scholarly journals Gluconeogenesis in the kidney cortex. Effects of d-malate and amino-oxyacetate

1970 ◽  
Vol 116 (3) ◽  
pp. 483-491 ◽  
Author(s):  
R. Rognstad ◽  
J. Katz
Keyword(s):  
Malate Dehydrogenase ◽  
High Speed ◽  
Tricarboxylic Acid Cycle ◽  
Rat Kidney ◽  
Supernatant Fraction ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
High Concentrations ◽  
Cortex Slices ◽  
Kidney Cortex Slices

1. Rat kidney-cortex slices incubated with d-malate alone formed very little glucose. d-Malate, however, augmented gluconeogenesis from l-lactate and inhibited gluconeogenesis from pyruvate and l-malate. 2. d-Malate had little effect on the rate of the tricarboxylic acid cycle with or without other substrates added. 3. d-Malate inhibited the activity of the l-malate dehydrogenase in a high-speed-supernatant fraction from kidney cortex. 4. It was concluded that d-malate inhibited either the operation of the cytoplasmic l-malate dehydrogenase or malate outflow from the mitochondria in the intact kidney-cortex cell. This supports the hypothesis of Lardy, Paetkau & Walter (1965) and Krebs, Gascoyne & Notton (1967) on the role of malate as carrier for carbon and reducing equivalents in gluconeogenesis. 5. Gluconeogenesis from l-lactate in kidney-cortex slices was strongly inhibited by a low concentration (0.1mm) of amino-oxyacetate, whereas glucose formation from pyruvate, malate, aspartate and several other compounds was only slightly affected. 6. High concentrations of l-aspartate largely reversed the inhibition of gluconeogenesis from l-lactate caused by amino-oxyacetate. 7. Amino-oxyacetate inhibited strongly the glutamate–oxaloacetate transaminase in the 30000g supernatant fraction of a kidney-cortex homogenate. The presence of l-aspartate decreased the inhibition of the transaminase by amino-oxyacetate. 8. Detritiation of l-[2-3H]aspartate was inhibited by 90% during an incubation of kidney-cortex slices with l-lactate and amino-oxyacetate. 9. Low concentrations (10μm) of artificial electron acceptors such as Methylene Blue and phenazine methosulphate abolished most of the inhibition of gluconeogenesis from l-lactate by amino-oxyacetate. This is interpreted as an activation of net malate outflow from the mitochondria by-passing the inhibited transfer of oxaloacetate. 10. These findings support the concept that transamination to aspartate is involved in the transfer of oxaloacetate from mitochondria to cytosol required in gluconeogenesis from l-lactate.

scholarly journals The intracellular ratio of cysteine and cystine in various tissues

1967 ◽  
Vol 105 (2) ◽  
pp. 891-896 ◽  
Author(s):  
J. C. Crawhall ◽  
S. Segal
Keyword(s):  
High Voltage ◽  
Rat Kidney ◽  
Reduced Form ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
High Concentrations ◽  
Cortex Slices ◽  
Free Media ◽  
Kidney Cortex Slices ◽  
High Voltage Electrophoresis

1. The cysteine–cystine ratio was measured in rat kidney cortex, diaphragm, jejunum, liver and brain. 2. This ratio was determined by incubating these tissues in buffer containing [35S]cystine and then homogenizing the tissue in a buffered solution of N-ethylmaleimide. The products of this reaction were separated by high-voltage electrophoresis and the radioactivity in the cystine and 2-(l-2′-amino-2′-carboxyethylthio)-N-ethylsuccinimide regions was determined. 3. In these tissues cyst(e)ine was mainly present in the reduced form. 4. After incubation of [35S]cystine with rat jejunal segments it was found that 36% of the cystine in the medium has been reduced. 5. Anaerobiosis, Na+-free media, glucose and high concentrations of cystine and lysine were found not to affect significantly the cysteine–cystine ratio in rat kidney-cortex slices.

Effect of metal ions on in vitro gluconeogenesis in rat kidney cortex slices

1965 ◽  
Vol 208 (5) ◽  
pp. 841-846 ◽  
Author(s):  
Julia Z. Rutman ◽  
Lawrence E. Meltzer ◽  
J. Roderick Kitchell ◽  
Robert J. Rutman ◽  
Philip George
Keyword(s):  
Amino Acids ◽  
Metal Ions ◽  
Tricarboxylic Acid Cycle ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
In Vitro Systems ◽  
Cortex Slices ◽  
Kidney Cortex Slices

The effect of metal ions on glucose formation from amino acids and glycolytic and tricarboxylic acid cycle intermediates has been examined in rat kidney cortex slices in vitro. Of the metals tested, only Mn++ and Ca++ have been shown to be stimulatory, while Zn++, Cu++, and Cd++ are inhibitory. The case of Mn++ activation is of particular interest because Mg++ ions are inactive in this system, despite the similarities usually observed in the in vitro systems. The stimulation of gluconeogenesis from α-keto acids is comparable for both Ca++ and Mn++, in contrast to the lack of a Mn++ effect with the homologous l-α-amino acids. Evidence is presented as to the possible significance of metal ions in regulating carbohydrate metabolism.

Effect of Pentobarbital Sodium on Uptake of PAH by Rat Kidney Cortex Slices in Vitro

1958 ◽  
Vol 195 (2) ◽  
pp. 343-346 ◽  
Author(s):  
E. J. Støren
Keyword(s):  
Oxygen Consumption ◽  
Renal Cortex ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Tissue Respiration ◽  
Rat Kidney Cortex ◽  
Pentobarbital Sodium ◽  
Cortex Slices ◽  
Kidney Cortex Slices

Active uptake of PAH by rat renal cortex slices was studied by the method of Cross and Taggart. Uptake was determined at low and at high medium concentrations of PAH. Pentobarbital sodium in concentrations comparable to those found in plasma during anesthesia, significantly depressed the uptake of PAH on all occasions. Simultaneously oxygen consumption was reduced. Acetate failed to stimulate PAH uptake in the presence of pentobarbital, although tissue respiration was restored to normal.

Tamm—Horsfall Glycoprotein Release from Rat Kidney Cortex Slices in Vitro

1984 ◽  
Vol 67 (5) ◽  
pp. 529-534 ◽  
Author(s):  
P. K. Wirdnam ◽  
R. D. G. Milner
Keyword(s):  
Cell Membrane ◽  
Ethacrynic Acid ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
The Media ◽  
Cortex Slices ◽  
Kidney Cortex Slices ◽  
Krebs Henseleit Buffer

1. Rat kidney cortex slices were incubated for 30 min at 37°C in unmodified Krebs-Henseleit buffer containing aldosterone, vasopressin, theophylline, ethacrynic acid, frusemide, spironolactone or ouabain. 2. Tamm—Horsfall glycoprotein (THG) released into the media was measured by radioimmunoassay and at the end of each experiment the slices were homogenized and assayed for THG content. 3. Incubation of kidney cortex slices in unmodified buffer resulted in a significant increase in the slice THG content when compared with pre-incubation levels. The increase was prevented by puromycin or cycloheximide. 4. Incubation in ethacrynic acid (1 mmol/l) or frusemide (10 mmol/l) resulted in a significant increase in release of THG when compared with unmodified buffer. Puromycin or cycloheximide failed to prevent the increased release. 5. THG release induced by ethacrynic acid or frusemide is probably the result of an aggregation-disaggregation reaction on the cell membrane. It is suggested that the action of the chloride inhibiting diuretics, ethacrynic acid and frusemide, is mediated in some way via THG.

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