Seasonal changes in plasma amino acid levels in the winter flounder (Pseudopleuronectes americanus)

1979 ◽  
Vol 57 (7) ◽  
pp. 1438-1442 ◽  
Author(s):  
E. James Squires ◽  
Douglas E. Hall ◽  
L. A. W. Feltham
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Seasonal Variations ◽  
Seasonal Changes ◽  
Feeding Habits ◽  
Winter Flounder ◽  
Plasma Amino Acids ◽  
Total Plasma ◽  
Pseudopleuronectes Americanus ◽  
Amino Acid Levels

Amino acid analyses were performed on plasma samples taken monthly over a period of 2 years from 305 mature winter flounder. All plasma amino acids showed wide seasonal variations. A very low basal level of the total plasma amino acids was found during the winter months from December through until June. In July, the total levels rose from six to seven times the basal level and then stabilized during August through to November at a level three to four times the basal level. Both male and female flounder showed similar patterns of seasonal amino acid variations. These seasonal variations in plasma amino acids may be related to the feeding habits of the flounder. However, an increase in the plasma level of alanine and threonine during November correlates with the initiation of antifreeze protein synthesis.

scholarly journals Amino acid homeostasis and signalling in mammalian cells and organisms

2017 ◽  
Vol 474 (12) ◽  
pp. 1935-1963 ◽  
Author(s):  
Stefan Bröer ◽  
Angelika Bröer
Keyword(s):  
Amino Acids ◽  
Protein Synthesis ◽  
Amino Acid ◽  
Food Intake ◽  
Essential Amino Acids ◽  
Acid Oxidation ◽  
Plasma Amino Acids ◽  
Amino Acid Oxidation ◽  
Amino Acid Levels ◽  
Amino Acid Depletion

Cells have a constant turnover of proteins that recycle most amino acids over time. Net loss is mainly due to amino acid oxidation. Homeostasis is achieved through exchange of essential amino acids with non-essential amino acids and the transfer of amino groups from oxidised amino acids to amino acid biosynthesis. This homeostatic condition is maintained through an active mTORC1 complex. Under amino acid depletion, mTORC1 is inactivated. This increases the breakdown of cellular proteins through autophagy and reduces protein biosynthesis. The general control non-derepressable 2/ATF4 pathway may be activated in addition, resulting in transcription of genes involved in amino acid transport and biosynthesis of non-essential amino acids. Metabolism is autoregulated to minimise oxidation of amino acids. Systemic amino acid levels are also tightly regulated. Food intake briefly increases plasma amino acid levels, which stimulates insulin release and mTOR-dependent protein synthesis in muscle. Excess amino acids are oxidised, resulting in increased urea production. Short-term fasting does not result in depletion of plasma amino acids due to reduced protein synthesis and the onset of autophagy. Owing to the fact that half of all amino acids are essential, reduction in protein synthesis and amino acid oxidation are the only two measures to reduce amino acid demand. Long-term malnutrition causes depletion of plasma amino acids. The CNS appears to generate a protein-specific response upon amino acid depletion, resulting in avoidance of an inadequate diet. High protein levels, in contrast, contribute together with other nutrients to a reduction in food intake.

Plasma Amino Acid Levels in Huntington's Chorea

1978 ◽  
Vol 132 (4) ◽  
pp. 394-397 ◽  
Author(s):  
J. A. G. Watt ◽  
W. L. Cunningham
Keyword(s):  
Amino Acids ◽  
Drug Therapy ◽  
Amino Acid ◽  
Consistent Pattern ◽  
Plasma Amino Acid ◽  
Plasma Amino Acids ◽  
Huntington's Chorea ◽  
Isoleucine Leucine ◽  
Specific Factors ◽  
Amino Acid Levels

SummaryConcentrations of plasma amino acids in nine patients with Huntington's chorea and nine control patients were studied while diet and drug therapy were controlled. Significantly low values for threonine, alanine, isoleucine, leucine, lysine and histidine were found in the Huntington's chorea patients. However, since different investigators have failed to establish a consistent pattern of abnormality, it is considered that the findings are probably due to non-specific factors.

Quantitative Changes in Plasma Amino Acids Induced by Oral Contraceptives

1971 ◽  
Vol 41 (4) ◽  
pp. 301-307 ◽  
Author(s):  
I. L. Craft ◽  
T. J. Peters
Keyword(s):  
Amino Acids ◽  
Oral Contraceptives ◽  
Plasma Concentrations ◽  
Plasma Amino Acids ◽  
Total Plasma ◽  
Hormone Production ◽  
Contraceptive Pills ◽  
High Concentrations ◽  
Normal Women ◽  
Quantitative Changes

1. Plasma amino acids have been determined in healthy untreated women and in those receiving synthetic steroids to suppress ovulation. Both groups were studied early in the cycle when endogenous sex hormone production is low, and again later in the same cycle, when endogenous or exogenous hormones are at high concentrations respectively. 2. In normal women there is a significant decrease in plasma concentrations of serine, glutamate and ornithine, and of total amino acids in the second half of the cycle. 3. At this time those taking oral contraceptives have significant decreases in plasma concentrations of proline, glycine, alanine, valine, leucine and tyrosine, and of total plasma amino acids. In addition plasma glutamate, glycine, isoleucine and tyrosine concentrations are significantly lower than in normal women. 4. In the interval between completing one course of contraceptive pills and commencing the next, total plasma amino acid concentration reverts to normal, but a significant decrease in plasma glycine concentration persists. 5. It is suggested that these changes are due to the influence of endogenous and exogenous sex hormones respectively.

CIRCADIAN PERIODICITY OF BLOOD AMINO ACIDS IN THE NEONATE

PEDIATRICS ◽  
1970 ◽  
Vol 45 (5) ◽  
pp. 782-791
Author(s):  
Ralph D. Feigin ◽  
Morey W. Haymond
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Detailed Analysis ◽  
Normal Values ◽  
Time Of Day ◽  
Plasma Amino Acids ◽  
Older Children ◽  
Total Blood ◽  
Term Infants ◽  
Plasma Tyrosine

Blood amino acids were obtained every 4 hours for 24 hours from 46 full-term infants who were between 1 hour and 120 hours of age when first sampled. Blood was also obtained at 0400 and 1200 hours on the same day from 10 additional infants, aged 48 to 72 hours at the time of study, for more detailed analysis of individual blood amino acids. Periodicity of total blood amino acids was demonstrated as early as the first day of life in some infants. This blood amino acid rhythmicity was similar but not identical to that previously observed in adults and older children. Concentrations of blood amino acids were minimal at 0400 hours and peaked between 1200 and 2000 hours. Periodicity of individual blood amino acids was similar to that for total blood amino acids but much less consistent. The presence of periodicity for plasma tyrosine was demonstrable even in two patients with neonatal tyrosinemia. Since plasma amino acids vary normally as a function of time, "normal values" must be standardized for time of day.

Interrelationship between hepatic ureagenesis and gluconeogenesis in early sepsis

1991 ◽  
Vol 260 (3) ◽  
pp. E453-E458 ◽  
Author(s):  
Y. Ohtake ◽  
M. G. Clemens
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Substrate Preference ◽  
Hormone Sensitivity ◽  
Urea Production ◽  
Urea Release ◽  
Amino Acid Levels ◽  
Early Sepsis ◽  
Septic Group

This study was performed to investigate the interrelationship between gluconeogenesis and ureagenesis during sepsis. In isolated perfused livers, gluconeogenesis was assessed using either lactate or a combination of lactate, glutamine, and alanine as substrate. Ureagenesis was assessed using either NH4Cl or glutamine plus alanine as substrate. NH4Cl stimulated urea production in livers from both septic and sham-operated control rats. Urea release was approximately 1.2 and 2.0 mg urea nitrogen.g-1.h-1 for 1 and 5 mM NH4Cl, respectively, and was equal for both groups. With amino acids as substrate, urea production was significantly greater in livers from septic animals compared with controls. Phenylephrine stimulated urea production in the sham-operated group by about twofold, whereas in the septic group urea release was slightly inhibited. Gluconeogenesis from lactate was inhibited by NH4Cl (1 and 5 mM) in both groups, with no difference between groups. In contrast to enhanced ureagenesis from amino acids in septic rats, gluconeogenesis was decreased by approximately 24% (P less than 0.5). Similarly, phenylephrine (1 microM) stimulated gluconeogenesis by 13 +/- 1 mumol.g-1.h-1 in sham-operated rats but only by 9 +/- 1 mumol.g-1.h-1 in septic rats (P less than 0.02). These results suggest that hepatic gluconeogenic and ureagenic pathways are intact in sepsis but that altered substrate preference and hormone sensitivity may result in decreased gluconeogenesis in the presence of elevated amino acid levels.

scholarly journals The Amino Acid Need for Milk Synthesis Is Defined by the Maximal Uptake of Plasma Amino Acids by Porcine Mammary Glands

2004 ◽  
Vol 134 (9) ◽  
pp. 2182-2190 ◽  
Author(s):  
Xinfu Guan ◽  
Brian J. Bequette ◽  
Pao K. Ku ◽  
Robert J. Tempelman ◽  
Nathalie L. Trottier
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Mammary Glands ◽  
Plasma Amino Acids

scholarly journals Amino acids whose intracellular levels change most during aging alter chronological lifespan of fission yeast

2020 ◽  
Author(s):  
Charalampos Rallis ◽  
Michael Mülleder ◽  
Graeme Smith ◽  
Yan Zi Au ◽  
Markus Ralser ◽  
...  
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Fission Yeast ◽  
Yeast Cells ◽  
Total Amino Acid ◽  
Wild Type ◽  
Chronological Lifespan ◽  
Biomarkers Of Aging ◽  
Concentration Changes ◽  
Amino Acid Levels

AbstractAmino acid deprivation or supplementation can affect cellular and organismal lifespan, but we know little about the role of concentration changes in free, intracellular amino acids during aging. Here, we determine free amino-acid levels during chronological aging of non-dividing fission yeast cells. We compare wild-type with long-lived mutant cells that lack the Pka1 protein of the protein kinase A signalling pathway. In wild-type cells, total amino-acid levels decrease during aging, but much less so in pka1 mutants. Two amino acids strongly change as a function of age: glutamine decreases, especially in wild-type cells, while aspartate increases, especially in pka1 mutants. Supplementation of glutamine is sufficient to extend the chronological lifespan of wild-type but not of pka1Δ cells. Supplementation of aspartate, on the other hand, shortens the lifespan of pka1Δ but not of wild-type cells. Our results raise the possibility that certain amino acids are biomarkers of aging, and their concentrations during aging can promote or limit cellular lifespan.

Food Intake Regulation: Amino Acid Toxicity and Changes in Rat Brain and Plasma Amino Acids

1973 ◽  
Vol 103 (4) ◽  
pp. 608-617 ◽  
Author(s):  
Y. Peng ◽  
J. Gubin ◽  
A. E. Harper ◽  
M. G. Vavich ◽  
A. R. Kemmerer
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Food Intake ◽  
Rat Brain ◽  
Plasma Amino Acids ◽  
Food Intake Regulation ◽  
Acid Toxicity ◽  
Intake Regulation

Effect of free fatty acids on blood amino acid levels in human

1986 ◽  
Vol 250 (6) ◽  
pp. E686-E694 ◽  
Author(s):  
E. Ferrannini ◽  
E. J. Barrett ◽  
S. Bevilacqua ◽  
R. Jacob ◽  
M. Walesky ◽  
...  
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Plasma Insulin ◽  
Plasma Free Fatty Acid ◽  
Blood Levels ◽  
Experimental Conditions ◽  
Lipid Infusion ◽  
Amino Acid Levels ◽  
Branched Chain

Raised plasma free fatty acid (FFA) levels effectively impede glucose uptake in vivo, thereby conserving plasma glucose and sparing glycogen. To test whether FFA have any effect on blood amino acid levels, we infused Intralipid plus heparin or saline into healthy volunteers under four different experimental conditions: A) overnight fast; B) euglycemic hyperinsulinemia (approximately 100 microU/ml); C) hyperglycemic (approximately 200 mg/100 ml) hyperinsulinemia (approximately 50 microU/ml); and D) hyperglycemic (approximately 300 mg/100 ml) normoinsulinemia (approximately 20 microU/ml). In the fasting state (A), lipid infusion was associated with lower blood levels of most amino acids, both branched chain and glucogenic. This effect, however, could not be ascribed to lipid infusion alone, because plasma insulin levels were also stimulated. The clamp studies (B, C, and D) allowed to assess the influence of lipid on blood amino acid levels at similar plasma insulin and glucose levels. It was thus observed that lipid infusion has a significant hypoaminoacidemic effect of its own under both euglycemic (B) and hyperglycemic (C) conditions; this effect involved many glucogenic amino acids (alanine, glycine, phenylalanine, serine, threonine, and cystine) but none of the branched-chain amino acids (leucine, isoleucine, and valine). In marked contrast, normoinsulinemic hyperglycemia (D), with or without lipid infusion, caused no change in the blood level of any measured amino acid. We conclude that lipid infusion has a hypoaminoacidemic action. We also suggest that this action is permitted by insulin and may involve specific metabolic interactions (e.g., reduced availability of glucose-derived pyruvate or glycerophosphate) as well as enhanced uptake by the liver.

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