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At least 1,135 records · Page 63Linked to original sources
PubMed1995

Effect of cortisol on energy expenditure and amino acid metabolism in humans.

Hydrocortisone was infused overnight into nine normal healthy adults on three occasions at 0, 80, and 200 micrograms.kg-1.h-1, producing plasma cortisol concentrations of 10.6 +/- 1.2, 34.0 +/- 2.0, and 64.9 +/- 4.3 micrograms/dl, respectively. L-[1-13C]leucine, L-[phenyl-2H5]phenylalanine, and L-[2-15N]glutamine were infused during the last 7 h of hypercortisolemia to measure amino acid kinetics. During the last 3.5 h, somatostatin, glucagon, and insulin were infused to reduce the cortisol-induced elevation in plasma insulin to basal. Hypercortisolemia increased plasma glucose, free fatty acid (FFA), and insulin concentrations. Institution of the somatostatin clamp returned insulin to basal but increased glucose and FFA. Acute hypercortisolemia increased protein breakdown 5-20%, as measured by increases in leucine and phenylalanine appearance rates. Normalizing insulin during hypercortisolemia did not alter phenylalanine flux but enhanced leucine appearance rate, the latter result indicating that insulin was affecting leucine metabolism during hypercortisolemia. The fraction of the leucine flux that was oxidized was not significantly increased with hypercortisolemia, but disposal by the nonoxidative route of leucine uptake for protein synthesis was increased. Hypercortisolemia increased cycling of amino acids by increasing protein breakdown and synthesis, but the increase in this process could have increased resting energy expenditure (REE) only 1-2%. Hypercortisolemia increased glutamine flux in a dose-dependent fashion through an increase in de novo synthesis, which presumably reflects increased release from skeletal muscle. Hypercortisolemia increased REE 9-15% at the 80 and 200 micrograms.kg-1.h-1 infusion rates. Respiratory quotient did not rise with cortisol infusion but tended to decrease, suggesting that the increase in REE was fueled by increased oxidation of fat. These data demonstrate that hypercortisolemia increases metabolic rate and may be in part responsible for the hypermetabolic state in injury.

Adult↗
PubMed1994

Altered amino acid metabolism in lrp mutants of Escherichia coli K12 and their derivatives.

An Escherichia coli lrp mutant, lacking the leucine-responsive regulatory protein and the global response it controls, is deregulated in the expression of many genes, but is nevertheless able to grow in glucose-minimal medium at 37 degrees C. In the presence of isoleucine and valine, the growth rate of the lrp mutant at 37 degrees C is significantly increased by exogenous L-serine or L-leucine (or both), suggesting that synthesis of these amino acids is limiting. In the absence of isoleucine and valine, however, growth is severely inhibited by both L-serine and L-leucine. A shift to 42 degrees C or to anaerobiosis makes the lrp mutant auxotrophic for L-serine. Three double mutants carrying lrp and another known mutation, acquire new auxotrophies: lrp relA, lacking the stringent response to amino acid limitation, requires leucine; lrp ssd with numerous metabolic perturbations and antibiotic resistances, requires serine and leucine; and lrp pnt, lacking pyridine nucleotide transhydrogenase, requires glutamate or aspartate (or the corresponding amides). The lrp mutant, although able to achieve balanced growth in some conditions, is clearly on the edge of a metabolic precipice, unable to tolerate many physiological and genetic perturbations which are inocuous to wild-type E. coli.

Amino Acids↗
PubMed1995

Sulfur amino acid metabolism in infants on parenteral nutrition.

In the infant on parenteral nutrition, cysteine supplementation has been suggested due to low levels of hepatic cystathionase activity limiting synthesis from methionine. We have examined the plasma concentrations of sulfur amino acids in four groups of post-surgical infants requiring parenteral nutrition receiving (A) a low methionine + cysteine + taurine formula, (B) a high methionine formula (non-steady state), (C) a high methionine formula (steady state), and (D) a high methionine + cysteine formula. Plasma methionine concentrations were above the normal reference range (2.2-4.9 micromol/dL) of normal breast-fed infants in Groups B (15.9 +/- 10.7 micromol/dL) and D (5.7 +/- 1.9 micromol/dL) and at the upper limit for Group C (4.9 +/- 1.7 micromol/dL). Total cysteine/cystine concentrations (normal reference range, 10.2-20.4 micromol/dL) were highest in Groups A (18.9 +/- 3.5 micromol/dL) and D (16.8 +/- 5.3 micromol/dL) that received cysteine HCI supplementation, and lowest in Group B (8.6 +/- 3.7 micromol/dL) that received no cysteine in non-steady state. All plasma free cystine concentrations were below the normal reference range (3.6-6.8 micromol/dL). Plasma taurine concentrations were not significantly different among the four groups and all were within the normal reference range (0.6-16.2 micromol/dL). The strikingly elevated methionine and low total cysteine/cystine values in Group B suggested the existence of a feedback loop of methionine conversion below the level of homocysteine. Equilibrium of methionine and cysteine/cystine plasma concentrations did occur, in time. Parenteral cysteine administration resulted in a greater proportion of plasma free cysteine concentration, but not cystine. The proportion of free to bound cysteine/cystine, as well as the proportion of free cystine to cysteine, was not normal during parenteral nutrition with or without cysteine HCI supplementation. Little benefit in plasma concentrations was derived from cysteine HCI supplementation to a high methionine formulation.

Journal Article↗
PubMed1982

[Postoperative amino acid metabolism].

According to literature, anabolism is present in the visceral organs also during stress and early poststress-periods. During early periods of fasting, those enzyme structures of the visceral organs which are of prime importance are being catabolized. Therefore, an adequate nutrition is not only reasonable, but obligatory especially in those patients severely ill. As for the parenteral management of protein nutrition, solutions of L-amino acids (a.a.) are the only types suitable. These solutions should contain at least proportionate quantities of the 8 essential a.a., histidine, arginine, proline, alanine, glutamic acid and glycine with each single a.a. being within the respective physiologic regulation range. Different pattern of the a.a. requirement of adults are being established for different metabolic conditions. These types of a.a. pattern are highly dependent on the alterations of the functional requirement of one or more a.a. For the clinical need of total parenteral nutrition (t.p.n.) of adults, at least 3 types of different compositions of L-a.a. solution should be available: a) a standard a.a. solution (adapted to the physiologic requirement of adults) for long-term t.p.m. b) an a.a. solution with a high E/T-ratio for the t.p.n. of uremic patients (this solution is the one also used for t.p.n. of infants), c) an a.a. solution with high concentrations of branched-chain a.a. for the therapy of portosystemic encephalopathy. The metabolic significant and clinical importance of other special a.a. solutions are discussed.

Adult↗