Plasma amino acid abnormalities in liver disease. Comparative analysis of idiopathic portal hypertension, extrahepatic portal occlusion and liver cirrhosis.

Ouchi, Kiyoaki; Matsubara, Seishiro; Fukuhara, Kenzo; Matsuno, Seiki

doi:10.1620/tjem.158.171

Cited by 9 publications

(5 citation statements)

References 16 publications

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“…6 Cholestasis leads to secondary hepatocyte injury as reflected by increased plasma levels of liver enzymes like ALT. Hepatocyte impairment is known to lead to reduced levels of branched-chain amino acids for example in cirrhotic patients (Ouchi et al, 1989) and in patients with mild-to-moderate cholestasis as well [2]. In our model we find reduced plasma levels of BCAA throughout the period of administration, showing that similar to humans even moderate liver dysfunction impacts the BCAA metabolism.…”

Section: A) B)supporting

confidence: 55%

Characterization of a rat model of moderate liver dysfunction based on alpha-naphthylisothiocyanate-induced cholestasis

et al. 2017

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-Plasma amino acid level changes occur in mild, moderate and severe stages of liver injury in human patients. In animal models, however, data are mainly restricted to severe liver injury models in rats. Here we present the characterization of a rat model of moderate liver dysfunction secondary to alpha-napthylisothiocyanate (ANIT)-induced cholestasis. Rats treated with 30 mg/kg/day ANIT for 3 weeks exhibited a time-dependent increase in plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST) and bilirubin levels and a decrease in albumin concentration. According to a liver dysfunction evaluation based on the human Child-Pugh-Score, animals developed a moderate liver dysfunction in the first two weeks of ANIT treatment, while only a mild dysfunction was observed at the end of week 3 despite ongoing ANIT administration. Univariate analysis of branched-chain amino acid plasma levels indicated that reduced levels of branched chain amino acids were associated with the ANIT treatment. These data may set the stage for further research of amino acid disturbances and requirements in non-severe cholestasis.

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Section: A) B)supporting

confidence: 55%

Characterization of a rat model of moderate liver dysfunction based on alpha-naphthylisothiocyanate-induced cholestasis

et al. 2017

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“…Plasma concentrations of branched chain amino acids are reduced in cirrhosis and this may have a negative impact on skeletal muscle protein synthesis and breakdown [81,82]. As mentioned earlier, complications of cirrhosis have an adverse impact on skeletal muscle mass and energy metabolism in cirrhosis.…”

Section: Impact Of Complications Of Cirrhosis On Protein Turnovermentioning

confidence: 93%

“…This can be overcome by administering a balanced mixture of essential amino acids with leucine enrichment. Plasma concentrations of aromatic amino acids in cirrhosis are elevated and have been suggested to play a role in the development of hepatic encephalopathy [81]. Therefore, studies to determine the optimum concentration of appropriate amino acid supplementation to derive the maximum skeletal muscle protein response in cirrhotics are necessary.…”

Section: Nutriceuticals In Sarcopenia Of Cirrhosismentioning

confidence: 99%

Consilience in sarcopenia of cirrhosis

Dasarathy

2012

J cachexia sarcopenia muscle

215

225

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Cirrhosis is the consequence of progression of many forms of necro-inflammatory disorders of the liver with hepatic fibrosis, hepatocellular dysfunction, and vascular remodeling. Reversing the primary hepatic disorder, liver transplantation, and controlling the complications are the major management goals. Since the former options are not available to the majority of cirrhotics, treating complications remains the mainstay of therapy. Sarcopenia and/or cachexia is the most common complication and adversely affects survival, quality of life, development of other complications of cirrhosis, and outcome after liver transplantation. With the increase in number of cirrhotic patients with hepatitis C and nonalcoholic fatty liver disease, the number of patients waiting for a liver transplantation is likely to continue to increase above the currently estimated 72.3/100,000 population. One of the critical clinical questions is to determine if we can treat sarcopenia of cirrhosis without transplantation. No effective therapies exist to treat sarcopenia because the mechanism(s) of sarcopenia in cirrhosis is as yet unknown. The reasons for this include the predominantly descriptive studies to date and the advances in our understanding of skeletal muscle biology and molecular regulation of atrophy and hypertrophy not being translated into the clinical practice of hepatology. Satellite cell biology, muscle autophagy and apoptosis, and molecular signaling abnormalities in the skeletal muscle of cirrhotics are also not known. Aging of the cirrhotic and transplanted population, use of mTOR inhibitors, and the lack of definitive outcome measures to define sarcopenia and cachexia in this population add to the difficulty in increasing our understanding of hepatic sarcopenia/cachexia and developing treatment options. Recent data on the role of myostatin, AMP kinase, impaired mTOR signaling resulting in anabolic resistance in animal models, and the rapidly developing field of nutriceuticals as signaling molecules need to be evaluated in human cirrhotics. Finally, the benefits of exercise reported in other disease states with sarcopenia may not be safe in cirrhotics due to the risk of gastrointestinal variceal bleeding due to an increase in portal pressure. This article focuses on the problems facing both muscle biologists and hepatologists in developing a comprehensive approach to sarcopenia in cirrhosis.

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“…Eine Abnahme der Spiegel der verzweigtkettigen Aminos~iuren wurde bei idiopathischer portaler Hypertension, bei extrahepatischem Pfortaderverschlug wie auch in Tierversuchen mit Anlage eines portosystemischen Shunts gefunden [22]. Eine Abnahme der Spiegel der verzweigtkettigen Aminos~iuren wurde bei idiopathischer portaler Hypertension, bei extrahepatischem Pfortaderverschlug wie auch in Tierversuchen mit Anlage eines portosystemischen Shunts gefunden [22].…”

Section: Diskussionunclassified

Hepatische Enzephalopathie nach porto-systemischem shunt

Jentschura

Storz

Rumstadt

et al. 1996

Langenbecks Arch Chir

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A total of 28 cirrhotic patients with porto-systemic anastomosis were compared with 38 cirrhotic patients without porto-systemic shunts concerning their mental state and biochemical parameters of importance for hepatic encephalopathy. A group of 37 metabolically healthy individuals provided the reference values for the psychometric test results and the EEG power spectra. Laboratory values for both groups showed marginal elevation of bilirubin, while the ammonia levels were significantly increased in the operated group. A significant difference was found concerning both the tyrosine level and that of the branched-chain amino acids. None of the patients who had surgical treatment showed clinical evidence of hepatic encephalopathy. Regarding the results in the flicker photometry, the non-shunted cirrhotic patients differed significantly from the healthy control subjects. For both the shunted and non-shunted cirrhotic patients, the results of the Viennese determination test and the number connection test indicated subclinical encephalopathy. We conclude that the elevated ammonia level in patients with porto-systemic anastomosis does not cause a significant mental disturbance. In well-selected patients, the porto-systemic end-side shunt is an appropriate procedure in the treatment of esophageal varices.

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Plasma amino acid abnormalities in liver disease. Comparative analysis of idiopathic portal hypertension, extrahepatic portal occlusion and liver cirrhosis.

Cited by 9 publications

References 16 publications

Characterization of a rat model of moderate liver dysfunction based on alpha-naphthylisothiocyanate-induced cholestasis

Characterization of a rat model of moderate liver dysfunction based on alpha-naphthylisothiocyanate-induced cholestasis

Consilience in sarcopenia of cirrhosis

Hepatische Enzephalopathie nach porto-systemischem shunt

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