Renal gluconeogenesis: effects of Ca2+ and H+.

@article{Nagata1970RenalGE,
  title={Renal gluconeogenesis: effects of Ca2+ and H+.},
  author={Naokazu Nagata and Howard Rasmussen},
  journal={Biochimica et biophysica acta},
  year={1970},
  volume={215 1},
  pages={
          1-16
        }
}
...

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Observations suggest that cyclic AMP accelerates a rate-limiting gluconeogenic reaction between oxalacetate and the triose phosphates, which is consistent with a previously advanced hypothesis that cortical gluconeogenesis, ammonia production, and glutamate concentration may be interdependent.

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P pH, rather than CO(2) tension or [HCO(3) (-)], is the most important acid-base variable affecting renal gluconeogenesis, and the findings suggest that a decrease in extracellular fluid pH enhances renal gluc oneogenesis through direct stimulation of one of the rate-limiting reactions involved in the conversion of oxalacetate to glucose.

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    The Journal of clinical investigation
  • 1967
The inhibition of citrate oxidation caused by increasing pH and [HCO(3) (-)] in slices of renal cortex and kidney mitochondria is an in vitro representation of the inhibition ofcitrate reabsorption in the nephron that occurs in metabolic alkalosis.

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It is proposed that the increase of PEPCK activity is the key event in the ammoniagenesis and gluconeogenesis which follow on metabolic acidosis, which is constantly related to increases of urinary ammonia.

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Evidence is presented as to the possible significance of metal ions in regulating carbohydrate metabolism and the stimulation of gluconeogenesis from α-keto acids is comparable for both Ca and Mn ++.

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Results are consonant with the view that alanine is metabolized by transamination with alpha-ketoglutarate to form glutamate, which is subsequently deaminated oxidatively to liberate ammonia.