scholarly journals Quantitative metabolomics analysis of amino acid metabolism in recombinant Pichia pastoris under different oxygen availability conditions

2012 ◽  
Vol 11 (1) ◽  
pp. 83 ◽  
Author(s):  
Marc Carnicer ◽  
Angela ten Pierick ◽  
Jan van Dam ◽  
Joseph J Heijnen ◽  
Joan Albiol ◽  
...  
2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 177-177
Author(s):  
Yue Guo ◽  
Andrea Hanson ◽  
Lei Wang ◽  
Brian Kerr ◽  
Pedro Urriola ◽  
...  

Abstract Feeding oxidized lipids compromises growth performance of pigs, but the metabolic events contributing to this adverse effect are not well defined. In this study, oxidized corn oil (OCO) was prepared by heating control corn oil (CCO) at 185 oC for 12 h. Weanling pigs (initial BW = 6.3 ± 1.4 kg) were fed 4 isocaloric diets containing 9% CCO, 6% CCO + 3% OCO, 3% CCO + 6% OCO, and 9% OCO, respectively. Pigs were provided ad libitum access to experimental diets in 3 phases (phase 1 = 4 d, phase 2 = 10 d and phase 3 = 21 d) for 35 d. Pig body weight (BW) and feed disappearance were determined at the d 0, 4, 14 and 35 to calculate average daily gain (ADG), average daily feed intake (ADFI) and gain to feed (G:F) ratio. Serum and liver samples collected on d 35 of feeding were analyzed by the liquid chromatography-mass spectrometry (LC-MS)-based metabolomics analysis. Growth performance data were analyzed using the MIXED procedure of SAS and metabolomics data were analyzed by two-tailed student’s t test for comparison between different doses of OCO and CCO treatments. The result showed that dietary OCO decreased G:F ratio (P < 0.05) dose-dependently, but did not ADFI. Metabolomics analysis showed that OCO fed pigs decreased the levels of serum alanine (P < 0.01), tryptophan (P < 0.05), carnosine (P < 0.01), and glutamic acid (P < 0.05), while the levels of threonine (P < 0.05) was increased compared to CCO. Moreover, consuming OCO decreased the hepatic metabolites from threonine catabolism pathways, including α-ketobutyrate (P < 0.01), α-amino-butyrate (P < 0.05), and propionic acid (P < 0.05), compared to CCO treatment. In addition, OCO increased hepatic NAD level by activating tryptophan-NAD+ metabolic pathway. Overall, OCO selectively modulated amino acid metabolism in nursery pigs, which may further affect growth performance.


BBA Clinical ◽  
2016 ◽  
Vol 5 ◽  
pp. 151-158 ◽  
Author(s):  
Noriko Yoshimi ◽  
Takashi Futamura ◽  
Keiji Kakumoto ◽  
Alireza M. Salehi ◽  
Carl M. Sellgren ◽  
...  

2014 ◽  
Vol 28 (10) ◽  
pp. 1707-1718 ◽  
Author(s):  
Mounia Tannour-Louet ◽  
Brian York ◽  
Ke Tang ◽  
Erin Stashi ◽  
Hichem Bouguerra ◽  
...  

Disturbances in amino acid metabolism are increasingly recognized as being associated with, and serving as prognostic markers for chronic human diseases, such as cancer or type 2 diabetes. In the current study, a quantitative metabolomics profiling strategy revealed global impairment in amino acid metabolism in mice deleted for the transcriptional coactivator steroid receptor coactivator (SRC)-1. Aberrations were hepatic in origin, because selective reexpression of SRC-1 in the liver of SRC-1 null mice largely restored amino acids concentrations to normal levels. Cistromic analysis of SRC-1 binding sites in hepatic tissues confirmed a prominent influence of this coregulator on transcriptional programs regulating amino acid metabolism. More specifically, SRC-1 markedly impacted tyrosine levels and was found to regulate the transcriptional activity of the tyrosine aminotransferase (TAT) gene, which encodes the rate-limiting enzyme of tyrosine catabolism. Consequently, SRC-1 null mice displayed low TAT expression and presented with hypertyrosinemia and corneal alterations, 2 clinical features observed in the human syndrome of TAT deficiency. A heterozygous missense variant of SRC-1 (p.P1272S) that is known to alter its coactivation potential, was found in patients harboring idiopathic tyrosinemia-like disorders and may therefore represent one risk factor for their clinical symptoms. Hence, we reinforce the concept that SRC-1 is a central factor in the fine orchestration of multiple pathways of intermediary metabolism, suggesting it as a potential therapeutic target that may be exploitable in human metabolic diseases and cancer.


1979 ◽  
Vol 7 (1) ◽  
pp. 261-262
Author(s):  
E. V. ROWSELL

1985 ◽  
Vol 4 ◽  
pp. 141-146 ◽  
Author(s):  
K VESTERBERG ◽  
J BERGSTROM ◽  
P FURST ◽  
U LEANDER ◽  
E VINNARS

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