scholarly journals Metabolism of 3H- and 14C-labelled lactate in starved rats

1981 ◽  
Vol 194 (2) ◽  
pp. 525-540 ◽  
Author(s):  
Fumikazu Okajima ◽  
Maymie Chenoweth ◽  
Robert Rognstad ◽  
Arnold Dunn ◽  
Joseph Katz
Keyword(s):  
Amino Acids ◽  
Steady State ◽  
Transit Time ◽  
Bolus Injection ◽  
Mean Transit Time ◽  
Specific Radioactivity ◽  
Vena Cava ◽  
The Body ◽  
Replacement Rate ◽  
Kinetics Of

1. [2-3H,U-14C]- or [3-3H,U-14C]-Lactate was administered by infusion or bolus injection to overnight-starved rats. Tracer lactate was injected or infused through indwelling cannulas into the aorta and blood was sampled from the vena cava (A–VC mode), or it was administered into the vena cava and sampled from the aorta (V–A mode). Sampling was continued after infusion was terminated to obtain the wash-out curves for the tracer. The activities of lactate, glucose, amino acids and water were followed. 2. The kinetics of labelled lactate in the two modes differed markedly, but the kinetics of labelled glucose were much the same irrespective of mode. 3. The kinetics of 3H-labelled lactate differed markedly from those for [U-14C]lactate. Isotopic steady state was attained in less than 1h of infusion of [3H]lactate but required over 6h for [U-14C]lactate. 4. 3H from [2-3H]lactate labels glucose more extensive than does that from [3-3H]lactate. [3-3H]Lactate also labels plasma amino acids. The distribution of 3H in glucose was determined. 5. Maximal radioactivity in 3HOH in plasma is attained in less than 1min after injection. Near-maximal radioactivity in [14C]glucose and [3H]glucose is attained within 2–3min after injection. 6. The apparent replacement rates for lactate were calculated from the areas under the specific-radioactivity curves or plateau specific radioactivities after primed infusion. Results calculated from bolus injection and infusion agreed closely. The apparent replacement rate for [3H]lactate from the A–VC mode averaged about 16mg/min per kg body wt. and that in the V–A mode about 8.5mg/min per kg body wt. The apparent rates for [14C]lactate (‘rate of irreversible disposal’) were 8mg/min per kg body wt. for the A–VC mode and 5.5mg/min per kg body wt. for the V–A mode. Apparent recycling of lactate carbon was 55–60% according to the A–VC mode and 35% according to the V–A mode. 7. The specific radioactivities of [U-14C]glucose at isotopic steady state were 55% and 45% that of [U-14C]lactate in the A–VC and V–A modes respectively. We calculated, correcting for the dilution of 14C in gluconeogenesis via oxaloacetate, that over 70% of newly synthesized glucose was derived from circulating lactate. 8. Recycling of 3H between lactate and glucose was evaluated. It has no significant effect on the calculation of the replacement rate, but affects considerably the areas under the wash-out curves for both [2-3H]- and [3-3H]-lactate, and calculation of mean transit time and total lactate mass in the body. Corrected for recycling, in the A–VC mode the mean transit time is about 3min, the lactate mass about 50mg/kg body wt. and the lactate space about 65% of body space. The V–A mode yields a mass and lactate space about half those with the A–VC mode. 9. The area under the wash-out curve for [14C]lactate is some 20–30 times that for [3H]lactate, and apparent carbon mass is 400–500mg/kg body wt. and presumably includes the carbon of glucose, pyruvate and amino acids, which are exchanging rapidly with that of lactate.

Metabolism of tritium- and 14C-labeled alanine in rats

1981 ◽  
Vol 241 (2) ◽  
pp. E121-E128 ◽  
Author(s):  
S. Golden ◽  
M. Chenoweth ◽  
A. Dunn ◽  
F. Okajima ◽  
J. Katz
Keyword(s):  
Continuous Infusion ◽  
Transit Time ◽  
Bolus Injection ◽  
Specific Activity ◽  
Mean Transit Time ◽  
Vena Cava ◽  
Maximal Activity ◽  
Total Body Mass ◽  
Arterial Blood ◽  
Specific Activities

[3-3H]- and [U-14C]alanine were administered to starved rats by bolus injection and by continuous infusion. The specific activities of alanine, glucose, and lactate in blood were followed. The tracer kinetics of alanine depended on the site of tracer administration and sampling. Tracer was either administered into the aorta and blood sampled from the vena cava (A-VC mode) or tracer was administered into the vena cava and arterial blood sampled (V-A mode) (Katz, J. F. Okajima, and A. Dunn. Biochem J. 194: 513-524, 1981). When tracer was infused in the A-VC mode the plateau specific activity of alanine was about half that obtained in the V-A mode. The parameters of alanine turnover were calculated from the specific activities obtained in the A-VC mode. The calculated apparent replacement rate averaged 1.9 mg.min-1.kg-1 for [U-14C]- and 3.9 mg.min-1.kg-1 for [3-3H]alanine, indicating a carbon recycling of about 50%. The apparent contribution of alanine carbon to that of glucose is 15%. The maximal activity in plasma water is attained at about 5 min after bolus injection of [3-3H]alanine and that of [14C]glucose in blood is attained about 10 min after the injection of [U-14C]alanine. Maximal specific activity of [3H]- and [14C]lactate is attained within about 1 min after injection. The apparent mean transit time and alanine mass were calculated from the areas of washout curves after the continuous infusion was terminated. The mean transit time for [3H]alanine was 10 min and apparent total body mass of alanine of the order of 40 mg/kg. The apparent means transit time for [U-14C]alanine ranged from 33 to 66 min corresponding to a mass of the order of 100 mg/kg of alanine or 40 mg/kg of alanine carbon.

Kinetics of Na+ uptake and transcellular transit by the pancreas

1975 ◽  
Vol 228 (4) ◽  
pp. 1199-1205 ◽  
Author(s):  
M Rossier ◽  
SS Rothman
Keyword(s):  
Steady State ◽  
Transit Time ◽  
Mean Transit Time ◽  
Uptake Curve ◽  
Rabbit Pancreas ◽  
In Series ◽  
The Mean ◽  
22Na Uptake ◽  
Kinetics Of

22Na uptake into strips of rabbit pancreas was measured for up to 10 min. The uptake curve was characterized by the presence of two plateaus separated by an inflexion point; a first "plateau" or an approximation of steady-state uptake was observed between 1 and 3 min; betwen 3 and 4 min the slope of the uptake curve increased again, finally decreasing to a new and higher steady-state uptake between 4 and 6 min. The data suggest that the first part of the uptake curve (from 0 to 3 min) represents uptake into most if not all cells, and the second part (from 3 to 10 min) represents the sum of "quasi" steady-state cellular uptake and of the equilibration of the ductal compartment in series with the cells. In this model a substantial delay (2.5-3.25 min) elapses between the filling of cellular and ductal compartments which is apparently of intracellular origin, implying restricted Na+ diffusion within the cytoplasm and an intracellular Na+ gradient. If this model is correct, then the mean transit time for Na+ across the whole organ should be approximately 3-4 min and be primarily the result of transcellular transit. The mean transit time for Na+ across the whole organ in vitro was measured and found to be 3.5 min on the average. The step that accounts for most of this time appears to be the transepithelial transit of Na+.

The Effects of Thromboxane Antagonism on the Transit Time of Platelets Through the Spleen

1985 ◽  
Vol 54 (02) ◽  
pp. 495-497 ◽  
Author(s):  
A M Peters ◽  
I F Lane ◽  
M Sinclair ◽  
J T C Irwin ◽  
C N McCollum
Keyword(s):  
Transit Time ◽  
Mean Transit Time ◽  
Thromboxane A2 ◽  
Time Measurement ◽  
Thromboxane A2 Receptor ◽  
Group Research ◽  
The Mean ◽  
A Site ◽  
Kinetics Of ◽  
Transit Time Measurement

SummaryThe spleen is well-known as a site for platelet pooling, although the mechanisms controlling intrasplenic platelet transit are essentially unknown. We tested the possibility that thromboxane A2 might be involved in this control by measuring intrasplenic platelet transit time in 10 subjects receiving a specific thromboxane A2 receptor antagonist (AH23848B; 70 mg; Glaxo Group Research Ltd), in 10 receiving aspirin (300 mg) plus dipyridamole (75 mg), and in 9 receiving placebo. All doses were administered 3 times daily commencing 4 days prior to transit time measurement.Mean intrasplenic platelet transit time was measured by monitoring the kinetics of equilibration of 111In radiolabelled platelets between blood and spleen following intravenous injection. There was no difference between the mean transit time in the 3 groups of subjects, lending no support to the hypothesis that thromboxane A2 is involved in the control of platelet traffic through the spleen.

scholarly journals KINETICS OF AMINO ACID INCORPORATION INTO SERUM PROTEINS

1955 ◽  
Vol 38 (3) ◽  
pp. 283-293 ◽  
Author(s):  
H. Green ◽  
H. S. Anker
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Serum Protein ◽  
Transit Time ◽  
Serum Proteins ◽  
Amino Acid Incorporation ◽  
Acid Incorporation ◽  
Amino Acid Analogues ◽  
Kinetics Of

1. The effect of varying body temperature on the rate of amino acid incorporation into serum protein does not give support to the idea that the rate of this process is adjusted in vivo to restore those protein molecules destroyed by thermal denaturation. The experimentally observed Q10 was about 3.9. 2. When amino acids are injected into the blood of animals in a steady state of serum protein turnover, a period of time elapses before these amino acids can be found in the serum proteins. This has been called transit time. At a given temperature (31°) it is the same in rabbits, turtles, and Limulus (1 hour). In rabbits and turtles it has a Q10 of 3.2. It appears to be specifically related to the process of synthesis (or release) of serum proteins. 3. It was not possible to affect the transit time or the incorporation rate by the administration of amino acid analogues.

Tritium Loss from Iron Meteorites by Solar Wind Hydrogen

1967 ◽  
Vol 22 (10) ◽  
pp. 1483-1488 ◽  
Author(s):  
K. Wagener
Keyword(s):  
Solar Wind ◽  
Steady State ◽  
Hydrogen Content ◽  
Cosmic Ray ◽  
The Body ◽  
Iron Meteorites ◽  
Tritium Content ◽  
Diffusion Data ◽  
Meteoritic Iron ◽  
Kinetics Of

An estimate of the diffusion loss of tritium from iron meteorites in space cannot be based, in a direct manner, on the results of diffusion measurements in the laboratory, because the hydrogen content of the samples in the laboratory is always higher by many orders of magnitude than is the tritium content of iron meteorites in space, which results from bombardement by cosmic rays. This is true because the kinetics of gas loss from a metal change with concentration and temperature, especially the kinetics of hydrogen loss from meteoritic iron, where the amounts of cosmic rayproduced tritium are sufficiently small to be trapped completely by chemisorption of nickel. Estimates based on diffusion data for hydrogen in the laboratory lead to much higher rates of hydrogen loss than can be expected for cosmic ray-produced tritium in meteorites.In this connection, however, the fact has to be considered that meteoritic iron in space may not only contain hydrogen isotopes derived from cosmic ray-induced spallation processes, but also derived from solar wind bombardement. The steady-state hydrogen content of an iron meteorite, resulting from such bombardement in outer space, depends, of course, on the size and the structure of the meteoritic body. In general, the body will have to be assumed to possess a grain structure and this complicates the situation considerably. In any case, it can be shown that the steady-state hydrogen content is much higher than the tritium content and this makes it possible to use laboratory diffusion data in a calculation of the diffusion losses of tritium. By using the laboratory data of Festag, Fechtig and Schultes, it can be shown that cosmogenic tritium will be lost almost completely whenever the temperature is close to 0°C, or higher. Only meteorites consisting of grains of a size exceeding several millimeters retain tritium at such temperatures.

Comparison in Rabbits of Chole-Scintigraphic Properties of Several 99mTc-IDA Derivatives

1986 ◽  
Vol 25 (05) ◽  
pp. 188-193 ◽  
Author(s):  
J. Liniecki ◽  
K. Durski ◽  
Mikiciuk-Olasik Elzbieta ◽  
J. Kapuscinski
Keyword(s):  
Transit Time ◽  
Plasma Clearance ◽  
Mean Transit Time ◽  
Optimal Parameters ◽  
Time Activity ◽  
Time Activity Curve ◽  
Urinary Elimination ◽  
Activity Curve ◽  
Kinetics Of ◽  
Peak Value

Pathways and kinetics of excretion were compared to four 99mTc-IDA derivatives in healthy rabbits of both sexes. Assessment of differences between the compounds was based upon: plasma clearance, characteristics of time-activity curves measured scintigraphically over the liver (time of the peak Tmax; time for decline of activity to half the peak value - T50%), and hepatocytic mean transit time (MTT) as derived after deconvolution of the hepatic time-activity curve. Hepatocyte transit time was short and similar to 99mTc-complexes of Mebrofenin, 2,4-diethyl IDA (HEPIDA) and 3-iodo-2,6- diethylphenylcarbamoylmethyliminodiacetic acid (JODIDA); it was evidently longer for 99mTc-p-butyl-IDA (BIDA). 99mTc-HEPIDA displayed significant urinary elimination; the remaining three compounds were excreted practically completely via the biliary route. It is concluded that optimal parameters were displayed by 99mTc-Mebrofenin and 99mTc-JODIDA.

Kinetics of l-[1-13C]leucine when ingested with free amino acids, unlabeled or intrinsically labeled casein

2000 ◽  
Vol 278 (6) ◽  
pp. E1000-E1009 ◽  
Author(s):  
Cornelia C. Metges ◽  
Antoine E. El-Khoury ◽  
Ambalini B. Selvaraj ◽  
Rita H. Tsay ◽  
Alan Atkinson ◽  
...  
Keyword(s):  
Amino Acids ◽  
Free Amino Acids ◽  
Free Amino ◽  
The Body ◽  
Metabolic Fate ◽  
Fed State ◽  
Amino Acid Requirements ◽  
Balance Technique ◽  
Condition C ◽  
Kinetics Of

In two groups of five adults, each adapted to two different dietary regimens for 6 days, the metabolic fate of dietary [1-13C]leucine was examined when ingested either together with a mixture of free amino acids simulating casein (extrinsically labeled; condition A), along with the intact casein (extrinsically labeled; condition B), or bound to casein (intrinsically labeled; condition C). Fed state leucine oxidation (Ox), nonoxidative leucine disposal (NOLD), protein breakdown, and splanchnic uptake have been compared using an 8-h oral [1-13C]leucine and intravenous [2H3]leucine tracer protocol while giving eight equal hourly mixed meals. Lower leucine Ox, increased NOLD, and net protein synthesis were found with condition Ccompared with condition A (19.3 vs. 24.9; 77 vs. 55.8; 18.9 vs. 12.3 μmol ⋅ kg−1 ⋅ 30 min−1; P < 0.05). Ox and NOLD did not differ between conditions B and C. Splanchnic leucine uptake calculated from [1-13C]- and [2H3]leucine plasma enrichments was between 24 and 35%. These findings indicate that the form in which leucine is consumed affects its immediate metabolic fate and retention by the body; the implications of these findings for the tracer balance technique and estimation of amino acid requirements are discussed.

scholarly journals Kinetic analysis of the internalization and recycling of [3H]TRH and C-terminal truncations of the long isoform of the rat thyrotropin-releasing hormone receptor-1

2000 ◽  
Vol 346 (3) ◽  
pp. 711-718 ◽  
Author(s):  
Tomas DRMOTA ◽  
Graeme MILLIGAN
Keyword(s):  
Amino Acids ◽  
Steady State ◽  
Thyrotropin Releasing Hormone ◽  
Peptide Ligands ◽  
Full Length ◽  
Hek 293 ◽  
Releasing Hormone ◽  
293 Cells ◽  
Kinetics Of ◽  
Trh Receptor

The C-terminal tail of the long splice variant of the rat thyrotropin-releasing hormone (TRH) receptor-1 (TRHR-1L) comprises around 93 amino acids. A series of C-terminal truncations was constructed and expressed transiently in HEK-293 cells. The extent of steady-state internalization of these in response to [3H]TRH was dependent upon the degree of truncation. Little effect was produced by deletion of the C-terminal to 50 amino acids, although there was a substantial decrease in the extent of internalization by deletion to 45-46 amino acids. The rate of internalization of TRHR-1L in response to ligand was substantially decreased by the acid-wash procedures often used in the analysis of cellular distribution of receptors with peptide ligands, and thus an alternative procedure using a Mes-containing buffer was employed in the present study. Apart from a truncation anticipated to eliminate post-translational acylation of the re-ceptor, which altered both the association and dissociation rates of [3H]TRH, the kinetics of ligand binding were unaffected by C-terminal truncation. Equally, the rate of recycling to the plasma membrane of internalized receptors was unaffected by C-terminal truncation. Although the extent of internalization of the full-length receptor was impaired by pre-exposure of cells to TRH, this was not true of C-terminal truncation mutants, which displayed limited steady-state internalization ratios. A mutant with a substantial C-terminal deletion also displayed decreased functional desensitization compared with the full-length receptor.

Evaluation of role of G-CSF in the production, survival, and release of neutrophils from bone marrow into circulation

Blood ◽  
2002 ◽  
Vol 100 (3) ◽  
pp. 854-861 ◽  
Author(s):  
Sunanda Basu ◽  
George Hodgson ◽  
Melissa Katz ◽  
Ashley R. Dunn
Keyword(s):  
Bone Marrow ◽  
Steady State ◽  
Transit Time ◽  
Bone Marrow Cells ◽  
Mean Transit Time ◽  
Wild Type ◽  
Blast Cells ◽  
And Control ◽  
Deficient Mice

Abstract In steady-state hematopoiesis, G-CSF (granulocyte-colony stimulating factor) regulates the level of neutrophils in the bone marrow and blood. In this study, we have exploited the availability of G-CSF–deficient mice to evaluate the role of G-CSF in steady-state granulopoiesis and the release of granulocytes from marrow into circulation. The thymidine analogue bromodeoxyuridine (BrdU) was used to label dividing bone marrow cells, allowing us to follow the release of granulocytes into circulation. Interestingly, the labeling index and the amount of BrdU incorporated by blast cells in bone marrow was greater in G-CSF–deficient mice than in wild-type mice. In blood, 2 different populations of BrdU-positive granulocytes, BrdUbright and BrdUdim, could be detected. The kinetics of release of the BrdUbright granulocytes from bone marrow into blood was similar in wild-type and G-CSF–deficient mice; however, BrdUdim granulocytes peaked earlier in G-CSF–deficient mice. Our findings suggest that the mean transit time of granulocytes through the postmitotic pool is similar in G-CSF–deficient and control mice, although the transit time through the mitotic pool is reduced in G-CSF–deficient mice. Moreover, the reduced numbers of granulocytes that characterize G-CSF–deficient mice is primarily due to increased apoptosis in cells within the granulocytic lineage. Collectively, our data suggest that at steady state, G-CSF is critical for the survival of granulocytic cells; however, it is dispensable for trafficking of granulocytes from bone marrow into circulation.

scholarly journals A model for measurement of lactate disappearance with isotopic tracers in the steady state

1988 ◽  
Vol 256 (3) ◽  
pp. 1035-1038 ◽  
Author(s):  
W C Stanley ◽  
S L Lehman
Keyword(s):  
Steady State ◽  
Infusion Rate ◽  
Specific Radioactivity ◽  
Compartment Model ◽  
The Body ◽  
Total Carbon ◽  
Isotopic Tracers ◽  
Arterial Lactate ◽  
Lactate And Pyruvate ◽  
Almost All

1. The irreversible disappearance of lactate carbon from the body (RdL) is commonly calculated from data obtained with a continuous infusion of isotopically labelled lactate tracer. The tracer infusion rate divided by the steady-state lactate specific radioactivity in blood is taken to give the rate of lactate disappearance. 2. Measurement of lactate disappearance is complicated by the fact that it is reversibly converted into pyruvate as well as being irreversibly removed from the system. 3. We analysed a four-compartment model of lactate metabolism, representing blood lactate, tissue lactate and pyruvate carbon pools. 4. The standard method of calculating RdL from the lactate tracer infusion rate divided by the specific radioactivity of lactate was not validated. 5. We found that RdL can be calculated from the infusion rate and the pyruvate specific radioactivity, multiplied by the fraction of the total carbon flow out of pyruvate that goes to lactate. 6. Therefore, if almost all of the pyruvate carbon flows back to lactate, then RdL approaches the tracer infusion rate divided by the pyruvate specific radioactivity. On the other hand, if the rate of oxidation is large in relation to the rate of pyruvate conversion into lactate, than RdL is overestimated when calculated from the pyruvate specific radioactivity. 7. Calculation of RdL with the arterial lactate specific radioactivity results in an underestimate of the true RdL.

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