The Gluconeogenetic Ability of Hepatocytes in Various Types of Acute Uraemia

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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.

Section: Introductionmentioning

confidence: 99%

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

Djovkar¹,

Hörl

Heidland

1983

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“…Furthermore, some substrates other than glycine must be considered as precursors of serine. Several studies have shown a key role of serine in liver and skeletal muscle metabolism of acutely uremic rats [3][4][5][15][16][17][18][19][20], Fortunately, extrarenal serine synthesis may prevent serine deficiency even fol lowing bilateral nephrectomy.…”

Section: Discussionmentioning

confidence: 99%

“…Renal metabolism of amino acids at their normal plasma concentration is highly selective: there is a renal uptake of glutamine and glycine; on the other hand, there is a significant renal production rate only for serine and alanine [1], Serine and alanine are important substrates for hepatic gluconeogenesis [2][3][4][5]. In the intact organism serine is produced primarily from glycine in the kidney [6], Therefore, the question arises as to what extent a serine deficit exists after bilateral nephrectomy.…”

Section: Introductionmentioning

confidence: 99%

Kidney Independent Serine Synthesis in the Rat

Hörl¹,

Kluthe²,

Gierlach³

et al. 1985

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The potential role ofthe kidney in renal serine synthesis was elucidated in rats following dietary serine as well as serine and glycine depletion for 6 weeks. Serine deficient diet caused a significant rise in blood serine and glycine values. In contrast, blood glycine concentration decreased significantly following serine and glycine depletion, whereas blood serine levels remained unchanged. Bilateral nephrectomy caused a significant decrease of blood serine values of control and serine deficient rats. Serine concentration, however, was not affected by bilateral nephrectomy following serine and glycine deficiency indicating kidney-independent serine synthesis under these conditions. There was a significant increase of blood lactate and pyruvate levels under serine and serine/glycine deficient diet compared with control animals, whereas blood ketone bodies fell. In contrast, 24 h after bilateral nephrectomy blood ketone bodies rose and blood lactate and pyruvate concentrations decreased significantly. 24 h after bilateral nephrectomy there was a marked rise in blood citrate values of female rats compared with male animals indicating sex dependency of kidney citrate metabolism in the rat.

“…We have shown that the gluconeogenetic function of isolated liver cells depends on the type of acute uraemia as well as on the substrates used [28]. The present study was undertaken to elucidate the effects of different hormones on the gluconeogenetic abil ity of rat hepatocytes in different models of acute uraemia.…”

Section: According To Katz and Emmanuelmentioning

confidence: 95%

Effect of Hormones on Hepatocyte Gluconeogenesis in Different Models of Acute Uraemia

Riegel

Stępiński

Hörl

et al. 1982

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Hepatocytes isolated from the livers of starved, sham-operated, bilaterally nephrectomised and ureter-ligated rats as well as rats with ischaemic acute renal failure were used for a comparative study of the effects of different hormones on gluconeogenesis. In all tested groups dibutyryl-3′: 5′-adenosine monophosphate inhibits glucose synthesis from pyruvate whereas this process is not affected by glucagon and only slightly activated by adrenalin. In contrast, gluconeogenesis from dihydroxyacetone was stimulated by all three hormones at the expense of the conversion of dihydroxyacetone to lactate. In the presence of I-serine adrenalin, glucagon and dibutyryl cAMP also stimulate glucose synthesis, which is more marked in bilaterally nephrectomised and ureter-ligated animals. In half of the experiments with bilaterally nephrectomised rats (group BN 2), lack of sensitivity of hepatocytes to all tested hormones on gluconeogenesis from serine or dihydroxyacetone was observed. The beta-adrenergic antagonist propranolol reduced the stimulatory effect of adrenalin on glucose synthesis from serine and abolished the influence of catecholamines in the presence of dihydroxyacetone and pyruvate. This suggests that both alpha- and beta-receptors are involved in the activation of hepatic gluconeogenesis. Insulin and parathyroid hormone did not change the rate of glucose synthesis in any of the experimental groups.