Possible sites of interaction of acute renal failure with amino acid utilization for gluconeogenesis in isolated perfused rat liver

Fröhlich, Jürgen; Hoppe-Seyler, G.; Schollmeyer, P.; Maier, K. P.; Gerok, W.

doi:10.1111/j.1365-2362.1977.tb01603.x

Cited by 18 publications

(15 citation statements)

References 39 publications

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“…Fröhlich et al [2,3] found a stimulation of gluconeogenesis in the presence of amino acids in liver per fusion experiments in acutely uraemic rats. Stimulation of glucose synthesis from serine in acute uraemia induced by a maximal activation of serine dehydratase has also been described by Fröhlich et al [4], Furthermore, serine may be important for the regulation of glycogen metabolism in skeletal muscle of acutely uraemic rats.…”

Section: Introductionmentioning

confidence: 99%

Glycogen Synthesis from Serine in Isolated Perfused Hindquarters of Acutely Uraemic Rats

Djovkar¹,

Hörl

Heidland

1983

Nephron

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Isolated hindquarters of bilaterally nephrectomized and sham-operated rats were perfused in the presence and absence of ¹⁴C-labelled serine, respectively. After a perfusion period of 30 min ¹⁴C-serine was 4,074 ± 270 dpm/ml in the perfusion medium of sham-operated animals and decreased to 2,800 ± 190 dpm/ml in the medium of acutely uraemic rats. Muscle glycogen concentration in sham-operated animals was 1.10 ± 0.04 mg/g wet weight in the absence and 1.03 ± 0.11 mg/g in the presence of serine. In contrast, in acutely uraemic rats there was a glycogen concentration of 0.57 ± 0.09 mg/g in the absence of serine. Glycogen was increased in the presence of serine in the perfusion medium, the value being 1.50 ± 0.13 mg glycogen/g wet weight. Incorporation of labelled serine into skeletal muscle glycogen was significantly higher in acutely uraemic animals (15 ± 0.5 µmol/g glycogen) than in sham-operated animals (10 ± 0.4 µmol/g). The results are compatible with the hypothesis that serine increases muscle glycogen synthesis in acute uraemia.

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Section: Introductionmentioning

confidence: 99%

Glycogen Synthesis from Serine in Isolated Perfused Hindquarters of Acutely Uraemic Rats

Djovkar¹,

Hörl

Heidland

1983

Nephron

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“…The key regulatory enzymes of ureagenesis and gluconeogenesis are located in the same zone of hepatic acinus, showing a parallel behavior of these pathways. Therefore, in the situations of high blood-urea concentrations, gluconeogenesis, in general (18), and from serine, in particular (27), are stimulated; meanwhile, when urea production is inhibited, gluconeogenesis (9) and even serine dehydratase also decrease. This relationship leads us to assume some degree of channeling between substrates and initial products of both pathways; for example, the carbon backbone of amino acids that give up their NH 3 group for urea synthesis is channelled to glucose production.…”

Section: Discussionmentioning

confidence: 99%

Downregulation in the expression of the serine dehydratase in the rat liver during chronic metabolic acidosis

López-Flores

Peragón²,

Valderrama³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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. Downregulation in the expression of the serine dehydratase in the rat liver during chronic metabolic acidosis. Am J Physiol Regul Integr Comp Physiol 291: R1295-R1302, 2006. First published June 22, 2006 doi:10.1152/ajpregu.00095.2006.-Blood pH controls the activity of important regulatory enzymes in the metabolism. Serine dehydratase (SerDH) transforms L-serine into pyruvate and ammonium and is involved in the regulation of gluconeogenesis from serine in the rat liver. In this work, we investigate the effect of chronic metabolic acidosis on the kinetics, specific protein level, tissue location, and mRNA levels of rat liver SerDH. Experimental acidosis was induced in rats by ingestion of 0.28 M ammonium chloride solution for 10 days. Acidosis significantly (P Ͻ 0.05) decreased SerDH activity at all substrate concentrations assayed. Moreover, the V max value was 38.50 Ϯ 3.51 mU/mg (n ϭ 7) of mitochondrial protein in the acidotic rats and 92.49 Ϯ 6.79 mU/mg (n ϭ 7) in the control rats. Western blot analysis revealed a significant reduction (14%) in the level of SerDH protein content in the rat liver during acidosis. Immunohistochemical analysis showed that SerDH location did not change in response to chronic metabolic acidosis and confirmed previous results on SerDH protein levels. Moreover, the SerDH mRNA level, estimated by RT-PCR, was also significantly 33.8% lower than in control. These results suggest that during experimental acidosis a specific repression of rat-liver SerDH gene transcription could result, lowering the amount and activity of this enzyme. The changes found in SerDH expression are part of an overall metabolic response of liver to maintain acid-base homeostasis during acidosis. NH 4Cl; reverse transcriptase-polymerase chain reaction; serine catabolism ACIDOSIS IS A METABOLIC STATE in which, for different causes, blood pH and bicarbonate fall. In these cases, the organism attempts to compensate for these imbalances by increasing the respiratory frequency or adapting its metabolism to facilitate the removal of protons via renal excretion and thus restore the serum-bicarbonate level. For this, major metabolic adaptations occur in liver and kidney. During this situation, liver metabolism helps maintain the acid-base balance by controlling the ammonium supply to kidney in the form of glutamine (1, 21, 50). In parallel, amino-acid breakdown (34, 42) and gluconeogenesis (9, 26) are also regulated. In this situation, the hepatic synthesis of urea and glucose are inhibited, and glutamine metabolism shifts to the net release of this amino acid to serum (1,21,50). In kidney, the fall in blood pH values intensifies the catabolism of glutamine and gluconeogenesis (26). The increased glutamine catabolism increases the renal excretion of protons in the form of ammonium and gluconeogenesis as one end pathway of the metabolism of the carbon backbone of glutamine. These changes are due to an induction of glutaminase, glutamate dehydrogenase, and phosphoenolpyruvate carboxykinase (PEPCK) during this situation ...

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“…A large pro portion of the amino acids administered with the ENAA regimen was degraded to urea. This may be explained by experimental datas of Fröhlich et al [22,23], who demonstrated an enhanced propensity for the liver to catabolize circulating amino acids in acutely ure mic rats. Should these observations reflect the metabolic alterations obtained in humans with ARF, then one might predict that intra venous infusions of larger quantities of amino acids may lead to an enhanced rate of amino acid degradation in the liver [19], So, neither a great quantity of nitrogen intake nor the administration of a 50:50 ENAA solution seems to play the key role in reducing hypercatabolism.…”

Section: Reduction Of Negative Nitrogen Balance As a Current Principlmentioning

confidence: 99%

Nutrition in Acute Renal Failure

Teschner¹,

Heidland²

1985

Blood Purif

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An important prognostic factor of acute renal failure (ARF) is the nutritional status of the patient. Malnutrition in ARF is mainly a consequence of profound catabolism, caused by alterations of the hormonal milieu, physical inactivity, infection, an enhanced proteolytic activity and the hemodialysis process. In the management of these patients, optimal nutritional intake must especially be discussed under the aspect of reducing catabolism. In catabolic ARF, an energy intake of about 50 kcal/kg/day provided by hypertonic glucose, may be adequate. The requirement of essential and nonessential amino acid solutions in respect of their composition and quantity is not clearly defined. High doses of amino acids failed to improve negative nitrogen balance in catabolic ARF. Recent approaches in order to reduce net protein breakdown imply new combinations of amino acid formulations or pharmacological trials for instance with antiproteolytic substances.

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Possible sites of interaction of acute renal failure with amino acid utilization for gluconeogenesis in isolated perfused rat liver

Cited by 18 publications

References 39 publications

Glycogen Synthesis from Serine in Isolated Perfused Hindquarters of Acutely Uraemic Rats

Glycogen Synthesis from Serine in Isolated Perfused Hindquarters of Acutely Uraemic Rats

Downregulation in the expression of the serine dehydratase in the rat liver during chronic metabolic acidosis

Nutrition in Acute Renal Failure

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