scholarly journals Hepatic Proteomic Analysis Reveals That Enhanced Carboxylic Acid Metabolism and Oxidoreduction Promote Muscle and Fat Deposition in Muscovy Duck

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2180
Author(s):  
Wanli Yang ◽  
Xingyong Chen ◽  
Congcong Wei ◽  
Yutong Zhao ◽  
Zhengquan Liu ◽  
...  
Keyword(s):  
Carboxylic Acid ◽  
Acid Metabolism ◽  
Triosephosphate Isomerase ◽  
Subcutaneous Fat ◽  
Lipid Synthesis ◽  
Reduction Process ◽  
Fat Deposition ◽  
Muscovy Duck ◽  
Dependent Manner ◽  
Muscovy Ducks

Liver is responsible for 90% of lipid synthesis in poultry; thus, it plays an important role in the growth of Muscovy ducks, which have a high fat deposition ability in a time-dependent manner. Therefore, male Muscovy ducks at 14, 28, 42, and 56 days were selected for body weight (BW), carcass weight (CW), subcutaneous fat thickness (SFT), abdominal fat weight (AFW), intramuscular fat content (IMF), and breast muscle fiber (BMF) diameter and density determination. Two-dimensional electrophoresis (2-DE) combining liquid chromatography linked to tandem mass spectrometry (LC-MS/MS) was used to analyze proteomic changes in liver at each stage. The BW, CW, AFW, SFT, and BMF diameter and density were significantly increased, while IMF content was significantly decreased at 28 to 42 days of age (p < 0.05). There were 57 differentially abundant protein (DEP) spots representing 40 proteins identified among the ages, in which 17, 41 and 4 spots were differentially abundant at 14 vs. 28, 28 vs. 42, and 42 vs. 56, respectively. Gene Ontology enrichment analysis found that DEPs were mostly enriched in the oxidation-reduction process, carboxylic acid metabolism, etc. Protein–protein interaction showed that catalase (CAT), triosephosphate isomerase (TPI), and protein disulfide-isomerase (PDI) were the key proteins responsible for the growth of Muscovy duck. In conclusion, 28 to 42 days of age is the crucial period for Muscovy ducks, and the ability of metabolism and antioxidants were significantly enhanced in liver.

scholarly journals Myostatin regulates fatty acid desaturation and fat deposition through MEF2C/miR222/SCD5 cascade in pigs

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Hongyan Ren ◽  
Wei Xiao ◽  
Xingliang Qin ◽  
Gangzhi Cai ◽  
Hao Chen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Muscle Growth ◽  
Subcutaneous Fat ◽  
Fat Deposition ◽  
Wild Type ◽  
Binding Prediction ◽  
Stearoyl Coa Desaturase

Abstract Myostatin (MSTN), associated with the “double muscling” phenotype, affects muscle growth and fat deposition in animals, whereas how MSTN affects adipogenesis remains to be discovered. Here we show that MSTN can act through the MEF2C/miR222/SCD5 cascade to regulate fatty acid metabolism. We generated MSTN-knockout (KO) cloned Meishan pigs, which exhibits typical double muscling trait. We then sequenced transcriptome of subcutaneous fat tissues of wild-type (WT) and MSTN-KO pigs, and intersected the differentially expressed mRNAs and miRNAs to predict that stearoyl-CoA desaturase 5 (SCD5) is targeted by miR222. Transcription factor binding prediction showed that myogenic transcription factor 2C (MEF2C) potentially binds to the miR222 promoter. We hypothesized that MSTN-KO upregulates MEF2C and consequently increases the miR222 expression, which in turn targets SCD5 to suppress its translation. Biochemical, molecular and cellular experiments verified the existence of the cascade. This novel molecular pathway sheds light on new targets for genetic improvements in pigs.

scholarly journals Transcriptional Insights into Key Genes and Pathways Underlying Muscovy Duck Subcutaneous Fat Deposition at Different Developmental Stages

Animals ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 2099
Author(s):  
Liping Guo ◽  
Congcong Wei ◽  
Li Yi ◽  
Wanli Yang ◽  
Zhaoyu Geng ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Differentially Expressed Genes ◽  
Molecular Mechanisms ◽  
Fatty Acid Biosynthesis ◽  
Developmental Stages ◽  
Subcutaneous Fat ◽  
Fat Deposition ◽  
Differentially Expressed ◽  
Muscovy Duck ◽  
Key Genes

Subcutaneous fat is a crucial trait for waterfowl, largely associated with meat quality and feed conversion rate. In this study, RNA-seq was used to identify differentially expressed genes of subcutaneous adipose tissue among three developmental stages (12, 35, and 66 weeks) in Muscovy duck. A total of 138 and 129 differentially expressed genes (DEGs) were identified between 35 and 12 weeks (wk), and 66 and 35 wk, respectively. Compared with 12 wk, subcutaneous fat tissue at 35 wk upregulated several genes related to cholesterol biosynthesis and fatty acid biosynthesis, including HSD17B7 and MSMO1, while it downregulated fatty acid beta-oxidation related genes, including ACOX1 and ACSL1. Notably, most of the DEGs (92.2%) were downregulated in 66 wk compared with 35 wk, consistent with the slower metabolism of aging duck. Protein network interaction and function analyses revealed GC, AHSG, FGG, and FGA were the key genes for duck subcutaneous fat from adult to old age. Additionally, the PPAR signaling pathway, commonly enriched between the two comparisons, might be the key pathway contributing to subcutaneous fat metabolism among differential developmental stages in Muscovy duck. These results provide several candidate genes and pathways potentially involved in duck subcutaneous fat deposition, expanding our understanding of the molecular mechanisms underlying subcutaneous fat deposition during development.

scholarly journals High Fat Activates O-GlcNAcylation and Affects AMPK/ACC Pathway to Regulate Lipid Metabolism

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1740
Author(s):  
Yuning Pang ◽  
Xiang Xu ◽  
Xiaojun Xiang ◽  
Yongnan Li ◽  
Zengqi Zhao ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
High Fat Diet ◽  
Lipid Synthesis ◽  
Fat Deposition ◽  
Liver Fat ◽  
Lipid Homeostasis ◽  
High Fat ◽  
Dual Inhibitor ◽  
Regulate Lipid Metabolism

A high-fat diet often leads to excessive fat deposition and adversely affects the organism. However, the mechanism of liver fat deposition induced by high fat is still unclear. Therefore, this study aimed at acetyl-CoA carboxylase (ACC) to explore the mechanism of excessive liver deposition induced by high fat. In the present study, the ORF of ACC1 and ACC2 were cloned and characterized. Meanwhile, the mRNA and protein of ACC1 and ACC2 were increased in liver fed with a high-fat diet (HFD) or in hepatocytes incubated with oleic acid (OA). The phosphorylation of ACC was also decreased in hepatocytes incubated with OA. Moreover, AICAR dramatically improved the phosphorylation of ACC, and OA significantly inhibited the phosphorylation of the AMPK/ACC pathway. Further experiments showed that OA increased global O-GlcNAcylation and agonist of O-GlcNAcylation significantly inhibited the phosphorylation of AMPK and ACC. Importantly, the disorder of lipid metabolism caused by HFD or OA could be rescued by treating CP-640186, the dual inhibitor of ACC1 and ACC2. These observations suggested that high fat may activate O-GlcNAcylation and affect the AMPK/ACC pathway to regulate lipid synthesis, and also emphasized the importance of the role of ACC in lipid homeostasis.

Airway synthesis of 20-hydroxyeicosatetraenoic acid: metabolism by cyclooxygenase to a bronchodilator

1999 ◽  
Vol 276 (2) ◽  
pp. L280-L288 ◽  
Author(s):  
Elizabeth R. Jacobs ◽  
Richard M. Effros ◽  
John R. Falck ◽  
K. Malla Reddy ◽  
William B. Campbell ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Gas Chromatography ◽  
Arachidonic Acid ◽  
Airway Resistance ◽  
Acid Metabolism ◽  
Gas Chromatography Mass Spectrometry ◽  
Dependent Manner ◽  
Hydroxyeicosatetraenoic Acid ◽  
Polar Metabolites ◽  
H 20

Rabbit airway tissue is a particularly rich source of cytochrome P-4504A protein, but very little information regarding the effect(s) of 20-hydroxyeicosatetraenoic acid (20-HETE) on bronchial tone is available. Our studies examined the response of rabbit bronchial rings to 20-HETE and the metabolism of arachidonic acid and 20-HETE from airway microsomes. 20-HETE (10−8 to 10−6 M) produced a concentration-dependent relaxation of bronchial rings precontracted with KCl or histamine but not with carbachol. Relaxation to 20-HETE was blocked by indomethacin or epithelium removal, consistent with the conversion of 20-HETE to a bronchial relaxant by epithelial cyclooxygenase. A cyclooxygenase product of 20-HETE also elicited relaxation of bronchial rings. [14C]arachidonic acid was converted by airway microsomes to products that comigrated with authentic 20-HETE (confirmed by gas chromatography-mass spectrometry as 19- and 20-HETE) and to unidentified polar metabolites. [3H]20-HETE was metabolized to indomethacin-inhibitable products. These data suggest that 20-HETE is an endogenous product of rabbit airway tissue and may modulate airway resistance in a cyclooxygenase-dependent manner.

scholarly journals Short-Term Effects of γ-Irradiation on 1-Aminocyclopropane-1-Carboxylic Acid Metabolism in Early Climacteric Cherry Tomatoes

1990 ◽  
Vol 92 (3) ◽  
pp. 577-581 ◽  
Author(s):  
Christian Larrigaudière ◽  
Alain Latché ◽  
Jean Claude Pech ◽  
Christian Triantaphylidès
Keyword(s):  
Carboxylic Acid ◽  
Acid Metabolism ◽  
Short Term ◽  
Γ Irradiation ◽  
Cherry Tomatoes ◽  
Short Term Effects

Abstract 1394: Sublethal Levels of Aldehydes Augmented Cardiac Anti-Oxidant Defense through Activation of eIF2 α -ATF4 Pathway via GCN2 Kinase

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Takaharu Katayama ◽  
Motoaki Sano ◽  
Jin Endo ◽  
Kentaro Hayashida ◽  
Tomohiro Matsuhashi ◽  
...  
Keyword(s):  
Amino Acid ◽  
Amino Acid Metabolism ◽  
Acid Metabolism ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Special Importance ◽  
Dependent Manner ◽  
Protein Levels

[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.

scholarly journals ETV5 regulates hepatic fatty acid metabolism through PPAR signaling pathway

2020 ◽  
Author(s):  
Ada Admin ◽  
Zhuo Mao ◽  
Mingji Feng ◽  
Zhuoran Li ◽  
Minsi Zhou ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Association Studies ◽  
Sequencing Analysis ◽  
Dependent Manner ◽  
Alcoholic Fatty Liver ◽  
Hepatic Fatty Acid ◽  
Ppar Signaling

ETV5 is an ETS transcription factor which has been associated with obesity in genomic association studies. However, little is known about the role of ETV5 in hepatic lipid metabolism and non-alcoholic fatty liver disease (NAFLD). In the present study, we found that ETV5 protein expression was increased in diet- and genetic-induced steatotic liver. ETV5 responded to the nutrient status in an mTORC1 dependent manner and in turn regulated mTORC1 activity. Both viral-mediated and genetic depletion of ETV5 in mice led to increased lipid accumulation in the liver. RNA sequencing analysis revealed that PPAR signaling and fatty acid degradation/metabolism pathways were significantly downregulated in ETV5 deficient hepatocytes <i>in vivo</i> and <i>in vitro. </i>Mechanistically, ETV5 could bind to the PPRE region of PPAR downstream genes and enhance its transactivity. Collectively, our study identifies ETV5 as a novel transcription factor for the regulation of hepatic fatty acid metabolism which is required for the optimal β oxidation process. ETV5 may provide a therapeutic target for the treatment of hepatic steatosis.<br>

scholarly journals Retrospective analysis of post-mortem findings in domestic ducks and geese from non-commercial flocks in Sweden, 2011–2020

2021 ◽  
Vol 63 (1) ◽  
Author(s):  
Désirée Seger Jansson ◽  
Faruk Otman ◽  
Elisabeth Bagge ◽  
Ylva Lindgren ◽  
Pernille Engelsen Etterlin ◽  
...  
Keyword(s):  
Retrospective Analysis ◽  
Viral Infections ◽  
Muscovy Duck ◽  
Post Mortem ◽  
National Veterinary Institute ◽  
Domestic Ducks ◽  
Yeast Infection ◽  
Wide Range ◽  
Causes Of Mortality ◽  
Muscovy Ducks

Abstract Background Small poultry flock ownership has become a popular hobby in Europe and North America in recent years but there is a general lack of information regarding bird health and welfare. This retrospective analysis of routine post-mortem cases of non-commercial anseriform poultry aimed at providing information on causes of mortality mostly in relation to mortality events. For this purpose, birds that were submitted for routine post-mortem diagnostics to the National Veterinary Institute (SVA) in Sweden in 2011–2020 were retrospectively reviewed to determine main causes of mortality. Results Records from 79 necropsy submissions involving 120 birds (domestic ducks n = 41, Muscovy ducks n = 45, hybrid ducks n = 2 and domestic geese n = 32) were retrieved and analysed. Most submissions (72.2%) represented flock disease events and unexpected mortality was the most common cause of submission (70.9% of submissions). Twenty-two submissions (27.8%) were referred by veterinarians. There was a wide range of diagnoses of infectious and noninfectious aetiologies. Infectious causes of mortality included parasitic (19.2%), bacterial (13.3%), fungal (10.0%) and viral infections (3.3%) (at bird level of all 120 birds). Some of these infections such as duck virus enteritis (DVE), highly pathogenic influenza (HPAI H5N8) in Muscovy ducks and leucocytozoonosis (Leucocytozoon sp.) in all three species were most likely acquired from contact with wild free-living waterfowl. Generalised yeast infection (Muscovy duck disease) was diagnosed in Muscovy ducks and in a Muscovy duck/domestic duck hybrid. Other diseases were related to generalised noninfectious causes (27.5% of all birds) including diseases such as kidney disease, amyloidosis, cardiac dilatation, reproductive diseases and idiopathic inflammatory conditions. Nutritional or management-related diseases were diagnosed in 14.2% of all birds including rickets and gastrointestinal impaction/obstruction. Congenital/developmental, neoplastic, toxic and traumatic causes of mortality were rare. Conclusions The information obtained in this study can be used to identify and evaluate risks and help owners and veterinarians to prevent disease and provide adequate veterinary care for non-commercial anseriform poultry.

Effects of polymethoxylated flavone metabolites on apoB100 secretion and MTP activity in Huh7.5 cells

2021 ◽  
Vol 18 ◽  
Author(s):  
Danielle R. Gonçalves ◽  
Thais B. Cesar ◽  
John A. Manthey ◽  
Paulo I. Costa
Keyword(s):  
Lipid Synthesis ◽  
Dependent Manner ◽  
Transfer Protein ◽  
Low Concentrations ◽  
Wide Range ◽  
Cell Assays ◽  
Polymethoxylated Flavones ◽  
High Concentrations

Background: Citrus polymethoxylated flavones (PMFs) reduce the synthesis of liver lipoproteins in animal and in vitro cell assays, but few studies have evaluated the direct effects of their metabolites on this highly regulated process. Objective: To investigate the effects of representative metabolites of PMF on the secretion of liver lipoproteins using the mammalian cell Huh7.5. Method: In this study, the influences of three PMFs and five previously isolated PMF metabolites on hepatic apoB-100 secretion and microsomal transfer protein (MTP) activity were evaluated. Tangeretin (TAN), nobiletin (NOB) and 3,5,6,7,8,3′,4′-heptamethoxyflavone (HMF), and their glucuronides (TAN-Gluc, NOB-Gluc and HMF-Gluc) and oxidatively demethylated metabolites (TAN-OH, NOB-OH, HMF-OH) were incubated with Huh7.5 cells to measure their inhibitory effects on lipid synthesis. Results: The results showed that TAN, HMF and TAN-OH reduced the secretion of apoB-100 in a dose-dependent manner, while NOB and the other tested metabolites showed no inhibition. MTP activity in the Huh7.5 cells was significantly reduced in the presence of low concentrations of TAN, and in high concentrations of NOB-OH. This study also showed that PMFs and PMF metabolites produced a wide range of effects on apoB-100 secretion and MTP activity. Conclusion: The results suggest that while PMFs and their metabolites control dyslipidemia in vivo, the inhibition of MTP activity cannot be the only pathway influenced by these compounds.

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