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Isabel M Carreira - One of the best experts on this subject based on the ideXlab platform.
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metabolic biomarkers of prenatal disorders an exploratory nmr metabonomics study of second trimester maternal urine and blood plasma
Journal of Proteome Research, 2011Co-Authors: Silvia O Diaz, Joana Pinto, Goncalo Graca, Iola F Duarte, Antonio S Barros, Eulalia Galhano, Cristina Pita, Maria Do Ceu Almeida, Brian J Goodfellow, Isabel M CarreiraAbstract:This work describes an exploratory NMR metabonomic study of second trimester maternal urine and plasma, in an attempt to characterize the metabolic changes underlying prenatal disorders and identify possible early biomarkers. Fetal malformations have the strongest metabolic impact in both biofluids, suggesting effects due to hypoxia (leading to hypoxanthine increased excretion) and a need for enhanced gluconeogenesis, with higher ketone bodies (acetone and 3-hydroxybutyric acid) production and TCA cycle demand (suggested by Glucogenic Amino Acids and cis-aconitate overproduction). Choline and nucleotide metabolisms also seem affected and a distinct plasma lipids profile is observed for mothers with fetuses affected by central nervous system malformations. Urine from women who subsequently develop gestational diabetes mellitus exhibits higher 3-hydroxyisovalerate and 2-hydroxyisobutyrate levels, probably due to altered biotin status and Amino acid and/or gut metabolisms (the latter possibly related to high...
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metabolic biomarkers of prenatal disorders an exploratory nmr metabonomics study of second trimester maternal urine and blood plasma
Journal of Proteome Research, 2011Co-Authors: Silvia O Diaz, Joana Pinto, Goncalo Graca, Iola F Duarte, Antonio S Barros, Eulalia Galhano, Cristina Pita, Maria Do Ceu Almeida, Brian J Goodfellow, Isabel M CarreiraAbstract:This work describes an exploratory NMR metabonomic study of second trimester maternal urine and plasma, in an attempt to characterize the metabolic changes underlying prenatal disorders and identify possible early biomarkers. Fetal malformations have the strongest metabolic impact in both biofluids, suggesting effects due to hypoxia (leading to hypoxanthine increased excretion) and a need for enhanced gluconeogenesis, with higher ketone bodies (acetone and 3-hydroxybutyric acid) production and TCA cycle demand (suggested by Glucogenic Amino Acids and cis-aconitate overproduction). Choline and nucleotide metabolisms also seem affected and a distinct plasma lipids profile is observed for mothers with fetuses affected by central nervous system malformations. Urine from women who subsequently develop gestational diabetes mellitus exhibits higher 3-hydroxyisovalerate and 2-hydroxyisobutyrate levels, probably due to altered biotin status and Amino acid and/or gut metabolisms (the latter possibly related to higher BMI values). Other urinary changes suggest choline and nucleotide metabolic alterations, whereas lower plasma betaine and TMAO levels are found. Chromosomal disorders and pre-preterm delivery groups show urinary changes in choline and, in the latter case, in 2-hydroxyisobutyrate. These results show that NMR metabonomics of maternal biofluids enables the noninvasive detection of metabolic changes associated to prenatal disorders, thus unveiling potential disorder biomarkers.
Sreekumaran K Nair - One of the best experts on this subject based on the ideXlab platform.
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erratum hyperglucagonemia mitigates the effect of metformin on glucose production in prediabetes cell reports 2016 15 7 1394 1400 s2211124716304375 10 1016 j celrep 2016 04 024
Cell Reports, 2018Co-Authors: Adam R Konopka, Raul Ruiz Esponda, Matthew M Robinson, Matthew L Johnson, Rickey E Carter, Michele Schiavon, Claudio Cobelli, Fredric E Wondisford, Ian R Lanza, Sreekumaran K NairAbstract:(Cell Reports 15, 1394–1400; May 17, 2016) In the originally published version of this article, the labels “Placebo” and “Metformin” were mistakenly switched in Table S2, which displayed plasma concentrations of Amino Acids. We have corrected this error as well as the following additional errors, which we would like to bring to the attention of the readers: 1. The third bullet point within the Highlights now reads “…metformin increases Glucogenic Amino Acids …” rather than “… metformin decreases Glucogenic Amino Acids …”2. The last sentence of the In Brief blurb now reads “… increased glucagon and Glucogenic precursors” rather than “increased glucagon and decreased Glucogenic precursors” (the word “decreased” was removed).3. In paragraph 6, line 21 of page 1396, the text now reads “.. including decreased metabolites of the urea pathway …” rather than “including elevated metabolites of the urea pathway”4. In paragraph 6, line 26 of page 1396, the text now reads “.. revealed an increase in Glucogenic AAs” rather than “.. revealed a decline in Glucogenic AAs”Although Amino acid metabolites are not the primary outcome of the work described in this paper and these errors do not alter the main conclusions outlined therein, the authors regret the errors.
Silvia O Diaz - One of the best experts on this subject based on the ideXlab platform.
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metabolic biomarkers of prenatal disorders an exploratory nmr metabonomics study of second trimester maternal urine and blood plasma
Journal of Proteome Research, 2011Co-Authors: Silvia O Diaz, Joana Pinto, Goncalo Graca, Iola F Duarte, Antonio S Barros, Eulalia Galhano, Cristina Pita, Maria Do Ceu Almeida, Brian J Goodfellow, Isabel M CarreiraAbstract:This work describes an exploratory NMR metabonomic study of second trimester maternal urine and plasma, in an attempt to characterize the metabolic changes underlying prenatal disorders and identify possible early biomarkers. Fetal malformations have the strongest metabolic impact in both biofluids, suggesting effects due to hypoxia (leading to hypoxanthine increased excretion) and a need for enhanced gluconeogenesis, with higher ketone bodies (acetone and 3-hydroxybutyric acid) production and TCA cycle demand (suggested by Glucogenic Amino Acids and cis-aconitate overproduction). Choline and nucleotide metabolisms also seem affected and a distinct plasma lipids profile is observed for mothers with fetuses affected by central nervous system malformations. Urine from women who subsequently develop gestational diabetes mellitus exhibits higher 3-hydroxyisovalerate and 2-hydroxyisobutyrate levels, probably due to altered biotin status and Amino acid and/or gut metabolisms (the latter possibly related to high...
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metabolic biomarkers of prenatal disorders an exploratory nmr metabonomics study of second trimester maternal urine and blood plasma
Journal of Proteome Research, 2011Co-Authors: Silvia O Diaz, Joana Pinto, Goncalo Graca, Iola F Duarte, Antonio S Barros, Eulalia Galhano, Cristina Pita, Maria Do Ceu Almeida, Brian J Goodfellow, Isabel M CarreiraAbstract:This work describes an exploratory NMR metabonomic study of second trimester maternal urine and plasma, in an attempt to characterize the metabolic changes underlying prenatal disorders and identify possible early biomarkers. Fetal malformations have the strongest metabolic impact in both biofluids, suggesting effects due to hypoxia (leading to hypoxanthine increased excretion) and a need for enhanced gluconeogenesis, with higher ketone bodies (acetone and 3-hydroxybutyric acid) production and TCA cycle demand (suggested by Glucogenic Amino Acids and cis-aconitate overproduction). Choline and nucleotide metabolisms also seem affected and a distinct plasma lipids profile is observed for mothers with fetuses affected by central nervous system malformations. Urine from women who subsequently develop gestational diabetes mellitus exhibits higher 3-hydroxyisovalerate and 2-hydroxyisobutyrate levels, probably due to altered biotin status and Amino acid and/or gut metabolisms (the latter possibly related to higher BMI values). Other urinary changes suggest choline and nucleotide metabolic alterations, whereas lower plasma betaine and TMAO levels are found. Chromosomal disorders and pre-preterm delivery groups show urinary changes in choline and, in the latter case, in 2-hydroxyisobutyrate. These results show that NMR metabonomics of maternal biofluids enables the noninvasive detection of metabolic changes associated to prenatal disorders, thus unveiling potential disorder biomarkers.
Christian Demigne - One of the best experts on this subject based on the ideXlab platform.
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effect of dietary supplementation with glutamic acid or glutamine on the splanchnic and muscle metabolism of Glucogenic Amino Acids in the rat
Journal of Nutritional Biochemistry, 1993Co-Authors: Corinne Moundras, Daniel Bercovici, Christian Remesy, Christian DemigneAbstract:Abstract The aim of the present study was to examine the metabolic effects of a high availability of dietary glutamic acid or glutamine. A 15% casein diet was supplemented with 7.2% glutamic acid or glutamine. The present results show that both supplementations produced only a slight modification in the circulating concentrations of glutamate. Glutamic acid supplementation noticeably enhanced (+ 19%) the arterial concentrations of glutamine, but to a lesser extent than glutamine supplementation itself (+ 54%). Large amounts of alanine were released by the digestive tract in rats fed the various diets; this release was enhanced by glutamine (+ 33%) and, more markedly, by glutamic acid (+ 80%) supplementation. In the liver, glutamic acid and glutamine supplementation produced an increase in the catabolism of glycine, serine, and threonine that resulted in a drop of their peripheral concentrations, especially in muscles. The decrease in serine and threonine concentrations could be ascribed to the elevation of the serine(threnine)dehydratase activity (three fold), and the drop in glycine concentration seems to be connected to serine metabolism. It appears that the administration of glutamine (but not of glutamic acid) by the oral route could be effective in increasing its availability in peripheral tissues.
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influence of Glucogenic Amino Acids on the hepatic metabolism of threonine
Biochimica et Biophysica Acta, 1992Co-Authors: Corinne Moundras, Daniel Bercovici, Christian Remesy, Christian DemigneAbstract:The supplementation of a low-protein diet with l -threonine leads to a marked accumulation of threonine in plasma and liver, whereas increasing dietary protein generally leads to an induction of threonine dehydratase in the liver, hence depressed availability for extrasplanchnic tissues. The aim of the present study was, thus, to further investigate the factors which control the utilization of threonine by the liver. Increasing the dietary supply of threonine led to parallel increases in the afferent and hepatic concentrations and in the rate of utilization by the liver; however, the fractional extraction tended to decrease. It appears that the addition of a mixture of Glucogenic Amino Acids to the diet prevented the accumulation of threonine in plasma induced by exogenous threonine. The Glucogenic Amino Acids increased the fractional hepatic uptake of threonine, and counteracted its accumulation in the liver. These effects reflect the fact that the Glucogenic Amino Acids elicited a potent induction of the threonine dehydratase, whereas threonine alone ws uneffective. Our results suggest that, besides the well-established effect of Glucogenic conditions, the availability of some Glucogenic Amino Acids is an important factor in the control of threonine catabolism.
Adam R Konopka - One of the best experts on this subject based on the ideXlab platform.
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erratum hyperglucagonemia mitigates the effect of metformin on glucose production in prediabetes cell reports 2016 15 7 1394 1400 s2211124716304375 10 1016 j celrep 2016 04 024
Cell Reports, 2018Co-Authors: Adam R Konopka, Raul Ruiz Esponda, Matthew M Robinson, Matthew L Johnson, Rickey E Carter, Michele Schiavon, Claudio Cobelli, Fredric E Wondisford, Ian R Lanza, Sreekumaran K NairAbstract:(Cell Reports 15, 1394–1400; May 17, 2016) In the originally published version of this article, the labels “Placebo” and “Metformin” were mistakenly switched in Table S2, which displayed plasma concentrations of Amino Acids. We have corrected this error as well as the following additional errors, which we would like to bring to the attention of the readers: 1. The third bullet point within the Highlights now reads “…metformin increases Glucogenic Amino Acids …” rather than “… metformin decreases Glucogenic Amino Acids …”2. The last sentence of the In Brief blurb now reads “… increased glucagon and Glucogenic precursors” rather than “increased glucagon and decreased Glucogenic precursors” (the word “decreased” was removed).3. In paragraph 6, line 21 of page 1396, the text now reads “.. including decreased metabolites of the urea pathway …” rather than “including elevated metabolites of the urea pathway”4. In paragraph 6, line 26 of page 1396, the text now reads “.. revealed an increase in Glucogenic AAs” rather than “.. revealed a decline in Glucogenic AAs”Although Amino acid metabolites are not the primary outcome of the work described in this paper and these errors do not alter the main conclusions outlined therein, the authors regret the errors.