Urea Synthesis After Protein Feeding Reflects Hepatic Mass in Rats† ‡

Brewer, Thomas G.; Berry, William R.; Harmon, John W.; Walker, Strothers H.; Dunn, Michael A.

doi:10.1002/hep.1840040520

Cited by 15 publications

(5 citation statements)

References 34 publications

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“…No significant differences were found between the different groups o f animals within this short time period o f 2 weeks. The urea synthesis rate was in the same range as previously reported by others [7,8] and no significant differences were found between the different groups o f rats in this study (table 3).…”

Section: Resultssupporting

confidence: 79%

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Effect of Rearterialization on Short-Term Graft Function in Orthotopic Rat Liver Transplantation

Svensson

Aldenborg²,

Karlberg³

1991

Eur Surg Res

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The orthotopic liver transplant model in rats has been very useful for immunological studies. However, differing opinions exist as to whether rearterialization of the graft is necessary for such experiments. Therefore, in this study we evaluted the short-term allograft function when rearterialized was compared to restored venous portal flow only and in situ hepatic artery ligation. The technique of orthotopic liver transplantation in the rat with and without rearterialization of the graft is described in detail. In addition, we evaluated the technical feasibility of sutured vascular anastomosis as compared to the traditional cuff technique. Urea synthesis rate was used as a sensitive marker of integrated liver function, including uptake, synthesis and excretion. Standard liver test of bilirubin, plasma aspergine aminotransferase and alanine aminotransferase were measured. We found no significant differences in the biochemical markers between allografts with portal venous flow only compared to the combination with arterial flow. Autopsy was performed after the biochemical studies at day 14. Histopathological analyses revealed no differences between the two groups of transplanted rats. The patency of sutured anastomoses was in our hands found to be superior to that of the cuff technique, with a success rate of more than 90% in rats with portal venous flow. This rat model in which vascular anastomosis is performed with a running suture technique and without rearterialization seems to be excellent for short-term studies of preservation and liver function after orthotopic liver transplantation.

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Section: Resultssupporting

confidence: 79%

“…FR G ). Urea pool size was assumed to be equal to a body water space o f 0.63 X BW [7], Calculations o f synthesis rate and pool size enabled the synthesis rate to be deter mined as pmol/h or pmol/BW/min.…”

Section: Biochemical Methodsmentioning

confidence: 99%

Effect of Rearterialization on Short-Term Graft Function in Orthotopic Rat Liver Transplantation

Svensson

Aldenborg²,

Karlberg³

1991

Eur Surg Res

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“…The diversion of portal blood flow causes hepatocellular atrophy and a decrease in the enzyme activities of the urea cycle in experi mental animals (99); furthermore, the shunting of portal blood to the sys temic circulation not only reduces the ammonia immediately available for extraction by the liver, but also reduces the concentrations of amino acids necessary for maximal activity of the urea cycle. Finally, a direct correlation between decreased liver mass produced by partial hepatectomy and urea synthesis was demonstrated in rats (12). The administration of corticosteroids to patients with cirrhosis and chronic active hepatitis results in an increase in urea synthesis (64).…”

Section: Urea Synthesismentioning

confidence: 97%

Liver Disease and Protein Needs

Mezey

1982

Annu. Rev. Nutr.

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Protein deficiency is often associated with liver disease. The principal cause of protein deficiency is decreased dietary intake. Deficiencies in digestion and absorption that are common in alcoholics contribute to protein deficiency in alcoholic liver disease. The protein requirements in most patients with compensated chronic liver disease are not different from normal, but increase during episodes of hepatocellular deterioration. An increased demand for protein after liver injury drains nitrogen from other organs such as muscle. Aromatic amino acids released from muscle in increased amounts accumulate in the circulation of patients with chronic liver disease because of their decreased hepatic metabolism. By contrast branched chain amino acids decrease in the circulation because of their preferential uptake by extrahepatic tissues. Decreases in urea synthesis in liver disease result in the accumulation of ammonia. The causes of the decrease in urea synthesis include decreases in the enzymes and substrates of the urea cycle, alterations in portal blood flow, and a decrease in total hepatic mass. The resulting increase in ammonia in association with an increased accumulation and entry of aromatic amino acids into the brain are important factors in the pathogenesis of hepatic encephalopathy. Circulating proteins synthetized by the liver, such as albumin and clotting factors, are frequently decreased in chronic liver disease. Vitamin deficiencies that are common in liver disease contribute to abnormalities of protein metabolism. Hepatic regeneration following hepatic resection or injury is adversely affected by protein and vitamin deficiencies and by alcohol ingestion.

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“…The amino acids has been shown to be decreased in patients and activity of benzoyl-CoA synthase, the enzyme catalyzing experimental animals with cirrhosis and to reflect the functhe rate-limiting step in benzoate metabolism, was retional liver cell mass. [3][4][5] The arterial b-hydroxybutyrate/aceduced by 25%, and the activity of benzoyl-CoA:glycine toacetate ratio, which is an indicator of the hepatic NADH/ N-transferase was reduced by 66% in BDL rats. The ac-NAD ratio and therefore of the function of the electron transtivity of benzoyl-CoA synthase was significantly inhibport chain in liver mitochondria, 6 has been proposed to reflect ited by lithocholate, suggesting that hepatic accumulaliver function and to be of prognostic significance in pation of hydrophobic bile acids could contribute to the tients 7,8 and in experimental animals with cirrhosis.…”

mentioning

confidence: 99%

Benzoic Acid Metabolism Reflects Hepatic Mitochondrial Function in Rats With Long–Term Extrahepatic Cholestasis

Krähenbühl¹,

Reichen²,

Talos³

et al. 1997

Hepatology

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Many of the metabolic pathways of liver mitochondria are Benzoic acid metabolism, which is primarily a funcessential not only for the function of the liver but for the tion of liver mitochondria, depending on the concentrawhole organism. Examples of vital hepatic mitochondrial tion of adenosine triphosphate (ATP), coenzyme A (CoA), functions include the first steps in gluconeogenesis, amino and glycine in the mitochondrial matrix, was investiacid metabolism, urea synthesis, and b-oxidation of fatty gated in both rats with long-term cholestasis caused by acids. A partial or complete loss of some of these functions bile duct ligation (BDL) and sham-operated control rats.in humans or experimental animals with liver disease may In isolated liver mitochondria, hippurate production therefore be critical for prognosis and survival. Some mitofrom benzoate in the presence of saturating glycine conchondrial functions have been investigated and proposed to centrations was reduced in BDL rats by 36% with L-glube useful as liver function tests in patients or animals with tamate as a source for ATP, by 21% in the presence of liver disease. For instance, Michaletz et al. described a breath succinate, and by 31% in the presence of ATP plus oligotest that measures the decarboxylation of a-ketoisocaproic mycine. This reduction in benzoate metabolism is in the acid, the first metabolite of leucine. 1 Assessment of a-ketoisosame range as the previously observed reduction in the caproic acid decarboxylation has been shown to reflect heactivity of the electron transport chain in liver mitopatic mitochondrial function in rats treated with the mitochondria from BDL rats. The mitochondrial CoA pool, chondrial toxin 4-pentenoic acid 1 and in alcoholics with or which can be rate-limiting for benzoic acid metabolism, without cirrhosis. 2 Similarily, urea production from infused was not different between BDL and control rats. The amino acids has been shown to be decreased in patients and activity of benzoyl-CoA synthase, the enzyme catalyzing experimental animals with cirrhosis and to reflect the functhe rate-limiting step in benzoate metabolism, was retional liver cell mass. [3][4][5] The arterial b-hydroxybutyrate/aceduced by 25%, and the activity of benzoyl-CoA:glycine toacetate ratio, which is an indicator of the hepatic NADH/ N-transferase was reduced by 66% in BDL rats. The ac-NAD ratio and therefore of the function of the electron transtivity of benzoyl-CoA synthase was significantly inhibport chain in liver mitochondria, 6 has been proposed to reflect ited by lithocholate, suggesting that hepatic accumulaliver function and to be of prognostic significance in pation of hydrophobic bile acids could contribute to the tients 7,8 and in experimental animals with cirrhosis. 7,9observed reduction of benzoate metabolism in BDL rats. The metabolism of benzoic acid (benzoate) has been shown Benzoate metabolism was also studied in vivo by monito be decreased in rats with fatty liver caused by long-term toring the urinary hippurate excretion af...

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Urea Synthesis After Protein Feeding Reflects Hepatic Mass in Rats† ‡

Cited by 15 publications

References 34 publications

Effect of Rearterialization on Short-Term Graft Function in Orthotopic Rat Liver Transplantation

Effect of Rearterialization on Short-Term Graft Function in Orthotopic Rat Liver Transplantation

Liver Disease and Protein Needs

Benzoic Acid Metabolism Reflects Hepatic Mitochondrial Function in Rats With Long–Term Extrahepatic Cholestasis

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