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At least 1,369 records · Page 76Linked to original sources
PubMed1989

Effect of ursodeoxycholic acid on bile acid metabolism in primary biliary cirrhosis.

We have compared the effect of ursodeoxycholic acid with placebo on the clinical state, blood liver chemistries and serum and urinary bile acids in four patients with primary biliary cirrhosis. All parameters were evaluated monthly, and bile acid composition was measured by capillary gas-liquid chromatography. At the time of admission, all patients showed intense pruritus, and their serum alkaline phosphatase, AST and ALT levels were elevated 4.3, 2.7 and 2.3 times over control values. Serum bile acids were elevated almost 38-fold with 2.5 times more cholic acid than chenodeoxycholic acid. Urinary bile acid output was elevated 28 times the control values, and 36% were 1 beta-hydroxycholic acid, 1 beta-hydroxydeoxycholic acid and hyocholic acid (3 alpha,6 alpha, 7 alpha-trihydroxy-5 beta-cholanoic acid). Three months of placebo administration did not significantly affect the clinical or biochemical presentations, and the serum and urinary bile acid composition did not change. In contrast, ursodeoxycholic acid feeding (12 to 15 mg per kg per day) for 6 months abolished pruritus in two and lessened itching in two subjects and reduced serum alkaline phosphatase, AST and ALT levels by 21, 35 and 47%, respectively. The mean values for the total serum bile acid concentrations in these patients declined 26% from the pretreatment value, but the proportion of ursodeoxycholic acid increased from 3 to 40% of the total bile acids; thus, total fasting serum endogenous bile acid levels decreased almost 50%. Similar changes were noted in the urinary bile acids, in which ursodeoxycholic acid became the major bile acid, and approximately 18% were hydroxylated at C-1, C-6 and C-21.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

[Total parenteral nutrition of premature infants: metabolic effects of an exogenous supply of L-aspartic acid and L-glutamic acid].

Within the scope of clinically indicated total parenteral nutrition of premature infants, a comparative randomized study was performed to examine--by means of nitrogen-balance studies and determination of the free amino acids in the serum--the metabolic effects of absent or parallel intake of 1.140 mumol L-aspartic acid plus 2.160 mumol L-glutamic acid per kg body weight per day in complete L-amino acid solutions with a comparative E/T-ratio and with identical intake of all other nutrients adapted to the requirement. 1. The nitrogen balance level was not affected by the absent or parallel intake of the dicarbonic acids. 2. Intravenous intakes of glycine plus L-serine, which are higher than 2.5 mmol per kg body weight and day, caused statistically significant increased serum concentrations of glycine and L-serine. Such intakes are obviously above the physiologic regulation range. 3. The absent intake of L-aspartic acid and L-glutamic acid resulted in parallel, statistically significant reduced serum concentrations of aspartic acid and asparagine as well as in homeostatic serum concentrations of glutamic acid and glutamine. Despite the only 15-20% higher intake of proline, alanine and arginine under the infusion regimen lacking dicarbonic acids, there was a parallel, statistically significant marked increase in the serum concentrations of proline, alanine, arginine and methionine as well as a statistically significant marked decrease in those of taurine. Under the infusion regimen containing dicarbonic acids exclusively, constant homeostatic serum concentrations of these amino acids as well as of aspartic acid and glutamic acid were measured. 4. A direct or indirect effect of the exogenous supply of L-aspartic acid and/or L-glutamic acid on the homeostasis of aspartic acid and asparagine, on the endogenous turnover of L-alanine and L-proline as well as on the physiologic course of the Krebs-Henseleit cycle and of the "transsulfuration pathway" must be discussed. 5. Since the supply rates of L-aspartic acid plus L-glutamic acid chosen in series 2 (when continuously administered during 24-hour periods) apparently do not cause any disturbance in amino-acid homeostasis, it is established that under the nutritional conditions given this intake lies within the respective physiologic regulation range and therefore is atoxic.

Amino Acids↗
PubMed1999

The pool of fatty acids covalently bound to platelet proteins by thioester linkages can be altered by exogenously supplied fatty acids.

The goals of this investigation were, first, to develop a chemical strategy to identify and quantitate the mass of fatty acid which is covalently bound to proteins by thioester linkage in unactivated platelets, and, second, to determine whether exogeneously added fatty acids can alter the fatty acid composition of thioester bound fatty acids. Studies with radiolabeled fatty acids cannot identify and quantitate the actual fatty acids bound to proteins because they permit analysis of only the radiolabeled fatty acids added and their metabolites. Therefore, in the absence of metabolic labeling by radiolabeled fatty acids, we isolated the thioester-linked fatty acids from platelet proteins using hydroxylamine at neutral pH to form fatty acid hydroxamates. The hydroxamates were subsequently converted to fatty acid methyl esters by acid methanolysis for quantitation by gas chromatography-mass spectrometry. Using platelet specimens from 14 subjects, 74% of the fatty acid recovered from the unactivated platelet proteins as thioester linked was palmitate. Importantly, however, 22% was stearic acid, and oleate was 4% of the total thioester bound fatty acid. There was minimal variability (2.6-fold at maximum) between the subjects in the amount of the thioester-linked palmitate and thioester-linked stearate. However, there was substantial variability (>100-fold at maximum) between subjects in the amount of thioester-linked oleate. We also demonstrated that incubation of platelets with exogenous fatty acids can alter the profile of fatty acids bound to platelet proteins by thioester linkages. Incubation of platelets with 100 microM palmitate for 3 h increased the amount of thioester-linked palmitate by up to 26%, and incubation of platelets with 100 microM stearate increased the amount of thioester-linked stearate up to 30%. In support of the observation that radiolabeled fatty acids other than palmitate were shown to be capable of binding to platelet proteins by thioester linkage, our results indicate that the fatty acids actually bound to unactivated platelet proteins include a significant amount of stearate, and variable amounts of oleate, as well as palmitate. In addition, the data show that palmitate and stearate can be increased, as a percentage of total protein-bound fatty acid, by incubation with exogenous palmitate and stearate, respectively.

Blood Platelets↗