Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect on free plasma amino acids before and after infusion of 1 mg glucagon was studied at rest after an overnight fast in seven patients with compensated liver cirrhosis and in seven healthy controls. Total aminoacidaemia in cirrhotic patients is significantly higher than in controls. Elevated basal levels in cirrhotics are found particularly in tyrosine, citrulline, tryptophane, threonine, phenylalanine, and methionine whereas ornithine and serine levels are decreased. Save for the redox couple cystine-cysteine which increases, glucagon elicits an decrease in most amino acids that is proportionate to their initial level. Total aminoacidaemia decreases in controls and cirrhotics by 14.6 and 9.1 per cent respectively. Serum ammonia level rises significantly in both groups, urea increases only in controls, uricaemia remains virtually unchanged.
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PMID:The effect of glucagon on free plasma amino acids in cirrhotics and healthy controls. 63 37

Derangements in glucose, amino acid and protein metabolism in patients with liver cirrhosis were examined with special reference to plasma levels of human growth hormone (HGH). Changes in blood glucose, IRI (immunoreactive insulin), HGH, FFA (free fatty acid) and plasma free amino acid levels were determined in controls and patients following either oral glucose load, protein feeding or intravenous arginine infusion. 1) In patients with liver cirrhosis, incidence of glucose intolerance after glucose tolerance test (GTT) was high and IRI levels were elevated in the fasting state as well as after glucose, protein or arginine loads. 2) Fasting levels of blood HGH were significantly higher in liver cirrhosis than in controls. GTT revealed that blood HGH levels decreased slightly during the rising phase of blood glucose, and conversely, increased during the falling phase of glucose (180 minutes after the glucose load) both in controls and in patients. In cirrhotic patients, marked increases in HGH levels were observed both 120 minutes after the protein load and 60 minutes after the arginine infusion. 3) Fasting levels of serum FFA were significantly higher in liver cirrhosis than in controls. Both controls and patients, however, showed a similar pattern of change in FFA levels following GTT or protein ingestion, i.e. a minimum value 120 minutes after the load and a gradual increase thereafter. 4) Fasting levels of plasma free amino acids were significantly higher in cirrhotic patients than in controls. After the glucose load, however, slight decrease was noted in some amino acid levels. All the amino acid levels examined were elevated following protein ingestion, particularly in cirrhotic patients. 5) A positive correlation was demonstrated in cirrhotic patients between total plasma free amino acids and maximal HGH responses following protein ingestion. Similar significant correlations were observed between the maximal HGH response and the plasma level of several amino acids such as His., Ser., Gly., Thr., Ala., and Ileu., respectively. 6) In cirrhotic patients, negative correlations were demonstrated between fasting levels of serum albumin and total plasma free amino acids or maximal HGH responses, respectively, after the protein ingestion. From these results it was inferred that derangements in the metabolism of protein and amino acids in cirrhotic patients may result in an increase in plasma free amino acid level which in turn stimulates HGH secretion. It was surmised that the HGH levels so elevated in the patients may cause FFA mobilization which in effect results in the glucose intolerance.
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PMID:[Studies on glucose, amino acid and protein metabolism in patients with liver cirrhosis in relation to plasma levels of human growth hormone (author's transl)]. 81 50

Although rat brain tryptophan is strikingly elevated following portacaval shunt, plasma total tryptophan is unchanged and plasma free tryptophan is not elevated to the same degree as brain tryptophan. Investigation of the concentrations of the neutral amino acids (phenylalanine, tyrosine, methionine, threonine, leucine, isoleucine, and valine) revealed that their distribution and the sum of their concentrations were altered following portacaval shunt, and that this pattern was similar to that seen in humans with cirrhosis of the liver. It is suggested that both the elevation in plasma free tryptophan and the decrease in the competing neutral amino acids, act together to increase the transport of tryptophan into brain when portal blood is diverted around the liver. The implications of these findings in therapy of hepatic coma is discussed.
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PMID:Brain tryptophan, plasma free tryptophan and distribution of plasma neutral amino acids. 126 41

Plasma amino acid and venous blood ammonia concentrations were measured in six patients with well-compensated cirrhosis and in six healthy volunteers, both in the fasting state and serially for 5 h following ingestion of 30 g mixed protein and 30 g amino acid mixture, administered on separate occasions. Mean fasting plasma concentrations of threonine, serine, proline, glycine, and of the three branched-chain amino acids, valine, isoleucine and leucine, were significantly reduced in the cirrhotic patients compared with the control subjects, while mean (+/- 1 s.d.) fasting venous blood ammonia concentrations were comparable 71.2 +/- 31.4 cf. 56.0 +/- 25.4 mumol/L. Following the oral protein and amino acid loads, increases were observed in plasma amino acid concentrations in the majority of subjects with a return to baseline values by the end of the study. Changes in the circulating concentrations of most amino acids were independent of their concentration in the oral protein and amino acid loads, and their relative distribution in the circulation varied over time. The increases in the concentrations of the three branched-chain amino acids did, however, reflect their concentrations in the two nitrogen loads and did remain constant, relative to one another, over time. There were wide intra- and inter-individual variations in plasma amino acid concentrations following protein and amino acid ingestion in both study groups, and in general no significant differences in responses were observed between them. Similarly, no significant inter-group differences were observed in the ammonia response to the two nitrogen loads. No fundamental differences exist in the ways in which patients with well-compensated cirrhosis handle oral protein or amino acid loads of the magnitude employed in the present study.
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PMID:Amino acid tolerance in cirrhotic patients following oral protein and amino acid loads. 210 85

Free amino acid (AA) concentrations in plasma and quadriceps femoris muscle were determined in 19 healthy volunteers and in 16 patients with hepatic cirrhosis and portal hypertension. Nutritional state was impaired as judged by overt muscle wasting (9/16), triceps skinfold thickness less than 70% of normal in 8/14 (57%), and creatinine-height index below 70% in 5/12 (42%). In the plasma of patients the typical amino acid pattern of cirrhosis was to be observed: Elevation of tyrosine and methionine (p less than 0.01), uniform reduction of branched chain amino acids (p less than 0.001) resulting in a decreased molar ratio of BCAA/AAA from 2.85 +/- 0.05 in normal individuals to 1.35 +/- 0.12 in cirrhotics (p less than 0.001). Levels of the gluconeogenic AA glutamine, glutamate, aspartate, alanine, glycine, threonine, serine and lysine were lowered (p less than 0.05). In muscle of cirrhotics, intracellular AA concentrations exhibited a similar pattern with two major exceptions: Tyrosine and phenylalanine were augmented (p less than 0.001). Surprisingly, BCAA levels were altered heterogeneously; those of gluconeogenic BCAA decreased: Valine from 0.34 +/- 0.03 to 0.20 +/- 0.03 mmol/l (p less than 0.001), isoleucine 0.09 +/- 0.01 to 0.05 +/- 0.02 mmol/l. However, the concentration of ketogenic leucine remained unaltered in muscle. Nevertheless, the molar ratio of BCAA/AAA was considerably reduced from 3.70 +/- 0.04 to 0.81 +/- 0.08 (p less than 0.001). Most of the gluconeogenic AA exhibited reduced intramuscular concentrations, but glutamine levels were normal. The pattern of plasma and muscle free AA in hepatic cirrhosis is thus characterized by accumulation of aromatic AA and by depletion of gluconeogenic AA, especially BCAA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characteristic pattern of free amino acids in plasma and skeletal muscle in stable hepatic cirrhosis. 231 39

Acetaldehyde, a product of ethanol oxidation which forms adducts with proteins, has been incriminated in the pathogenesis of alcoholic liver injury. High serum antibody titers against acetaldehyde-protein adducts have been found not only in alcoholics but also in patients with nonalcoholic liver disease, suggesting a contribution of acetaldehyde derived from sources other than exogenous ethanol. To investigate the effect of liver injury on the removal and the production of acetaldehyde, we produced fibrosis and cirrhosis (by chronic administration of carbon tetrachloride) and fatty liver (with very small doses of dimethylnitrosamine) in rats. Endogenous blood acetaldehyde levels increased by 38% in rats with severe liver injury (p less than 0.005), but not significantly in rats with fatty liver. However, an i.v. load of threonine (a physiological source of acetaldehyde), in amounts equivalent to the daily intake of this amino acid, increased blood and hepatic acetaldehyde levels in the rats with both types of liver injury more than in controls. Threonine dehydrogenase and dehydratase activities, involved in the major pathways for threonine degradation in mitochondria and cytosol, respectively, were markedly decreased in rats with liver injury with a resulting increase in hepatic threonine concentration. Moreover, the threonine aldolase activity, which splits threonine into glycine and acetaldehyde, remained unaffected or even slightly increased. Liver injury was also associated with impaired mitochondrial functions, including a 10 to 23% decrease in acetaldehyde oxidation (depending upon the severity of the lesions). As a consequence, administration of ethanol (an exogenous source of acetaldehyde) resulted in striking elevations in the levels of acetaldehyde in carbon tetrachloride-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High levels of acetaldehyde in nonalcoholic liver injury after threonine or ethanol administration. 251 Nov 35

The aim of this study was to evaluate the contribution of gluconeogenesis from amino acids in the development of fasting and absorptive hyperammonemia in cirrhosis. Somatostatin (SRIF), which is known to inhibit the hepatic disposal of gluconeogenic amino acids, was administered in a continuous infusion (500 micrograms/h) for 90 min before and 5 h after a protein meal (240 g of meat) in 11 overnight fasting patients. Plasma glucagon, insulin, gluconeogenic amino acids (GAA: alanine, serine, glycine, and threonine) and ammonia (NH3) were evaluated before the infusion, immediately before, and at 1, 3, and 5 h after the meal. As control study, the same protocol was randomly repeated in a different day with saline infusion. During the latter, a direct correlation was found between fasting glucagon and ammonia (r = 0.68; p less than 0.05). Fasting glucagon, insulin, and NH3 did not change, whereas alanine (p less than 0.05) and the GAA sum decreased (p less than 0.01). When SRIF was infused, fasting glucagon (p less than 0.05), insulin (p less than 0.05), and NH3 (p less than 0.05) decreased. Alanine did not change, and GAA sum increased (p less than 0.02). No correlations were found by plotting changes in glucagon or GAA sum and NH3. After the meal, SRIF infusion abolished the plasma response of glucagon and markedly reduced that of insulin, so that their area under the curve (AUC0-5) were reduced (p less than 0.005, for both), with respect to control study. Moreover, the AUC0-5 of alanine (p less than 0.005) and GAA sum (p less than 0.005) were increased, suggesting a reduced disposal of these compounds. In spite of this, the meal-induced early increase and the AUC0-5 of plasma NH3 observed during SRIF and saline infusion did not differ. Our results do not confirm the importance of gluconeogenesis from alpha-amino-nitrogens in determining the fasting ammonemia of cirrhosis, and suggest that this metabolic pathway does not significantly influence the protein meal-induced exacerbation of plasma ammonia.
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PMID:Role of gluconeogenesis from amino acids in determining fasting and absorptive levels of plasma ammonia in cirrhosis. 289 85

The purpose of our study was to evaluate the effect of somatostatin (500 microgram/h intravenously) upon insulin, c-peptide, glucagon and plasma amino acids concentrations in patients with and without cirrhosis of the liver. The typical plasma amino acid pattern in cirrhosis is characterised by increased concentrations of the aromatic amino acids and decreased concentrations of the branched chain amino acids and of alanine and glycine. After administration of somatostatin insulin, c-peptide and glucagon concentrations decreased and those of the branched chain amino acids in both groups increased; in addition in patients with cirrhosis the plasma concentrations of threonine, serine, glycine, alanine, lysine, and arginine increased also. Infusion of somatostatin plus insulin in patients with cirrhosis succeeded in preventing the increase in the branched chain amino acid concentrations, while the infusion of somatostatin plus glucagon decreased threonine, serine, glycine, alinine, phenylalanine, tyrosine, lysine and arginine concentrations. It is therefore suggested that the effect of somatostatin on the plasma amino acids may be because of the reduction of insulin and glucagon concentrations; however, other effects of somatostatin cannot be excluded at present.
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PMID:Correction of altered plasma amino acid pattern in cirrhosis of the liver by somatostatin. 614 82

By means of a radioimmunoassay, which utilized [125I]-epiglycanin and anti-epiglycanin antiserum induced in rabbits by injections of viable TA3-Ha ascites cells with Freund's complete adjuvant, picogram quantities of epiglycanin could be detected. Anti-epiglycanin antiserum was similarly produced in allogeneic mice. Unlabeled epiglycanin lost the capacity to compete with [125I]epiglycanin in the radioimmunoassay as a result of periodate oxidation or incubation with endo-alpha-N-acetyl-D-galactosaminidase (Diplococcus pneumoniae), an enzyme found to cleave only the disaccharide beta-D-galactopyranosyl-(1----3)-2-acetamido-2-deoxy-D-galactose chain from serine or threonine residues in epiglycanin. Glycosylhydrolases known to cleave alpha-D-mannose, beta-D-galactose (1,4-linked), beta-N-acetyl-D-glucosamine, and alpha-N-acetyl-D-galactosamine did not reduce the activity of epiglycanin. Neuraminidase enhanced the activity twofold to fivefold. The finding that little or no activity was demonstrated by the disaccharide, the reduced disaccharide, or other glycoproteins containing the same disaccharide chain suggested that the antigenic determinant probably involved the disaccharide and a unique amino acid sequence at the site of its attachment. By means of the radioimmunoassay epiglycanin cross-reactive antigens were detected in the peritoneal or pleural fluid and in the sera of patients with metastatic cancer. Lower concentrations of epiglycanin-like antigen(s) were found in the peritoneal fluid of patients with hepatitis or liver cirrhosis but not in normal serum.
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PMID:Antibody to epiglycanin and radioimmunoassay to detect epiglycanin-related glycoproteins in body fluids of cancer patients. 620 3

The amino acid solution, Aminofusin hepar, was evaluated for treatment of hepatic encephalopathy and for parenteral nutrition of patients with liver cirrhosis in correlation to changes in amino acid levels. In contrast to amino acid solutions used for the parenteral nutrition of patients without liver disease, this solution contains an increased proportion of branch chained amino acids and of arginine and ornithine, and a reduced proportion of phenylalanine, methionine, glycine and threonine. The changes in the plasma amino acid levels after infusion of this solution were measured in 4 cirrhotics. The concentration of leucine, isoleucine, valine, ornithine and arginine increased markedly, whereas phenylalanine, methionine, tyrosine, glycine and threonine decreased. The ammonia level in venous blood increased slightly. 4 cirrhotics with encephalopathy were treated for 7 days. In 3 of them the neuropsychiatric symptoms were completely reversed, whereas in the remaining 1 no clinical improvement was achieved in spite of normalization of the plasma aminogramm. In this patient a constant rise of blood ammonia was noted. The indications for special amino acid solutions in liver diseases are discussed.
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PMID:[Parenteral feeding of patients with liver cirrhosis with hepatic encephalopathy]. 677 52


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