Molecular cloning of the goose ACSL3 and ACSL5 coding domain sequences and their expression characteristics during goose fatty liver development

He, Hua; Liu, H. H.; Wang, Jiwen; Lu, Jia; Li, L.; Pan, Zhenxiao

doi:10.1007/s11033-014-3053-5

Cited by 10 publications

(7 citation statements)

References 24 publications

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“…ACSL3 gene expression was significantly downregulated in the VAT of the obese individuals compared with that of the controls. Considering the evidence of the important role of ACSL3 in hepatic lipogenesis and its regulation, the ACSL3 gene and protein can be assumed to be essential for triglyceride metabolism in VAT, regulated by the PPAR gene, in addition to preventing the development of lipotoxicity in peripheral tissues and contributing to the modulation of steroidogenic genes in adipose tissue2021. SUCGL and IDH2 gene expression was also downregulated in the VAT of obese individuals.…”

Section: Discussionmentioning

confidence: 99%

Different gene expression profiles in subcutaneous & visceral adipose tissues from Mexican patients with obesity

Ronquillo

Mellnyk

Cárdenas-Rodríguez

et al. 2019

Indian Journal of Medical Research

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Background & objectives: Obesity is a health problem that requires substantial efforts to understand the physiopathology of its various types and to determine therapeutic strategies for its treatment. The objective of this study was to characterize differences in the global gene expression profiles of subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) between control patients (normal weight) and patients with obesity (IMC≥30) using microarrays. Methods: Employing RNA isolated from SAT and VAT samples obtained from eight control and eight class I, II and III patients with obesity, the gene expression profiles were compared between SAT and VAT using microarrays and the findings were validated via real-time quantitative polymerase chain reaction. Results: A total of 327 and 488 genes were found to be differentially expressed in SAT and VAT, respectively ( P ≤0.05). Upregulation of PPAP2C, CYP4A11 and CYP17A1 genes was seen in the VAT of obese individuals. Interpretation & conclusions: SAT and VAT exhibited significant differences in terms of the expression of specific genes. These genes might be related to obesity. These findings may be used to improve the clinical diagnosis of obesity and could be a tool leading to the proposal of new therapeutic strategies for the treatment of obesity.

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Section: Discussionmentioning

confidence: 99%

Different gene expression profiles in subcutaneous & visceral adipose tissues from Mexican patients with obesity

Ronquillo

Mellnyk

Cárdenas-Rodríguez

et al. 2019

Indian Journal of Medical Research

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“…Main themes for ACSL3 identified via profiling of its literature were: lipid droplet, liver, and goose fatty liver . Expression of ACSL3 has been described in various tissues including the brain (35), pancreatic islet cells (36), upper small intestine (37), vascular smooth muscle cells (38), liver (39–41), and fetal liver (42). Transcriptome data available via the BioGPS portal and depicted in Supplementary Figure 1 shows ACSL3 as the member of the family with the highest degree of restriction to the CNS.…”

Section: Review Of Acsl Family Members Function and Role In Diseasementioning

confidence: 99%

Long-Chain Acyl-CoA Synthetase 1 Role in Sepsis and Immunity: Perspectives From a Parallel Review of Public Transcriptome Datasets and of the Literature

et al. 2019

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A potential role for the long-chain acyl-CoA synthetase family member 1 (ACSL1) in the immunobiology of sepsis was explored during a hands-on training workshop. Participants first assessed the robustness of the potential gap in biomedical knowledge identified via an initial screen of public transcriptome data and of the literature associated with ACSL1. Increase in ACSL1 transcript abundance during sepsis was confirmed in several independent datasets. Querying the ACSL1 literature also confirmed the absence of reports associating ACSL1 with sepsis. Inferences drawn from both the literature (via indirect associations) and public transcriptome data (via correlation) point to the likely participation of ACSL1 and ACSL4, another family member, in inflammasome activation in neutrophils during sepsis. Furthermore, available clinical data indicate that levels of ACSL1 and ACSL4 induction was significantly higher in fatal cases of sepsis. This denotes potential translational relevance and is consistent with involvement in pathways driving potentially deleterious systemic inflammation. Finally, while ACSL1 expression was induced in blood in vitro by a wide range of pathogen-derived factors as well as TNF, induction of ACSL4 appeared restricted to flagellated bacteria and pathogen-derived TLR5 agonists and IFNG. Taken together, this joint review of public literature and omics data records points to two members of the acyl-CoA synthetase family potentially playing a role in inflammasome activation in neutrophils. Translational relevance of these observations in the context of sepsis and other inflammatory conditions remain to be investigated.

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“…So far, hepatic lipogenesis and lipid channeling have been investigated in the context of fatty liver induced by overfeeding1011. With the emergence of next generation sequencing (NGS) techniques, many genes have been identified as associated with goose fatty liver121314. A recent study suggests that the large amount of fat stored in goose liver results from an imbalance between the storage and secretion of exogenous and de novo synthesized endogenous lipids, as well as an absence of leptin gene homologs due to positive selection15.…”

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confidence: 99%

Prosteatotic and Protective Components in a Unique Model of Fatty Liver: Gut Microbiota and Suppressed Complement System

Liu

Zhao

Wang

et al. 2016

Sci Rep

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Goose can develop severe hepatic steatosis without overt injury, thus it may serve as a unique model for uncovering how steatosis-related injury is prevented. To identify the markedly prosteatotic and protective mechanisms, we performed an integrated analysis of liver transcriptomes and gut microbial metagenomes using samples collected from overfed and normally-fed geese at different time points. The results indicated that the fatty liver transcriptome, initially featuring a ‘metabolism’ pathway, was later joined by ‘cell growth and death’ and ‘immune diseases’ pathways. Gut microbiota played a synergistic role in the liver response as microbial and hepatic genes affected by overfeeding shared multiple pathways. Remarkably, the complement system, an inflammatory component, was comprehensively suppressed in fatty liver, which was partially due to increased blood lactic acid from enriched Lactobacillus. Data from in vitro studies suggested that lactic acid suppressed TNFα via the HNF1α/C5 pathway. In conclusion, gut microbes and their hosts respond to excess energy influx as an organic whole, severe steatosis and related tolerance of goose liver may be partially attributable to gut microbiotic products and suppressed complement system, and lactic acid from gut microbiota participates in the suppression of hepatic TNFα/inflammation through the HNF1α/C5 pathway.

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Molecular cloning of the goose ACSL3 and ACSL5 coding domain sequences and their expression characteristics during goose fatty liver development

Cited by 10 publications

References 24 publications

Different gene expression profiles in subcutaneous & visceral adipose tissues from Mexican patients with obesity

Different gene expression profiles in subcutaneous & visceral adipose tissues from Mexican patients with obesity

Long-Chain Acyl-CoA Synthetase 1 Role in Sepsis and Immunity: Perspectives From a Parallel Review of Public Transcriptome Datasets and of the Literature

Prosteatotic and Protective Components in a Unique Model of Fatty Liver: Gut Microbiota and Suppressed Complement System

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