycolic acid added to the urines of 12 persons was 100.6 +/- 4.7% (1 S.D., n=12) without, and 101.9 +/- 5.3% (1 S.D., n=12) with correction for isotope dilution of [1-14C]glycolic acid, respectively, using 0.5-ml sample volumes. The variation coefficients of a single determination were 1.5 and 2.1% without and with correction for isotope dilution, respectively (n=7). The method was checked by mass fragmentography. The following normal values were found in adults (n=15; x +/- 1 S.D. (range)): 47.3 +/- 10.1 (24.4--63.7) mmol/mol creatinine and 0.60 +/- 0.15 (0.29--0.91) mmol/day or 45.8 +/- 11.3 (22.2--69.0) mg/day. Two patients (F.G. and A.S.) with primary hyperoxaluria type I excreted glycolic acid between 112 and 379 mmol/mol creatinine and 1.21--5.64 mmol/day or 92--429 mg/day. Under vitamin B-6 treatment, urinary excretion decreased in one patient (F.G.) to 71--131 mmol/mol creatinine and 0.92--2.0 mmol/day or 70--152 mg/day.

Adult↗

PubMed1977

Pyruvate kinase mutants of Saccharomyces cerevisiae: biochemical and genetic characterisation.

Mutants of Saccharomyces cerevisiae lacking pyruvate kinase (EC 2.7.1.40) are described. These have less than 0.5% of the pyruvate kinase activity of the wild type. All the other glycolytic enzymes are present in normal amounts in these mutants. The mutation is recessive and segregates in diploids as a single gene. Five alleles examined fail to complement one another. Tetrad analysis and mitotic recombination data place the mutation on the left arm of chromosome I distal to cys 1. The majority of single-step spontaneous revertants on glucose regain the enzyme activity fully and this activity appears, by a number of criteria, to be due to the same enzyme present in the wild type. Some of these revertants become nuclear petites. The mutants do neither grow on nor ferment sugars but do grow on ethyl alcohol or pyruvate. Glucose addition to cultures growing on alcohol arrests growth until glucose is exhausted. The steady state rate of glucose utilization is slower than in the wild type. This is associated with the accumulation of as much as 5 micronmoles P-enolpyruvate per g wet weight of cells and proportional amounts of 2-P-glyceric and 3-P glyceric acids. The mutation is believed to involve some regulatory element in the synthesis of pyruvate kinase.

Chromosome Mapping↗

PubMed1976

The inhibition of insulin secretion from the perfused rat pancreas after thyroxine treatment.

Thyroxine treatment did not significantly affect the immediate insulin secretory response of the perfused rat pancreas, but it inhibited the late phase of D-glucose-induced insulin secretion. Thyroxine treatment did not inhibit D-glyceraldehyde-, D-mannose-, and tolbutamide-induced insulin release from the perfused pancreas. An increase in the D-glucose concentration of the perfusion medium as well as feeding of the rats did not restore insulin secretion after thyroxine treatment. The inhibition of D-glucose-induced insulin release in response to thyroxine treatment was reversed after addition of either D-glyceraldehyde, dihydroxyacetone, DL-glyceric acid, pyruvate, or alpha-ketobutyrate to the perfusion medium. Tolbutamide, L-glucose, D-fructose, D-mannose, L-lactate, and propionic acid were not able to overcome the inhibition of D-glucose-induced insulin secretion. Except for alpha-ketobutyrate all substances which were effective in reversing the inhibition of D-glucose-induced insulin release were glycolytic intermediates. Comparing the glycolytic alpha-ketoacid pyruvate and the non-glycolytic ketoacid alpha-ketobutyrate, the only part common to both substances was the ketoacid moiety. It is concluded from these findings that the ketoacid moiety of the alpha-ketoacids plays an important role in reversing the effect of thyroxine on D-glucose-induced insulin release.

Animals↗

PubMed1979

Insulin secretion by isolated perfused rat and mouse pancreas.

A method for isolation and perfusion of a pancreas preparation consisting of pancreas, stomach, proximal duodenum, and spleen is described. Basic characteristics of regulation of insulin secretion from the perfused pancreas isolated from rats, albino mice, obese mice (ob/ob), and black mice were identical. Viability and stability of the pancreas preparation during perfusion were maintained as documented by measurements of oxygen consumption of the pancreas preparation, perfusion pressure, and pH of the perfusion medium. The insulin-secretory capacity of the pancreas of different animal species was compared. Insulin secretion by the perfused rat and obese (ob/ob) mouse pancreas was much more potent than that by the pancreas of lean albino and lean black mice. D-Glucose-induced insulin secretion from the pancreas was decreased after fasting of the animals and was dependent on glucose concentration and presence of calcium in the perfusion medium. D-Glyceraldehyde, tolbutamide, D-mannose, dihydroxyacetone, L-leucine, and L-arginine also induced insulin secretion from the pancreas. D-Fructose, D-galactose, L-glucose, 3-O-methyl-D-glucose, N-acetylglucosamine, D-xylose, D,L-glyceric acid, pyruvate, L-lactate, and theophylline did not provoke insulin secretion.

Animals↗

PubMed1978

[Role of pyruvate kinase in non-specific changes of carbon photosynthetic metabolism, caused by the photophosphorylation inhibition].

The decrease in the level of NADP reduction in chloroplasts under injections of cofactors of pseudocyclic FMN photophosphorylation (vitamin K3 and methylviologen) into pea, tomato and cucumber leaves resulted in the decrease of 14CO2 autotrophic accumulation rate and in the change of distribution of assimilated carbon among the assimilation products. The inhibition of synthesis of labelled sugars and the increase of the content of 3-phosphoglyceric and glyceric acids in the labelled low molecular fraction were observed in all the experiments. Similar changes in the distribution of synthesized in Kalvin cycle labelled products, associated with the inhibition of its reduction unit, were observed under the effect of photophosphorylation uncoupling agents. However, the decrease of ATP/NADP ratio in chloroplasts resulted in the simultaneous increase of fixed 14CO2 incorporation into alanine. The role of pyruvate kinase in "alanine" effect, characteristic of non-specific changes of carbon photosynthetic metabolism, is discussed on the basis of the authors' previous data on the effect of phosphorylation on glycolysis reactions and on the basis of results of ADP introduction into leaf cuts.

Alanine↗