scholarly journals Regulation of glutamine metabolism in dog kidney in vivo

1986 ◽  
Vol 29 (1) ◽  
pp. 68-79 ◽  
Author(s):  
Patrick Vinay ◽  
Guy Lemieux ◽  
André Gougoux ◽  
Mitchell Halperin
Keyword(s):  
Glutamine Metabolism ◽  
Dog Kidney

ATP turnover and renal response of dog tubules to pH changes in vitro

1986 ◽  
Vol 251 (5) ◽  
pp. F919-F932
Author(s):  
C. Manillier ◽  
P. Vinay ◽  
L. Lalonde ◽  
A. Gougoux
Keyword(s):  
Respiratory Acidosis ◽  
Maximum Activity ◽  
Tissue Response ◽  
Proximal Tubules ◽  
Glutamine Metabolism ◽  
Ammonia Production ◽  
Atp Turnover ◽  
Dog Kidney

In vivo the dog kidney responds to metabolic or respiratory acidosis by a marked increment of its ammonia production (expressed per 100 milliliters glomerular filtration rate). This phenomenon is related to a switch from metabolic utilization of nonammoniagenic (lactate) to ammoniagenic (glutamine) substrates to support ATP turnover in the proximal tubules. We have proposed that in vivo the maximum activity of the ammoniagenic process is fixed by the ATP turnover in this segment of the nephron. The maximal glutamine metabolism is reached when 100% of this turnover is supported by glutamine metabolism. We have studied how these concepts apply to the adaptation of glutamine metabolism and ammonia production to a low pH in vitro using proximal tubules of dogs incubated when one (lactate or glutamine) or several (glutamine plus lactate or plus palmitate) substrates are provided. At pH 7.4 glutamine alone supports already 71-76% of the tissue ATP turnover (minimal and maximal values). With acidification this fraction rises to nearly 87-94%, but this increases only modestly the ammonia production. Reducing the ATP turnover with ouabain at pH 7.4 decreases the absolute glutamine utilization, which now supports only 45-50% of the ATP turnover. Again acidification increases this fraction to 90-99%. Addition of lactate with glutamine displaces part of the glutamine metabolized, but greatly stimulates the synthesis of alanine. Fatty acids depress ammonia production and blunt the tissue response to acidification. Gluconeogenesis from lactate is minimally influenced by incubation pH. It is concluded that the ATP turnover limits the metabolism of glutamine by proximal tubules in vitro as in vivo in the dog, and that the response to acidification is small in vitro because of the absence of alternative substrates.

scholarly journals In vivo 13C MRS in the mouse brain at 14.1 Tesla and metabolic flux quantification under infusion of [1,6-13C2]glucose

2017 ◽  
Vol 38 (10) ◽  
pp. 1701-1714 ◽  
Author(s):  
Marta Lai ◽  
Bernard Lanz ◽  
Carole Poitry-Yamate ◽  
Jackeline F Romero ◽  
Corina M Berset ◽  
...  
Keyword(s):  
Mouse Brain ◽  
Metabolic Flux ◽  
Direct Detection ◽  
Tricarboxylic Acid Cycle ◽  
Quantitative Information ◽  
Glutamine Metabolism ◽  
Resonance Spectroscopy ◽  
Flux Analysis ◽  
Carboxylase Activity

In vivo 13C magnetic resonance spectroscopy (MRS) enables the investigation of cerebral metabolic compartmentation while, e.g. infusing 13C-labeled glucose. Metabolic flux analysis of 13C turnover previously yielded quantitative information of glutamate and glutamine metabolism in humans and rats, while the application to in vivo mouse brain remains exceedingly challenging. In the present study, 13C direct detection at 14.1 T provided highly resolved in vivo spectra of the mouse brain while infusing [1,6-13C2]glucose for up to 5 h. 13C incorporation to glutamate and glutamine C4, C3, and C2 and aspartate C3 were detected dynamically and fitted to a two-compartment model: flux estimation of neuron-glial metabolism included tricarboxylic acid cycle (TCA) flux in astrocytes (Vg = 0.16 ± 0.03 µmol/g/min) and neurons (VTCAn = 0.56 ± 0.03 µmol/g/min), pyruvate carboxylase activity (VPC = 0.041 ± 0.003 µmol/g/min) and neurotransmission rate (VNT = 0.084 ± 0.008 µmol/g/min), resulting in a cerebral metabolic rate of glucose (CMRglc) of 0.38 ± 0.02 µmol/g/min, in excellent agreement with that determined with concomitant 18F-fluorodeoxyglucose positron emission tomography (18FDG PET).We conclude that modeling of neuron-glial metabolism in vivo is accessible in the mouse brain from 13C direct detection with an unprecedented spatial resolution under [1,6-13C2]glucose infusion.

scholarly journals Dietary Supplement Enriched in Antioxidants and Omega-3 Promotes Glutamine Synthesis in Müller Cells: A Key Process against Oxidative Stress in Retina

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3216
Author(s):  
Maryvonne Ardourel ◽  
Chloé Felgerolle ◽  
Arnaud Pâris ◽  
Niyazi Acar ◽  
Khaoula Ramchani Ben Othman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Müller Cells ◽  
Nutritional Supplement ◽  
Glutamine Metabolism ◽  
Muller Cells ◽  
Omega 3 ◽  
Glutamine Synthesis ◽  
The Impact

To prevent ocular pathologies, new generation of dietary supplements have been commercially available. They consist of nutritional supplement mixing components known to provide antioxidative properties, such as unsaturated fatty acid, resveratrol or flavonoids. However, to date, only one preclinical study has evaluated the impact of a mixture mainly composed of those components (Nutrof Total®) on the retina and demonstrated that in vivo supplementation prevents the retina from structural and functional injuries induced by light. Considering the crucial role played by the glial Müller cells in the retina, particularly to regulate the glutamate cycle to prevent damage in oxidative stress conditions, we questioned the impact of this ocular supplement on the glutamate metabolic cycle. To this end, various molecular aspects associated with the glutamate/glutamine metabolism cycle in Müller cells were investigated on primary Müller cells cultures incubated, or not, with the commercially mix supplement before being subjected, or not, to oxidative conditions. Our results demonstrated that in vitro supplementation provides guidance of the glutamate/glutamine cycle in favor of glutamine synthesis. These results suggest that glutamine synthesis is a crucial cellular process of retinal protection against oxidative damages and could be a key step in the previous in vivo beneficial results provided by the dietary supplementation.

Interrelations of arsenate and phosphate transport in the dog kidney

1963 ◽  
Vol 205 (4) ◽  
pp. 707-714 ◽  
Author(s):  
J. M. Ginsburg ◽  
W. D. Lotspeich
Keyword(s):  
Phosphate Transport ◽  
Tubular Secretion ◽  
Tubular Reabsorption ◽  
Urine Flow ◽  
Phosphate Concentration ◽  
Plasma Phosphate ◽  
Osmotic Diuresis ◽  
Competitive Mechanism ◽  
Dog Kidney

The relation between arsenate and phosphate transport in the dog kidney was studied by measuring the renal clearance of arsenate labeled with its radioactive isotope As74. The experiments were performed during osmotic diuresis induced by mannitol. The results demonstrate certain similarities in the transport of these ions. Arsenate undergoes a net tubular reabsorption which is inhibited as the plasma phosphate concentration is raised. The inverse relationship between arsenate transport and the plasma As:P ratio suggests a competitive mechanism for the interaction between the two ions Like phosphate, arsenate transport is inhibited by glucose and this effect is reversed by phlorizin. An important difference between arsenate and phosphate transport is the sensitivity of arsenate transport to urine flow. In vivo reduction of arsenate to arsenite and a net tubular secretion of arsenite has been observed. The results are discussed in terms of the known ability of arsenate to substitute for phosphate in biochemical reactions.

Mechanism of maleic acid-induced glucosuria in dog kidney

1976 ◽  
Vol 231 (4) ◽  
pp. 1024-1032 ◽  
Author(s):  
M Silverman ◽  
L Huang
Keyword(s):  
Brush Border ◽  
Maleic Acid ◽  
Brush Border Membrane ◽  
Multiple Indicator Dilution ◽  
Dog Kidney ◽  
Proximal Tubular ◽  
Multiple Indicator ◽  
Prior Administration

The multiple indicator-dilution technique in vivo and isolated brush-border membranes in vitro have been used to explore the mechanism of maleic acid-induced glucosuria in dog kidney. The interaction of D-glucose with the antiluminal membrane from the peritubular fluid surface is unaltered. It is demonstrated that alpha-methyl-D-glucoside (alpha MG) enters and exits from the proximal tubular cell only across the brush-border membrane. Then using alphaMG as a reference indicator, it is shown that maleic acid does not cause complete inhibition of D-glucose interaction with the antiluminal membrane from the cytoplasmic surface. The binding of [3H]phlorizin both in vivo and in vitro is not affected by prior administration of maleic acid, indicating that D-glucose interaction with the outside surface of the brush border is also not affected by maleic acid. The data are therefore consistent with the concept that maleic acid-induced glucosuria is due either to i) partial inhibition of D-glucose movement from cytoplasm across the antiluminal membrane into the blood, ii) stimulated movement back across the brush-border membrane into urine, or iii) a combination of the two effects.

Regulation of glutamine metabolism in dog kidney cortex: effect of pH and chronic acidosis

1992 ◽  
Vol 262 (6) ◽  
pp. F1007-F1014
Author(s):  
A. C. Schoolwerth ◽  
B. C. Smith ◽  
K. Drewnowska
Keyword(s):  
Glutamate Dehydrogenase ◽  
Mitochondrial Membrane ◽  
Glutamine Metabolism ◽  
Kidney Cortex ◽  
Cytosolic Ph ◽  
Isolated Mitochondria ◽  
Significant Difference ◽  
Dog Kidney ◽  
Ammonium Production ◽  
Krebs Henseleit Buffer

To examine the interrelationships of proton compartmentation and ammoniagenesis, experiments were performed in tubules and mitochondria isolated from dog kidney cortex. Tubules were incubated in Krebs-Henseleit buffer at different pH (pHe), and cytosolic pH (pHi) was estimated with the fluorescent probe 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Mitochondrial pH (pHm) was determined simultaneously in intact tubules by use of dimethyloxazolidine-2,4-dione. Over the pHe range 6.9-7.7, pHi was similar in control and acidotic dogs and linearly related to pHe. At pHe 7.4 in control tubules. pHm was 7.78 +/- 0.07, and varied little over the pHe range of 7.0-7.7. The pH gradient across the mitochondrial membrane rose at acid pHe. pHm was more alkaline when estimated in tubules from acidotic dogs compared with controls. Ammonium and glucose productions from glutamine were inversely related to pHe and pHi in tubules from both control and acidotic animals and were higher in acidosis. In contrast, ammonium production by isolated mitochondria did not vary as pHe was altered. Enzyme fluxes, calculated from metabolite changes, demonstrated that glutamate dehydrogenase (GDH) flux was altered. Enzyme fluxes, calculated from metabolite changes, demonstrated that glutamate dehydrogenase (GDH) flux was inversely and glutaminase (PDG) flux was linearly related to pHe. Ammonium production was significantly greater in mitochondria from acidotic dogs because of accelerated flux through PDG but not GDH. The present study demonstrates significant difference between proton compartmentation and regulation of ammoniagenesis in kidneys from acidotic dog compared with rat.

scholarly journals Studies on glycolysis in the dog kidney in vivo

1972 ◽  
Vol 128 (3) ◽  
pp. 80P-81P
Author(s):  
J Costello ◽  
J M Scott ◽  
P Wilson ◽  
E Bourke
Keyword(s):  
Dog Kidney
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