5 results
Adaptation of in vivo amino acid kinetics facilitates increased amino acid availability for fetal growth in adolescent and adult pregnancies alike
- Minerva M. Thame, Jean W. Hsu, Raquel Gibson, Tameka M. Baker, Grace J. Tang, Asha V. Badaloo, Horace M. Fletcher, Alan A. Jackson, Farook Jahoor
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- Journal:
- British Journal of Nutrition / Volume 112 / Issue 11 / 14 December 2014
- Published online by Cambridge University Press:
- 17 October 2014, pp. 1779-1786
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- 14 December 2014
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During pregnancy, adult women with a normal BMI synthesise extra amino acids after an overnight fast by increasing body protein breakdown and decreasing amino acid oxidation. It is not known whether adolescent girls can make these adaptations during pregnancy. The present study aimed to measure and compare the protein, glutamine and alanine kinetics of adult women and adolescent girls at early-, mid- and late-pregnancy. Kinetics were measured in the overnight fasted state using intravenous infusions of 13C-leucine, 15N-glutamine and 15N-alanine in ten adults and twenty adolescents aged 14–17 years in the first and second trimesters (phase 1 study) and infusions of 13C-leucine and 15N2-urea in ten adults and eleven adolescents aged 16–17 years in the first and third trimesters (phase 2 study). In phase 1 study, there were no significant differences between the groups with regard to any of the kinetic parameters measured. In both groups, leucine flux increased (P< 0·05), the percentage of leucine flux oxidised decreased (P< 0·05) and non-oxidative leucine disposal to protein synthesis increased (P< 0·05) from the first to the second trimester. In phase2 study, leucine flux was significantly slower (P< 0·05) in the adult group than in the adolescent group during both trimesters, and whole-body leucine flux and non-oxidative leucine disposal increased significantly in the adolescent group (P< 0·05, respectively) and were higher in the adult group from the first to the third trimester. These results suggest that similar to their adult counterparts after an overnight fast, adolescent girls with a normal BMI provide extra amino acids required for net protein deposition during pregnancy by increasing protein breakdown and decreasing amino acid oxidation.
Tyrosine requirement during the rapid catch-up growth phase of recovery from severe childhood undernutrition
- Asha Badaloo, Jean W.-C. Hsu, Carolyn Taylor-Bryan, Marvin Reid, Terrence Forrester, Farook Jahoor
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- Journal:
- British Journal of Nutrition / Volume 104 / Issue 8 / 28 October 2010
- Published online by Cambridge University Press:
- 16 June 2010, pp. 1174-1180
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- 28 October 2010
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The requirement for aromatic amino acids during the rapid catch-up in weight phase of recovery from severe childhood undernutrition (SCU) is not clearly established. As a first step, the present study aimed to estimate the tyrosine requirement of children with SCU during the catch-up growth phase of nutritional rehabilitation using a diet enriched in energy and proteins. Tyrosine requirement was calculated from the rate of excretion of 13CO2 (F 13CO2) during [13C]phenylalanine infusion in thirteen children with SCU, five females and eight males, at about 19 d after admission when the subjects were considered to have entered their rapid catch-up growth phase and were consuming 627·3 kJ and about 3·5 g protein/kg per d. Measurements of F 13CO2 during [13C]phenylalanine infusion were made on two separate days with a 1 d interval. Three measurements at tyrosine intakes of 48, 71 and 95 mg/kg per d were performed on experimental day 1 and measurements at tyrosine intakes of 148, 195 and 241 mg/kg per d were performed on experimental day 2. An estimate of the mean requirement was derived by breakpoint analysis with a two-phase linear regression cross-over model. The breakpoint, which represents an estimate of the mean tyrosine requirement, is a value of 99 mg/kg per d when the children were growing at about 15 g/kg per d. The result indicates that the mean requirement for tyrosine during the catch-up growth phase of SCU is about 99 mg/kg per d under similar conditions to the present study.
Glutathione S-transferase polymorphisms may be associated with risk of oedematous severe childhood malnutrition
- Kwesi G Marshall, Sharon Howell, Marvin Reid, Asha Badaloo, Martin Farrall, Terrence Forrester, Colin A. McKenzie
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- Journal:
- British Journal of Nutrition / Volume 96 / Issue 2 / August 2006
- Published online by Cambridge University Press:
- 08 March 2007, pp. 243-248
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- August 2006
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It has been estimated that more than 50% of deaths before the age of 5 years have undernutrition as an underlying cause. Severe childhood malnutrition, an extreme form of undernutrition, occurs as oedematous and non-oedematous syndromes. The reasons why only some children develop oedematous severe childhood malnutrition (OSCM) have remained elusive, but the heterogeneity of clinical appearances among children from relatively homogeneous backgrounds suggests that interindividual variation in susceptibility to OSCM may exist. We investigated variants of four glutathione S-transferase (GST) genes in a retrospective study among subjects (n136) previously admitted to the Tropical Metabolism Research Unit, Jamaica, for the treatment of either OSCM (cases) or non-oedematous severe childhood malnutrition (controls). We found that GSTP1 Val105 homozygotes were significantly more common among the cases (odds ratio (OR) 3·5; 95% CI 1·1, 10·8). We also found an association of borderline significance between non-deletion GSTT1 genotypes (i.e. +/+ or +/0) and OSCM (OR 2·4; 95% CI 1·0, 5·9). There was no significant association between OSCM and any of the other GST variants. These preliminary findings suggest that genetic variation within the GST superfamily may contribute to the risk of OSCM. Additional, larger data sets and studies of variants in other candidate genes are required in order to properly assess the true contribution, if any, of genetic variation to risk of OSCM. Such studies may improve our understanding of the causes of clinical heterogeneity in malnutrition.
The transfer of 15N from urea to lysine in the human infant
- D. Joe Millward, Terrance Forrester, Eric Ah-Sing, Nana Yeboah, Neil Gibson, Asha Badaloo, M. Boyne, M. Reade, C. Persaud, Alan Jackson
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- Journal:
- British Journal of Nutrition / Volume 83 / Issue 5 / May 2000
- Published online by Cambridge University Press:
- 09 March 2007, pp. 505-512
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- May 2000
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To explore the nutritional significance of urea hydrolysis for human subjects, male infants being treated for severe undernutrition were given oral doses of 10 mg [15N15N]urea every 3 h for 36 h, on admission, during rapid growth and after repletion with either moderate or generous intakes of protein. Urea hydrolysis was calculated from the 15N enrichment of urinary urea, and where possible, lysine, alanine, glycine and histidine were isolated from urine by preparative ion-exchange chromatography for measurement of 15N enrichment. Sufficient N was obtained for 15N enrichment of lysine to be measured on fifteen occasions from six children. Urea hydrolysis accounted for half of all urea production with 130 (sd 85) mg N/kg hydrolysed per d, most of which appeared to be utilized in synthetic pathways. Of the samples analysed successfully, nine samples of lysine were enriched with 15N (mean atom percent excess 0·0102, range 0·0017–0·0208) with relative enrichment ratios with respect to lysine of 1·63 (range 0·18–3·15), 1·96 (range 0·7–3·73) and 0·9 (range 0·4–1·8) for glycine, alanine and histidine respectively. Enriched samples were identified at each treatment phase and 68 % of the variation in lysine enrichment was explained by the variation in urea enrichment with 54 % explained by the overall rate of delivery of 15N to the lower gastrointestinal tract. The results indicate a minimum of 4·7 mg lysine per kg body weight made available by de novo synthesis with the more likely value an order of magnitude higher. Thus, urea hydrolysis can improve the quality of the dietary protein supply by enabling an increased supply of lysine and other indispensable amino acids.To explore the nutritional significance of urea hydrolysis for human subjects, male infants being treated for severe undernutrition were given oral doses of 10 mg [15N15N]urea every 3 h for 36 h, on admission, during rapid growth and after repletion with either moderate or generous intakes of protein. Urea hydrolysis was calculated from the 15N enrichment of urinary urea, and where possible, lysine, alanine, glycine and histidine were isolated from urine by preparative ion-exchange chromatography for measurement of 15N enrichment. Sufficient N was obtained for 15N enrichment of lysine to be measured on fifteen occasions from six children. Urea hydrolysis accounted for half of all urea production with 130 (sd 85) mg N/kg hydrolysed per d, most of which appeared to be utilized in synthetic pathways. Of the samples analysed successfully, nine samples of lysine were enriched with 15N (mean atom percent excess 0·0102, range 0·0017–0·0208) with relative enrichment ratios with respect to lysine of 1·63 (range 0·18–3·15), 1·96 (range 0·7–3·73) and 0·9 (range 0·4–1·8) for glycine, alanine and histidine respectively. Enriched samples were identified at each treatment phase and 68 % of the variation in lysine enrichment was explained by the variation in urea enrichment with 54 % explained by the overall rate of delivery of 15N to the lower gastrointestinal tract. The results indicate a minimum of 4·7 mg lysine per kg body weight made available by de novo synthesis with the more likely value an order of magnitude higher. Thus, urea hydrolysis can improve the quality of the dietary protein supply by enabling an increased supply of lysine and other indispensable amino acids.To explore the nutritional significance of urea hydrolysis for human subjects, male infants being treated for severe undernutrition were given oral doses of 10 mg [15N15N]urea every 3 h for 36 h, on admission, during rapid growth and after repletion with either moderate or generous intakes of protein. Urea hydrolysis was calculated from the 15N enrichment of urinary urea, and where possible, lysine, alanine, glycine and histidine were isolated from urine by preparative ion-exchange chromatography for measurement of 15N enrichment. Sufficient N was obtained for 15N enrichment of lysine to be measured on fifteen occasions from six children. Urea hydrolysis accounted for half of all urea production with 130 (sd 85) mg N/kg hydrolysed per d, most of which appeared to be utilized in synthetic pathways. Of the samples analysed successfully, nine samples of lysine were enriched with 15N (mean atom percent excess 0·0102, range 0·0017–0·0208) with relative enrichment ratios with respect to lysine of 1·63 (range 0·18–3·15), 1·96 (range 0·7–3·73) and 0·9 (range 0·4–1·8) for glycine, alanine and histidine respectively. Enriched samples were identified at each treatment phase and 68 % of the variation in lysine enrichment was explained by the variation in urea enrichment with 54 % explained by the overall rate of delivery of 15N to the lower gastrointestinal tract. The results indicate a minimum of 4·7 mg lysine per kg body weight made available by de novo synthesis with the more likely value an order of magnitude higher. Thus, urea hydrolysis can improve the quality of the dietary protein supply by enabling an increased supply of lysine and other indispensable amino acids.To explore the nutritional significance of urea hydrolysis for human subjects, male infants being treated for severe undernutrition were given oral doses of 10 mg [15N15N]urea every 3 h for 36 h, on admission, during rapid growth and after repletion with either moderate or generous intakes of protein. Urea hydrolysis was calculated from the 15N enrichment of urinary urea, and where possible, lysine, alanine, glycine and histidine were isolated from urine by preparative ion-exchange chromatography for measurement of 15N enrichment. Sufficient N was obtained for 15N enrichment of lysine to be measured on fifteen occasions from six children. Urea hydrolysis accounted for half of all urea production with 130 (sd 85) mg N/kg hydrolysed per d, most of which appeared to be utilized in synthetic pathways. Of the samples analysed successfully, nine samples of lysine were enriched with 15N (mean atom percent excess 0·0102, range 0·0017–0·0208) with relative enrichment ratios with respect to lysine of 1·63 (range 0·18–3·15), 1·96 (range 0·7–3·73) and 0·9 (range 0·4–1·8) for glycine, alanine and histidine respectively. Enriched samples were identified at each treatment phase and 68 % of the variation in lysine enrichment was explained by the variation in urea enrichment with 54 % explained by the overall rate of delivery of 15N to the lower gastrointestinal tract. The results indicate a minimum of 4·7 mg lysine per kg body weight made available by de novo synthesis with the more likely value an order of magnitude higher. Thus, urea hydrolysis can improve the quality of the dietary protein supply by enabling an increased supply of lysine and other indispensable amino acids.
Comparison of urinary 5-L-oxoproline (L-pyroglutamate) during normal pregnancy in women in England and Jamaica
- Alan A Jackson, Chandarika Persaud, Geoff Werkmeister, Irene S. M McClelland, Asha Badaloo, Terrence Forrester
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- Journal:
- British Journal of Nutrition / Volume 77 / Issue 2 / February 1997
- Published online by Cambridge University Press:
- 09 March 2007, pp. 183-196
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- February 1997
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Urinary 5-L-oxoproline was measured during normal pregnancies in Southampton, England and Kingston, Jamaica. The CV of 5-L-oxoproline excretion in urine, determined over 7 d in a non-pregnant woman and three pregnant women, was 10–36%. Compared with non-pregnant women, urinary 5-L-oxoproline increased three to four times from early pregnancy in women in Southampton, a highly significant difference, and remained elevated at similar levels during mid and late pregnancy. For women in Kingston, the excretion of 5-L-oxoproline was similar to that of Southampton women in the non-pregnant group and during early pregnancy. However, there was a progressive increase in the excretion of 5-L-oxoproline as pregnancy advanced and by late pregnancy excretion was from three to ten times greater than the average for the non-pregnant women. There was a significant difference between the women in Southampton and the women in Kingston during mid and late pregnancy, with women in Kingston excreting twice as much 5-L-oxoproline during late pregnancy. If the excretion of 5-L-oxoproline is a measure of glycine insdciency, the results would indicate that in some pregnancies the ability of the mother to provide glycine for herself and the developing fetus is marginal or inadequate and the constraint appears more marked in Jamaica than in England.