Insulin, Glucagon, Aminoacid Imbalance, and Hepatic Encephalopathy

Soeters, P.B.; Fischer, J. E.

doi:10.1016/s0140-6736(76)90541-9

Cited by 249 publications

(95 citation statements)

References 33 publications

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“…Hepatic function: It is known that concentrations of plasma BCAA with hepatic disease are low level, and Fisher's ratio, it is the molar ratio of BCAA to aromatic amino acids, has been frequently used to evaluate hepatic function [34]. But these days, the BTR, it is the molar ratio of BCAA to tyrosine, has been used as a more simpler method.…”

Section: Discussionmentioning

confidence: 99%

Temporal Changes in Concentrations of Branched-Chain Amino Acids in Plasma on Healthy Mares and Foals from Birth to 24 Weeks of Age

Naito

Sasaki

Matsui

et al. 2009

The Journal of Veterinary Medical Science

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ABSTRACT. The concentrations of branched-chain amino acids ( BCAA; valine, leucine, isoleucine) were determined in plasma of 7 healthy thoroughbred mares and their foals from birth (0 week) to 24 weeks of age, using automated high-performance liquid chromatography. In foals, the concentrations of plasma valine were significantly high (p<0.05) at 16, 20 and 24 weeks. The concentrations of plasma leucine were significantly high (p<0.05) at 1 and 3 weeks. The concentrations of plasma isoleucine were significantly high (p<0.05) from 1 to 24 weeks. In mares, the concentrations of plasma valine were significantly high (p<0.05) at 16 and 24 weeks. The concentrations of plasma leucine and isoleucine were significantly high (p<0.05) at 16 weeks. It was clear that the concentrations of plasma BCAA in foals and mares were at different levels at various times after birth. Since mares and foals were kept in health during this study, we could get the base data of the concentrations of BCAA in plasma of healthy foals and mares from birth to 24 weeks.KEY WORDS: branched-chain amino acid, foal, mare, plasma.

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Section: Discussionmentioning

confidence: 99%

Temporal Changes in Concentrations of Branched-Chain Amino Acids in Plasma on Healthy Mares and Foals from Birth to 24 Weeks of Age

Naito

Sasaki

Matsui

et al. 2009

The Journal of Veterinary Medical Science

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“…The decrease of plasma free tryptophan may be the result of iniprovement of liver function, and this improvement may decrease the concentrations of substances that evoke coma to values below those effective in producing coma. The substances producing coma are reported to be 2-oxoglutaramate (2), ammonia (3), free fatty acids (4-7), methylinercaptan (7) and other false neurotransmitters (8)(9)(10)(11)(12); these components also act synergistically. We plan to study the effects of amino acid metabolism, mercaptan, ammonia and false transmitters and their mutual relations on the mechanism of the blood brain barrier.…”

Section: Discussionmentioning

confidence: 99%

“…Although the pathogenesis of hepatic encephalopathy in severe hepatic failure is not clearly understood, 2-oxoglutaramate (2), ammonia (3), free fatty acids (4-7), methylmercaptan (7) and other false neurotransmitters (8)(9)(10)(11)(12) are reported to be causes of hepatic coma. Tryptophan, the precursor of the putative neurotransmitter and serotonin, are reported to be involved in hepatic encephalopathy (13,14).…”

Section: Introductionmentioning

confidence: 99%

Determination of Free Tryptophan in Plasma and Its Clinical Applications

Hijikata¹,

Hara²,

Shiozaki³

et al. 1984

Clinical Chemistry and Laboratory Medicine

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Summary: Free tryptophan in plasma was separated by centrifugation through an Amicon Ultrafiltration membrane cone. The value obtained without control of pH was found to be lower than that obtained with control of pH by an improved method (Hijikata et al. (1981) Anal. Biochem. 118, 10-16).For determination of the total tryptophan concentration in the plasma, high performance liquid chromatography (HPLC) was better than the method of Denckla Dewey s modified by Bloxam & Warren ((1974) Anal. Biochem. 60,[621][622][623][624][625], s judged on the basis of sensitivity, recovery rate and coefficient of variance. The total tryptophan concentration in the plasma determined by HPLC was lower than that determined by theThe total tryptophan concentration (t-Trp), free tryptophan concentration (f-Trp) and f-Trp/t-Trp ratio were 55.8 ± 10.2 μιηοΐ/ΐ, 11.6 ± 1.5 μίηοΐ/ΐ and 0.211 ± 0.03 (mean ± l SD) respectively, in healthy subjects (co trols). No significant difference was observed between the values of controls and those of patients with liver cirrhosis, hepatocellular carcinoma, liver cirrhosis with hepatocellular carcinoma and hepatic encephalopathy of liver cirrhosis without bleeding. But in liver cirrhosis with bleeding, free tryptophan concentration (f-Trp, 48.0 ± 23.3 μτηοΐ/ΐ, p < 0.001) and f-Trp/t-Trp ratio (0.645 ± 0.289, p < 0.001) were significantly higher than those of controls. In fulminant hepatitis free tryptophan concentration, (f-Trp, 106.6 ± 79.9 μιηοΐ/ΐ, p < 0.02), and f-Trp/t-Trp ratio (0.973 ± 0.017, p < 0.001) were significantly higher than those of controls, and free tryptophan concentration (f-Trp) and f-Trp/t-Trp ratio (p < 0.005) were significantly higher than in liver cirrhosis with bleeding. In other words the increase of free tryptophan concentration in plasma may be related to the bleeding, and in fulminant hepatitis the binding ability of free tryptophan to albumin may decrease. In the examined cases of liver cirrhosis, the correlation of the concentration of plasma tryptophan with those of other amino acids and indicators of liver function was changed when hepatocellular carcinoma was also present.

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“…The reduced ratio of BCAAs to AAAs in plasma has been considered as one of the possible causes of hepatic encephalopathy (Soeters and Fisher, 1976). The accumulation of AAAs in the brain, especially phenylalanine, may interfere with the catecholamine biosynthesis of dopamine and noradrenaline, which normally act as neurotransmitters in the central nervous system.…”

Section: Discussionmentioning

confidence: 99%