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At least 19 recordsLinked to original sources
PubMed1979

Metabolism of palmitate in perfused rat liver. Effect of low and high ethanol concentrations at various concentrations of palmitate in the perfusion medium.

1. The effect of ethanol on the metabolism of [1-(14)C]palmitate in rat liver was investigated in a single-pass perfusion system at concentrations of 10mm- or 80mm-ethanol and 0.2mm- or 1mm-palmitate. 2. After the perfusion the hepatic lipid was isolated in subcellular fractions. The two major fractions contained triacylglycerol from cytoplasmic lipid droplets and from endoplasmic reticulum plus Golgi apparatus respectively. 3. In experiments with 0.2mm-palmitate perfusion with 10mm- or 80mm-ethanol did not measurably increase the esterification, and the oxidation was markedly decreased and the fatty acid uptake was not affected. 4. Perfusion with ethanol, at 1mm-palmitate, increased the fatty acid uptake, increased esterification and decreased oxidation. The effects of 10mm- and 80mm-ethanol were similar. The incorporation of [1-(14)C]palmitate into triacylglycerol in cytoplasmic lipid droplets was not affected statistically significantly by ethanol. Ethanol increased the incorporation of [1-(14)C]palmitate into di- and tri-acylglycerol in the membranous fraction. Estimated chemically, the contents of di- and tri-acylglycerol were only slightly affected by ethanol. These results suggest that the effect of ethanol was to increase the turnover of fatty acids in triacylglycerol rather than to increase its accumulation. 5. The results indicate that an increased concentration of fatty acids is more important for the formation of acute fatty liver in fed rats than are the direct effects of ethanol on hepatic fatty acid metabolism.

Animals↗
PubMed1979

Amniotic fluid palmitic acid/stearic acid ratios. Lecithin/sphingomyelin ratios and palmitic acid concentrations in the assessment of fetal lung maturity in diabetic pregnancies.

The lecithin/sphingomyelin (L/S) ratio, palmitic acid concentration and palmitic to stearic acid (P/S) ratio were estimated on samples of amniotic fluid obtained from 66 patients with diabetes. These were compared with similar estimates on amniotic fluid obtained from 127 non-diabetic patients. At 35 to 40 weeks, significant differences were observed between the L/S ratio and palmitic acid concentration in diabetics and non-diabetics, whereas the P/S ratio was similar in the two groups. The amniotic fluid L/S ratio, palmitic acid concentration, and P/S ratio were estimated on amniotic fluid obtained from 20 diabetic patients within 48 hours of induction, and the clinical outcome of the newborn infant was used to assess the predictive value of the three parameters. In 19 out of 20 diabetics the P/S ratio correctly predicted fetal lung maturity, whereas the palmitic acid concentration was correct in 12 patients and the L/S ratio in only 10 patients.

Amniotic Fluid↗
PubMed1979

Amniotic fluid lecithin/sphingomyelin ratio, palmitic acid, palmitic acid/stearic acid ratio, total cortisol, creatinine, and percentage of lipid-positive cells in assessment of fetal maturity and fetal pulmonary maturity: a comparison.

Lecithin/sphingomyelin (L/S) ratio, creatinine, percentage of lipid-positive cells, palmitic acid, palmitic acid/stearic acid (P/S) ratio, and total cortisol were analyzed as tests for fetal maturity and fetal pulmonary maturity in 164 samples of amniotic fluid from 121 patients. Fifty samples were taken within 72 hours of delivery. The best tests for fetal maturity (37 weeks) with differential percentages were L/S ratio, palmitic acid, and P/S ratio. In the assessment of fetal pulmonary maturity, we studied an additional 174 samples in which only L/S ratio, creatinine, and lipid-positive cells were analyzed. All tests showed a high predictive value of an immature (positive) result was much less for all six parameters; the three best tests were total cortisol (33%), lipid-positive cells (26%) and L/S ratio (14%).

Amniotic Fluid↗
PubMed2026

Weight and metabolic changes in patients with schizophrenia treated with paliperidone palmitate 6-month formulation versus paliperidone palmitate 3-month formulation: a post-hoc analysis.

OBJECTIVE: To determine the effect that paliperidone palmitate 6-month long-acting injectable formulation (PP6M) had on metabolic parameters including body weight (BW), and blood lipid profiles, a post-hoc analysis was conducted to assess changes in BW from baseline to the end of study based on age, body mass index (BMI), and changes in blood lipid profiles during a 12-month, phase 3, double-blind (DB) clinical study. Long term effects of PP6M on BW and BMI were further explored during a 24-month extension study in which participants were treated exclusively with PP6M. METHOD: In the 12-month DB phase, participants were randomized to receive PP6M or paliperidone palmitate 3-month long-acting injectable formulation (PP3M). The mean change in BW and abnormal weight percent change from baseline were calculated at endpoint by age, gender, and BMI. Additionally, treatment-emergent shifts from baseline for the four key lipid parameters (fasting low density lipoprotein [LDL], fasting triglycerides [TG], fasting total cholesterol [TC], and fasting high density lipoprotein [HDL]) during DB were assessed. Following this study, participants were given the opportunity to transition to a 24-month extension study and be treated with PP6M. The mean change and percent change in BW, and the mean change in BMI from DB baseline to the end of the extension study (36&#xa0;months total) were calculated. RESULTS: Participants who were treated with PP6M showed numerically less weight gain, BMI, waist circumference, and more weight decrease compared to PP3M group during 12-month DB phase, though the proportion of participants reporting an abnormal change (&#x2265;7% change) in BW did not significantly differ between PP3M and PP6M. The weight differences were more pronounced in the younger age group (18-25&#xa0;years) and those who were overweight (BMI: 25 to <30&#xa0;kg/m2. Numerical differences in favor of PP6M were found in fasting blood lipids (HDL, LDL, TG, and TC). The changes in BW and BMI over time remained consistent throughout the 24-month extension, favoring PP6M in each instance. CONCLUSIONS: This post-hoc analysis demonstrated that PP6M was comparable to PP3M in terms of metabolic parameters; however, it may have a beneficial effect on weight gain, especially in young patients. TRIAL REGISTRATION: Post-Hoc Analysis of Studies NCT03345342 and NCT04072575 (ClinicalTrials.gov). Significant outcomes The findings from this study have highlighted that participants who were treated with the 6-month long-acting injectable formulation of paliperidone exhibited less weight gain during treatment overall, and significantly less weight gain in adolescents and young adults. Importantly, this trend continued over the course of long-term treatment, regardless of age. Participants treated with the 6-month formulation also had fewer shifts in blood lipids outside of the normal range and had more favorable changes in body mass index and waist circumference. These results suggest that when considering metabolic dysregulation as a factor in choosing a long-acting injectable antipsychotic, the 6-month formulation is a viable alternative to the 3-month formulation, particularly in younger patients with schizophrenia. Limitations Because this is a post hoc analysis and the study was not powered to test weight and metabolic changes, most endpoints were summarized descriptively and the statistical test was limited to the main endpoint (abnormal percent weight gain and loss).

Adult↗
PubMed1992

Water-phase palmitate concentrations in equilibrium with albumin-bound palmitate in a biological system.

The palmitate (PA) binding and transport capacity of human and bovine red cell membranes enables us to establish, in a biological system, the existence of a well-defined monomer concentration in equilibrium with PA bound to bovine serum albumin (BSA, 30 microM) inside the resealed red cell ghosts. Supernatants of suspensions of the [3H]PA-labeled ghosts contain a tiny quantity of dissolved binding capacities besides the monomer PA. This is demonstrated by linear regression of supernatant tracer concentrations versus ghost concentrations in a dilution series. The extrapolated value, corresponding to zero ghost concentration, is the monomer PA concentration in equilibrium with PA bound to BSA within the ghosts in molar ratio (nu). Measurements have been carried out for nu between 0.1 and 1.5 and at 0 degrees C, 10 degrees C, 23 degrees C and 38 degrees C. The important nu-dependent binding of PA to the ghost membrane itself enables us to use preparations of BSA-free ghosts in the same way, whereas this is impossible in the case of arachidonic acid. Within the physiological range of nu the PA monomer concentrations are accounted for by an apparent dissociation equilibrium constant (Kd) 3.4 10(-8) M at 38 degrees C calculated on basis of three equivalent binding sites per mol BSA. Kd depends on temperature with a well-defined enthalpy of 38.4 kJ/mol.

Animals↗
PubMed1992

The origin of palmitic acid in brain of the developing rat.

A rat milk substitute containing lower amounts of palmitic and oleic acid in the triacylglycerols in comparison to natural rat milk was fed to artificially reared rat pups from day 7 after birth to day 14. Pups reared by their mother served as controls. Free trideuterated (D3) palmitic acid [(C2H3)(CH2)14COOH, 98 atom % D] and free perdeuterated (D31) palmitic acid [C15(2)H31COOH, 99 atom % D] in equal quantity were mixed into the triacylglycerols of the milk substitute in an amount equal to 100% of the palmitic acid in the triacylglycerols. A control milk substitute contained unlabeled free palmitic acid in an amount equal to 100% of the palmitic acid in the triacylglycerols of the milk substitute. The objective was to determine if palmitic acid in the diet contributed significantly to the palmitic acid content of developing brain and other organs. The methyl esters of the fatty acids were analyzed by gas chromatography and the palmitic acid methyl ester was examined by fast atom bombardment mass spectrometry. The proportion of deuterated methyl palmitate as a percentage of total palmitate was determined; 32% of the palmitic acid in liver and 12% of the palmitic acid in lung were trideuterated and perdeuterated palmitic acid in approximately equal amounts. The brain, by contrast, did not contain the deuterated palmitic acid moiety. Quantitation of palmitic acid and total fatty acids revealed a significant accumulation in organs in the interval from 7 to 14 days of age. Under our experimental conditions, labeled palmitic acid does not enter the brain. Consequently, we conclude that the developing brain produces all required palmitic acid by de novo synthesis.

Animals↗
PubMed1992

Palmitate metabolism by isolated sheep rumen epithelial cells.

Ruminal palmitate metabolism was examined using an isolated cell system. Palmitate oxidation to 14CO2 by rumen epithelial cells isolated from the rumens of mature sheep was linear during the course of a 2-h incubation (11.1 nmoles.million cells-1.2 h-1) and 3.6 times the rate of palmitate oxidation by cells isolated from neonatal rumen (3.1 nmoles.million cells-1.min-1). Subsequent experiments were conducted with mature rumen epithelial cells. Neither acetate (50 mM), propionate (10 mM), dibutyryl cAMP (.2 mM), nor insulin (10 mU/mL) altered palmitate oxidation to CO2. However, butyrate (10 mM) addition reduced (P less than .05), and ammonia (15 mM) tended to reduce (P less than .10), palmitate oxidation (51.6 and 82.0% of control, respectively), whereas addition of glucose (2.5 mM) increased (P less than .05) palmitate oxidation (151% of control). Of the compounds tested, only propionate, butyrate, and ammonia reduced palmitate oxidation to total acid-soluble metabolites. Propionate (10 mM) addition completely abolished palmitate oxidation to acid-soluble metabolites. Succinate addition (5 to 50 mM) increased palmitate oxidation to CO2 but exhibited no consistent effect on palmitate oxidation to either acid-soluble metabolites or beta-hydroxybutyrate. Propionate completely abolished palmitate oxidation to beta-hydroxybutyrate, suggesting that propionate-induced inhibition of palmitate oxidation is not mediated via succinate. The data indicate 1) that rumen epithelium is capable of oxidizing palmitate, 2) that ruminal palmitate oxidation may be subject to regulation by developmental factors, and 3) that palmitate metabolism seems to be influenced more by ruminally derived metabolites than by factors derived exclusively from the general circulation.

Ammonia↗
PubMed1989

Metabolism of methyl-branched iodo palmitic acids in cultured hepatocytes.

The metabolic fate of methyl-branched iodo fatty acids was studied in primary culture of rat hepatocytes. We compared 16-iodo-2-R,S-methyl palmitic acid (2-Me), which can be beta oxidized, with 16-iodo-3-R,S-methyl palmitic acid (3-Me) which can be beta oxidized only after an initial alpha oxydation and with 16-iodo-2,2-dimethyl palmitic acid (2,2-Me2) and 16-iodo-3,3-dimethyl palmitic acid (3,3-Me2) which cannot be beta oxidized at all. The normal fate of natural fatty acids was given by comparative experiments with [1-14C] palmitic acid. Monomethyl-branched iodo fatty acids were taken up in the same range as palmitic acid but more than dimethyl-branched iodo fatty acids. After a 15-h incubation, acido-soluble products (ASP) accounted for 75% of the radioactivity taken up as 16-iodo-2-methyl palmitic acid, 50% as other methyl-branched iodo fatty acids and only 30% as palmitic acid, which indicated that all the methyl-branched iodo fatty acids underwent a strong deiodination process. Fatty acids were esterified in the following order: palmitic acid greater than 16-iodo-3-R,S-methyl palmitic acid greater than 16-iodo-2-R,S-methyl palmitic acid greater than 16-iodo-2,2-dimethyl palmitic acid greater than 16-iodo-3,3-dimethyl palmitic acid. Cultured hepatocytes, labelled for 3 h with the various fatty acids and reincubated for 12 h without fatty acid, secreted large amounts of free dimethyl-branched iodo fatty acids as compared to the monomethyl ones and palmitic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Rapid clearance of surfactant-associated palmitic acid from the lungs of developing and adult animals.

Palmitic acid is a minor component of natural surfactant and has been used to modify lipid extracts of natural surfactants to optimize their in vitro surface properties. The metabolic fate of palmitic acid in surfactant is unknown. The clearance of surfactant-associated radiolabeled palmitic acid after intratracheal administration was investigated with trace doses of surfactant in the adult rabbit and with trace and treatment doses in the 28-d fetal rabbit and the 132-d fetal sheep. Palmitic acid was cleared rapidly from the airways, with less than 2% of the radiolabel recovered as free palmitic acid in the alveolar wash by 1 h in all models. Recovery as free palmitic acid in the total lung at 2 h was 2% in the adult rabbit and 3% both doses in the preterm rabbit. In the preterm sheep, the recovery as free palmitic acid in the total lung was approximately 2% of the trace dose and 1% of the treatment dose by 5 h. Between 5 and 15% of the instilled palmitic acid was used as substrate for phospholipid synthesis by the lung in the different models. About 30% of the palmitate derived label was recovered in lipid extracts of liver 30 min after tracheal instillation of labeled surfactant in adult rabbits, whereas only 5-10% of the palmitate derived label was found in liver lipids in the preterm animals. In contrast to palmitic acid, radiolabeled triglyceride was cleared much more slowly from the airspaces and lungs of preterm sheep. Inasmuch as large amounts of palmitic acid are cleared rapidly from airspaces and lung tissue, it will not have a prolonged effect on the surface properties of surfactant but it may serve as a precursor for lung lipid metabolism.

Animals↗
PubMed1991

Regulation of in vitro metabolism of palmitate by carnitine and propionate in liver from dairy cows.

Regulation of in vitro palmitate metabolism by carnitine and propionate was investigated in liver obtained by biopsy from fasted nonlactating cows and from cows during early lactation. Liver slices from nonlactating cows during a 7-d fast esterified less palmitate than those from the same cows before fasting. Carnitine added in vitro increased hepatic oxidation and decreased esterification of palmitate in fed cows, but effects of carnitine were less during fasting. Propionate added in vitro decreased oxidation of palmitate; the effect was greater during fasting. In liver slices from cows during early lactation, carnitine increased oxidation and total utilization of palmitate and decreased palmitate esterification. Addition of tetradecylglycidic acid, an inhibitor of carnitine palmitoyltransferase I, prevented the carnitine-induced changes in palmitate metabolism. Substantial carnitine-independent oxidation of palmitate was observed in the presence of tetradecylglycidic acid. Tetradecylglycidic acid decreased esterification of palmitate to triglycerides but increased esterification to diglycerides. Effects of tetradecylglycidic acid and either propionate or pyruvate on palmitate oxidation were additive, indicating that propionate and pyruvate affect palmitate oxidation at sites other than carnitine palmitoyltransferase I. No interactions were detected between carnitine and propionate, but both compounds were potent regulators of palmitate metabolism in liver slices from cows during early lactation.

Animals↗
PubMed1989

Palmitic acid stimulates glucose incorporation in the adipocyte by a mechanism likely involving intracellular calcium.

The effect of palmitic acid on basal and insulin-stimulated incorporation of glucose into rat adipocytes was studied. Palmitic acid (2.40 mM) stimulated basal as well as insulin-stimulated glucose incorporation in rat adipocytes three and twofold, respectively. Similar degrees of stimulation of basal glucose oxidation by palmitate were also observed. The ability of palmitic acid to stimulate glucose uptake was additive with respect to the stimulation induced by insulin and was proportional to the palmitic acid concentration between 0.15 mM and 2.40 mM. Stimulation of glucose incorporation by palmitic acid was inhibited by preincubating the cells with quin2-AM, which accumulates intracellularly yielding the trapped chelator form. quin2, which binds intracellular Ca2+.The concentration of quin2-AM required for half-maximal inhibition of palmitic acid stimulated glucose incorporation was 3.8 +/- 1.2 microM (mean +/- SEM). The inhibition of palmitic acid-stimulated glucose incorporation by quin2-AM (10 microM) was overcome by incubating cells with the Ca2+ ionophore, A23187, in the presence of extracellular Ca2+ (2.6 mM). Chelation of extracellular Ca2+ with EGTA did not significantly affect the magnitude of palmitic acid-stimulated glucose incorporation. Dantrolene (12.5-100 microM) failed to affect basal or palmitic acid-stimulated glucose incorporation. These findings suggest that palmitic acid stimulates incorporation of glucose in the adipocyte by a mechanism dependent upon intracellular but not extracellular Ca2+.

Adipose Tissue↗
PubMed1989

A method for examining turnover and synthesis of palmitate-containing brain lipids in vivo.

1. A theoretical three compartment model is presented which gives the rate of incorporation of plasma palmitate into brain, Jpalm, in terms of turnover and synthesis of palmitate-containing lipids, de novo synthesis of palmitate from acetate, and recycling of palmitate within lipids. 2. Jpalm equals 4 h brain radioactivity following intravenous injection of [U-14C]-palmitate (determined with quantitative autoradiography), divided by integrated plasma specific activity of palmitate. Jpalm follows the time course of brain lipid synthesis during development of the rat, but is age-invariant in the adult. 3. At 1-7 days after 5 min of bilateral carotid occlusion in the awake gerbil, intravascular [14C]-palmitate incorporation is reduced in the CA1 pyramidal layer of the hippocampus, consistent with delayed neuronal death, but is elevated in the CA3 and CA4 pyramidal layers and dentate gyrus, suggesting synthesis of new membrane during recovery from the ischaemic insult. 4. Several weeks after unilateral destruction of the cochlea in 11 day old rats, incorporation of [14C]-palmitate from plasma into appropriate central auditory regions is reduced, corresponding to reduced cell size and altered morphology. 5. [14C]-palmitate incorporation into the left hypoglossal nucleus is increased during and following axonal regeneration (up to 23% compared with control side) following transection of the left hypoglossal nerve in Fischer-344 rats, whereas incorporation is decreased 6-7% when regeneration is prevented. Time courses of incorporation in both cases correspond to histological changes. 6. The results show that the palmitate method can be used to examine regional turnover and synthesis of brain lipids following injury, sensory deprivation, development, regeneration and ageing.

Animals↗
PubMed1989

Palmitate oxidation by isolated working fetal and newborn pig hearts.

Palmitate oxidation and the effect of palmitate on glucose and lactate utilization were investigated in isolated, perfused, fetal (0.9 gestation), and neonatal (2 day old) pig hearts. Hearts were perfused under working conditions, developing a mean aortic pressure of 50-55 mmHg, paced at 180 beats/min for 30 min, with Krebs-Henseleit buffer containing 3% albumin, glucose (5 mM), and insulin (100 microU/ml). Palmitate (1 mM) and lactate (5 mM), either individually or in combination, were added to the perfusion buffer. Palmitate oxidation was assessed from 14CO2 production from [U-14C]-palmitate, glucose uptake as 3H2O production from D-[2-3H]-glucose, and lactate metabolism from changes in buffer lactate content. After perfusion, ATP, creatine phosphate, triglycerides, and glycogen were measured. Substantial palmitate oxidation was observed at both ages but was greater in neonatal hearts. Nevertheless, palmitate inhibited lactate utilization and glucose uptake similarly in fetal and neonatal hearts. Lactate also reduced palmitate uptake and oxidation by 40-60% in both fetal and neonatal hearts. During perfusions with palmitate, tissue concentrations of triglycerides increased approximately threefold in fetal hearts and were unaffected by lactate. Thus both palmitate and lactate can act as major energy substrates for the immature heart. Both substrates significantly (P less than 0.01) suppress glucose utilization, and each has suppressive effects on the other's metabolism.

Adenosine Triphosphate↗
PubMed1991

Regulation of in vitro palmitate oxidation in liver from dairy cows during early lactation.

Regulatory effects of carnitine, glucose, some glucogenic compounds (propionate, pyruvate, alanine, lactate, glycerol, and fructose), ketone bodies (acetate, acetoacetate, and beta-hydroxybutyrate), and insulin on oxidation of palmitate were studied in slices of liver obtained from high producing dairy cows during early lactation. A total of 77 biopsies of liver from 21 multiparous Holstein cows (36 +/- 16 d postpartum) was used. L-Carnitine increased oxidation of palmitate to CO2 by more than twofold and oxidation to acid-soluble products by about fourfold. Propionate decreased oxidation of palmitate in liver slices incubated without added carnitine, but the decrease was lessened by carnitine. Pyruvate, lactate, and alanine increased palmitate oxidation, especially in the presence of carnitine. Glycerol, glucose, and insulin tended to decrease palmitate oxidation in the absence of carnitine. Fructose tended to decrease oxidation to CO2 but did not affect oxidation to acid-soluble products. Acetate and acetoacetate decreased oxidation of palmitate, whereas beta-hydroxybutyrate decreased palmitate oxidation in the absence of carnitine but increased palmitate oxidation in its presence. In general, carnitine decreased the inhibitory effects of compounds that decreased palmitate oxidation but increased the stimulatory effects of compounds that increased palmitate oxidation.

Alanine↗
PubMedDate not supplied

Modeling of palmitate transport in the heart.

Transport of palmitate from the albumin-palmitate complex in the plasma to inside mitochondria where it undergoes beta-oxidation is a multistep process. Albumin's large size prevents permeation via interendothelial clefts. Palmitate dissociation from albumin in solution is too slow to provide an adequate supply of the unbound palmitate. The discovery that the dissociation occurs upon albumin binding to an endothelial surface receptor resolves the conundrum. Palmitate transport across the luminal surface membrane may be either carrier-mediated or passive. Fatty-acid binding protein inside endothelial and cardiac muscle cells facilitates diffusion through cytosol while maintaining the unbound palmitate concentration at a very low level. Within the interstitium, albumin is again the palmitate carrier. Still controversial is whether or not there is a saturable sarcolemmal transporter or simply passive exchange. Inside the myocyte palmitate is again bound to the fatty acid binding protein which buffers the free palmitate concentration, facilitates diffusion, and may facilitate further intracellular reactions.

Animals↗
PubMed1989

Study of amino acid formation during palmitate oxidation in rat brain mitochondria.

The interrelation of palmitate oxidation with amino acid formation in rat brain mitochondria has been investigated in purified mitochondria of nonsynaptic origin by measuring the formation of aspartate, alpha-ketoglutarate, and glutamate during palmitate oxidation, and also by assaying 14C-products of [1-14C]palmitate oxidation. Oxidation of palmitate (or [1-14C]palmitate) resulted in the formation of aspartate (or 14C-aspartate), and the oxidation was inhibited by aminooxyacetate (an inhibitor of transaminase). Palmitate oxidation also resulted in alpha-ketoglutarate formation, which was sensitive to the effect of aminooxyacetate. Addition of NH4Cl was found to increase 14C-products and formation of alpha-ketoglutarate, whereas glutamate formation was not increased unless the rate of palmitate oxidation was reduced by 50% by aminooxyacetate or alpha-ketoglutarate was added exogenously. Exogenous alpha-ketoglutarate was found to decrease 14C-products, but not aspartate formation. These results indicated that palmitate oxidation was closely related to aspartate formation via aspartate aminotransferase. During palmitate oxidation without aminooxyacetate or added alpha-ketoglutarate, however, alpha-ketoglutarate was not available for glutamate formation via glutamate dehydrogenase. We discuss the possibility that this was because (a) oxidative decarboxylation of alpha-ketoglutarate to form succinyl-CoA was favored over glutamate formation for the competition for alpha-ketoglutarate in the same pool, and (b) the pool of alpha-ketoglutarate produced in the aspartate aminotransferase reaction did not serve as substrate for glutamate formation.

Aminooxyacetic Acid↗