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3 Methylhistidine

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James G. Morris – One of the best experts on this subject based on the ideXlab platform.

  • Quantitative excretion of 3Methylhistidine in urine of cats as a measure of in vivo skeletal muscle protein catabolism
    The Journal of Nutritional Biochemistry, 1996
    Co-Authors: Stanley L. Marks, Quinton R. Rogers, James G. Morris
    Abstract:

    Abstract The purpose of this study was to evaluate the use of urinary 3Methylhistidine excretion as an index of in vivo skeletal muscle protein degradation in cats. The criterion for validation was the rapid and quantitative excretion of an intravenously administered dose of radiolabeled 3Methylhistidine (3-methyl-14C). Four adult cats were maintained in individual metabolism cages and allowed free access to a purified diet (43.5% protein) and water for 4 weeks. The cats were then injected intravenously with 740 kBq 3-[14C]Methylhistidine dihydrochloride diluted in 1 mL of saline. Twenty-four-hour urine samples were collected for 7 days. Total radioactivity in each urine sample was determined by direct counting. Quench correction was determined by using an external standard. The mean (±SEM) cumulative urinary recovery of 3-[14C]Methylhistidine from the four cats was 94.9 ±3.5% at 48 hr following radioisotope injection. The mean (±SEM) cumulative urinary recovery of radioactivity from the four cats was 103.9 ± 2.2% at 7 days following radioisotope administration. There was no detectable radioactivity found in expired CO2 and negligible amounts (mean ± SEM: 0.6 ± 0.5%) in the feces. Chromatography of urinary amino acids and radioactive urine metabolites revealed no significant radioactivity in any other peak besides 3Methylhistidine. Acid hydrolysis of urine resulted in no increase in 3Methylhistidine content or urine, indicating that there is no significant acetylation of 3Methylhistidine in this species. On the basis of these results, 3Methylhistidine does not appear to be metabolized and should therefore be a valid index of in vivo skeletal muscle protein degradation in the cat. Urinary 3Methylhistidine excretion should be useful for studying how nutritional, hormonal, and other physiological or pathological factors cause losses or gains in skeletal muscle protein in this species.

Stanley L. Marks – One of the best experts on this subject based on the ideXlab platform.

  • Quantitative excretion of 3Methylhistidine in urine of cats as a measure of in vivo skeletal muscle protein catabolism
    The Journal of Nutritional Biochemistry, 1996
    Co-Authors: Stanley L. Marks, Quinton R. Rogers, James G. Morris
    Abstract:

    Abstract The purpose of this study was to evaluate the use of urinary 3Methylhistidine excretion as an index of in vivo skeletal muscle protein degradation in cats. The criterion for validation was the rapid and quantitative excretion of an intravenously administered dose of radiolabeled 3Methylhistidine (3-methyl-14C). Four adult cats were maintained in individual metabolism cages and allowed free access to a purified diet (43.5% protein) and water for 4 weeks. The cats were then injected intravenously with 740 kBq 3-[14C]Methylhistidine dihydrochloride diluted in 1 mL of saline. Twenty-four-hour urine samples were collected for 7 days. Total radioactivity in each urine sample was determined by direct counting. Quench correction was determined by using an external standard. The mean (±SEM) cumulative urinary recovery of 3-[14C]Methylhistidine from the four cats was 94.9 ±3.5% at 48 hr following radioisotope injection. The mean (±SEM) cumulative urinary recovery of radioactivity from the four cats was 103.9 ± 2.2% at 7 days following radioisotope administration. There was no detectable radioactivity found in expired CO2 and negligible amounts (mean ± SEM: 0.6 ± 0.5%) in the feces. Chromatography of urinary amino acids and radioactive urine metabolites revealed no significant radioactivity in any other peak besides 3Methylhistidine. Acid hydrolysis of urine resulted in no increase in 3Methylhistidine content or urine, indicating that there is no significant acetylation of 3Methylhistidine in this species. On the basis of these results, 3Methylhistidine does not appear to be metabolized and should therefore be a valid index of in vivo skeletal muscle protein degradation in the cat. Urinary 3Methylhistidine excretion should be useful for studying how nutritional, hormonal, and other physiological or pathological factors cause losses or gains in skeletal muscle protein in this species.

S L Nissen – One of the best experts on this subject based on the ideXlab platform.

  • Estimation of 3Methylhistidine production in pigs by compartmental analysis.
    Journal of animal science, 1996
    Co-Authors: John A. Rathmacher, S L Nissen, R E Paxton, D B Anderson
    Abstract:

    Direct in vivo methodology is not available to accurately evaluate muscle turnover in pigs. Urinary 3Methylhistidine (3MH) excretion, which is used as an in vivo marker of muscle protein breakdown in humans and cattle, is not a valid indicator for pigs. The present study proposes that data from a single bolus dose of 3-[methyl- 2 H 3 ]Methylhistidine tracer can mathematically describe 3MH metabolism in pigs. Plasma concentration of the tracer is described by a linear time-invariant three-compartment model by using the SAAM/CONSAM computer modeling program. The model defines masses and fluxes of 3MH within the pigs and, in particular, the intracellular de novo production of 3MH, which should reflect muscle proteolysis. The de novo production of 3MH as calculated by the model was 621 μmol/d, corresponding to a fractional breakdown rate of 2.28 %/d, which is similar to values reported by using indirect methodology. These data also suggest that certain model compartments may be indicators of body muscle mass (mass of compartment 3, r =.59, P =.006). The mathematical model developed does not depend on urine collections and can be used to assess changes in muscle proteolysis in vivo.

  • A compartmental model of 3Methylhistidine metabolism in humans
    American Journal of Physiology-Endocrinology and Metabolism, 1995
    Co-Authors: John A. Rathmacher, Paul J. Flakoll, S L Nissen
    Abstract:

    Urinary 3Methylhistidine (3MH) excretion has been proposed as a noninvasive in vivo marker of muscle protein breakdown, but such analysis requires quantitative collection of urine and yields few details about the metabolism of 3MH. In this study, we propose that data from a single bolus dose of tracer and serial blood samples over 72 h can be described by a kinetic model that defines 3MH metabolism in humans. Plasma concentration of the tracer was described by a linear time-invariant three-compartment model. The model defines masses and fluxes of 3MH within the subjects and, in particular, the intracellular de novo production of 3MH. The de novo production of 3MH as calculated by the model was not different from that calculated via the traditional collection of urinary 3MH (3.09 vs 2.57 mumol.kg-1.day-1, respectively; P > 0.30). These data indicate that 3MH production can be measured by a compartmental model that can be used to measure muscle proteolysis without quantitative urine collections.

  • measurement of 3 Methylhistidine production in lambs by using compartmental kinetic analysis
    British Journal of Nutrition, 1993
    Co-Authors: John A. Rathmacher, G Link, S L Nissen
    Abstract:

    The kinetics of 3Methylhistidine (3MH) metabolism in four crossbred lambs were studied. Each lamb was injected with an intravenous dose of 3-[ 2 H 3 ]Methylhistidine (d 33MH) and the stable isotisotope disappearance in plasma and appearance in both urine and muscle were measured. Immediately after the administration of tracer there was a phase of rapid disappearance of tracer from the plasma, which was followed by a more gradual decrease in d 33MH from the plasma during the last 4 d of the experiment. A minimum of three exponentials was required to describe the plasma decay curve adequately. The kinetic model of 3MH in the whole animal was constructed by using the SAAM/CONSAM computer modelling program. Two different configurations of a three-compartment model are described: (1) a simple three-pool model, in which plasma kinetics were entered into pool 1 out of which they had one undefinable exit; (2) a plasma-urinary three-pool model with two exits, in which the urinary kinetics were entered as an exit out of pool 1 and required a second exit out of pool 3 to produce an adequate fit. In addition, muscle kinetics from biopsies of the longissirnus dorsi were entered into either pool 2 or 3 using the plasma-urinary model. Steady-state mass and transport rate values were obtained for each model construct described, and a de novo production rate corresponding to a fractional breakdown rate of myofibrillar protein of approximately 5%/d was also calculated. The model predicted that only 15% of 3MH was excreted in urine as free 3MH, which is consistent with current knowledge of 3MH excretion in sheep. The simple three-pool plasma kinetic model, therefore, could be used to estimate, by a relatively simple injection-sampling technique, the extent of muscle protein turnover in lambs.

A. Ferro-luzzi – One of the best experts on this subject based on the ideXlab platform.

Quinton R. Rogers – One of the best experts on this subject based on the ideXlab platform.

  • Quantitative excretion of 3Methylhistidine in urine of cats as a measure of in vivo skeletal muscle protein catabolism
    The Journal of Nutritional Biochemistry, 1996
    Co-Authors: Stanley L. Marks, Quinton R. Rogers, James G. Morris
    Abstract:

    Abstract The purpose of this study was to evaluate the use of urinary 3Methylhistidine excretion as an index of in vivo skeletal muscle protein degradation in cats. The criterion for validation was the rapid and quantitative excretion of an intravenously administered dose of radiolabeled 3Methylhistidine (3-methyl-14C). Four adult cats were maintained in individual metabolism cages and allowed free access to a purified diet (43.5% protein) and water for 4 weeks. The cats were then injected intravenously with 740 kBq 3-[14C]Methylhistidine dihydrochloride diluted in 1 mL of saline. Twenty-four-hour urine samples were collected for 7 days. Total radioactivity in each urine sample was determined by direct counting. Quench correction was determined by using an external standard. The mean (±SEM) cumulative urinary recovery of 3-[14C]Methylhistidine from the four cats was 94.9 ±3.5% at 48 hr following radioisotope injection. The mean (±SEM) cumulative urinary recovery of radioactivity from the four cats was 103.9 ± 2.2% at 7 days following radioisotope administration. There was no detectable radioactivity found in expired CO2 and negligible amounts (mean ± SEM: 0.6 ± 0.5%) in the feces. Chromatography of urinary amino acids and radioactive urine metabolites revealed no significant radioactivity in any other peak besides 3Methylhistidine. Acid hydrolysis of urine resulted in no increase in 3Methylhistidine content or urine, indicating that there is no significant acetylation of 3Methylhistidine in this species. On the basis of these results, 3Methylhistidine does not appear to be metabolized and should therefore be a valid index of in vivo skeletal muscle protein degradation in the cat. Urinary 3Methylhistidine excretion should be useful for studying how nutritional, hormonal, and other physiological or pathological factors cause losses or gains in skeletal muscle protein in this species.