Effects of dietary protein levels on the growth performance, digestive capacity and amino acid metabolism of juvenile Jian carp (Cyprinus carpiovar. Jian)

2009 ◽  
Vol 40 (9) ◽  
pp. 1073-1082 ◽  
Author(s):  
Yong Liu ◽  
Lin Feng ◽  
Jun Jiang ◽  
Yang Liu ◽  
Xiao-Qiu Zhou
Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Takaharu Katayama ◽  
Motoaki Sano ◽  
Jin Endo ◽  
Kentaro Hayashida ◽  
Tomohiro Matsuhashi ◽  
...  

[Introduction] Despite an increase in the levels of aldehydes, the heart from aldehyde dehydrogenase ( ALDH ) 2*2 -transgenic (Tg) mice, loss of function model of ALDH, exhibited a greater tolerance to oxidative stress via activation of amino acid metabolism leading to glutathione biosynthesis. This study was designed to identify the signaling cascades responsible for the activation of amino acid metabolism by aldehydes. [Methods & Results] (1) Phosphorylation of α -subunit of eukaryotic translation initiation factor 2 (eIF2 α ) and subsequent translational activation of ATF4 have been shown to induce amino acid metabolism as a common response to a wide variety of stressors. Consistent with this, phosphorylation levels of eIF2 α and protein expression of ATF4 were increased in ALDH2*2 -Tg hearts. (2) Among four eIF2 α kinases, general control non-depressible (GCN)2 kinase, a sensor for amino acid insufficiency, was activated in ALDH2*2 -Tg heart. (3) Quantification of intracellular amino acid demonstrated that free histidine concentration in ALDH2*2 -Tg heart was selectively reduced by 50% compared to that in non-Tg littermates. (4) To clarify the functional significance of observed reduction in histidine, ALDH2*2 -Tg mice were fed a high histidine diet. The phosphorylation levels of eIF2 α and the protein levels of ATF4 were diminished by 50% in ALDH2*2 -Tg mice fed the high histidine diet, in agreement with the normalization of histidine concentration. Accordingly, both enhanced tolerance to ischemia-reperfusion injury and elevated levels of glutathione were partially diminished in the heart from ALDH2*2 -Tg mice fed the high histidine diet compared to ALDH2*2 -Tg mice fed normal chow. (5) In culture, exposure to 4-hydroxy-2-nonenal (4-HNE) phosphorylated GCN2 and eIF2 α and increased protein levels of ATF4 in a time-dependent manner. (6) siRNA-mediated knockdown of GCN2 abrogated 4-HNE-induced induction of amino acid metabolic genes. [Conclusions] Activation of eIF2 α -ATF4 pathway via GCN2 kinase might be of special importance in the transcriptional control that coordinately promotes amino acid metabolism in response to aldehydes. Intracellular depletion of free histidine is at least partly involved in the activation of GCN2 kinase by aldehydes.


1981 ◽  
Vol 27 (2) ◽  
pp. 149-163 ◽  
Author(s):  
Yoshiaki FUJITA ◽  
Takashi YAMAMOTO ◽  
Toru RIKIMARU ◽  
Hidemichi EBISAWA ◽  
Goro INOUE

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.


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