Proteomic analysis of fatty liver induced by starvation of medaka fish larvae
Ontology highlight
ABSTRACT:
ORGANISM(S): Cellular Organisms
SUBMITTER: Kazutoshi Mori
PROVIDER: PXD041411 | JPOST Repository | Mon Apr 08 00:00:00 BST 2024
REPOSITORIES: jPOST
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| T56-TO-1-SC10-11-20-19.csv | Csv | |||
| T56-TO-1-SC10-11-20-19.txt | Txt | |||
| T56-TO-1-SC10-11-20-19.wiff | Wiff | |||
| T56-TO-1-SC10-11-20-19.wiff.scan | Wiff | |||
| T56-TO-2-SC10-11-20-19.csv | Csv |
Items per page: 5 1 - 5 of 8 |
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Project description:Starvation causes the accumulation of lipid droplets in the liver, a somewhat counterintuitive phenomenon that is nevertheless conserved from flies to humans. Much like fatty liver resulting from overfeeding, hepatic lipid accumulation (steatosis) during undernourishment can lead to lipotoxicity and atrophy of the liver. Here, we found that while surface populations of Astyanax mexicanus undergo this evolutionarily conserved response to starvation, the starvation-resistant cavefish larvae of the same species do not display an accumulation of lipid droplets upon starvation. Moreover, cavefish are resistant to liver atrophy during starvation, providing a unique system to explore strategies for liver protection. Using comparative transcriptomics between zebrafish, surface fish, and cavefish, we identified the fatty acid transporter slc27a2a/fatp2 to be correlated with the development of fatty liver. Pharmacological inhibition of slc27a2a in zebrafish rescues steatosis and atrophy of the liver upon starvation. Further, down-regulation of FATP2 in drosophila larvae inhibits the development of starvation-induced steatosis, suggesting the evolutionary conserved importance of the gene in regulating fatty liver upon nutrition deprivation. Overall, our study identifies a conserved, druggable target to protect the liver from atrophy during starvation.
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Project description:Novel DHA-enriched oils with high α-linolenic acid (ALA) content will be available in the near future as an alternative for dietary fish oil replacement in aquafeeds. As preliminary validation, we 1) assessed the ability of a diet containing a formulated oil blend (tuna oil + flaxseed oil, TOFX) with high DHA and ALA content to achieve fish oil-like omega-3 long-chain (≥C20) polyunsaturated fatty acids (n-3 LC-PUFA) tissue composition in Atlantic salmon smolts, and 2) applied liver proteomics as exploratory approach to understand the consequent nutritional changes. Comparisons were made on fish fed a fish oil-based diet (FO) and a commercial-like oil blend diet (fish oil + poultry oil, FOPO) over 89 days. Growth and feed efficiency ratio were lower on the TOFX diet. Fish tissue concentration of n-3 LC-PUFA and the n-3:n-6 ratio were significantly higher for TOFX than for FOPO, but not higher than for FO, while tissue retention efficiency of n-3 LC-PUFA was promoted by TOFX relative to FO. Proteomics analysis revealed an unexpected oxidative stress response as the main adaptive physiological mechanism in TOFX fish. While specific dietary fatty acid concentrations and balances and antioxidant supplementation may need further attention, the use of an oil with a high content of DHA and ALA can enhance tissue deposition of n-3 LC-PUFA in relation to a commercially used blend oil.
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Project description:Dietary effects of arachidonate-rich fungal oil and fish oil on murine hepatic and hippocampal gene expression.<BR> <LI><u>Brain:</u></LI><BR> GSM2558: Control<bR> GSM2559: Control <bR> GSM2560: Fungal oil (AA)<bR> GSM2561: Fungal oil (AA)<bR> GSM2562: Fish oil (DHA)<bR> GSM2563: Fish oil (DHA)<bR> GSM2564: Fish and Fungal oil (DHA + AA)<bR> <LI><u>Liver:</u></LI><bR> GSM2565: Control <bR> GSM2566: Control<bR> GSM2567: Control<bR> GSM2568: Control<bR> GSM2569: Fungal oil (AA)<bR> GSM2570: Fungal oil (AA)<bR> GSM2571: Fish oil (DHA)<bR> GSM2572: Fish oil (DHA)<bR> GSM2573: Fish + Fungal oil (DHA +AA)<bR> GSM2574: Fish + Fungal oil (DHA +AA)<bR> Keywords: ordered
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Project description:We used microarray analysis to examine which genes are differentially expressed in mice that received a combination of fish oil and indomethacin. We fed low density lipoprotein receptor knock-out (LDLR-/-) mice with 6% of olive oil (control) or fish oil diets in the presence or absence of indomethacin for 12 weeks. We collected total RNA from liver samples and pooled 6 RNA samples in each group for Affymetrix microarrays.
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Project description:Medaka fish were exposed to several concentrations of humic acid. Changes in liver protein profiles of control and exposed fish were studied using LC-MS/MS analysis.
2021-07-14 | PXD025749 | JPOST Repository
Project description:Dietary effects of arachidonate-rich fungal oil and fish oil on murine hepatic and hippocampal gene expression.; Brain:; GSM2558: Control; GSM2559: Control ; GSM2560: Fungal oil (AA); GSM2561: Fungal oil (AA); GSM2562: Fish oil (DHA); GSM2563: Fish oil (DHA); GSM2564: Fish and Fungal oil (DHA + AA); Liver:; GSM2565: Control ; GSM2566: Control; GSM2567: Control; GSM2568: Control; GSM2569: Fungal oil (AA); GSM2570: Fungal oil (AA); GSM2571: Fish oil (DHA); GSM2572: Fish oil (DHA); GSM2573: Fish + Fungal oil (DHA +AA); GSM2574: Fish + Fungal oil (DHA +AA)
2007-12-13 | E-GEOD-91 | biostudies-arrayexpress
Project description:Calorie restriction (CR) consistently extends longevity and delays age-related diseases across several animal models. We have previously shown that different dietary fat sources can modulate life span and mitochondrial ultrastructure, function and membrane fatty acid composition in mice maintained on a 40% CR. In particular, animals consuming lard as the main fat source (CR-Lard) lived longer than CR mice consuming diets with soybean oil (CR-Soy) or fish oil (CR-Fish) as the predominant lipid source. In the present work, a transcriptomic analysis in liver and skeletal muscle was performed in order to elucidate possible mechanisms underlying the changes in energy metabolism and longevity induced by dietary fat in CR mice. After 8 months of CR, transcription downstream of several mediators of inflammation was inhibited in liver. In contrast, proinflammatory signaling was increased in the CR-Fish versus other CR groups. Dietary fish oil induced a gene expression pattern consistent with increased transcriptional regulation by several cytokines (TNF, GM-CSF, TGF-b) and sex hormones when compared to the other CR groups. The CR-Fish also had lower expression of genes involved in fatty acid biosynthesis and increased expression of mitochondrial and peroxisomal fatty acid b-oxidation genes than the other CR diet groups. Our data suggest that a diet high in n-3 PUFA, partially reverts CR-related changes in gene expression of key processes, such as inflammation and steroid hormone signaling, and this may mitigate life span extension with CR in mice consuming diets high in fish oil. Sixteen male C57BL/6 mice were purchased at 14 weeks of age from the Jackson Laboratory (Sacramento, CA) and fed a commercial rodent chow diet (Harlan Teklad #7012). The mice were allowed ad libitum access to food and their food intake was monitored for two weeks. At 4 months of age, the animals were randomly assigned to four groups. The Control group received 95% of the daily ad libitum caloric intake (13.6 kcal/day) to avoid excessive weight gain and obesity, and the other three groups received 60% of the ad libitum consumption (8.6 kcal/day). A total of 31 mice samples (eight control, eight fish, eight lard and seven soy distributed in liver (n=16) and muscle (n=15) tissues) were analyzed by RNA-Sequencing. However, 2 samples (1071 control liver [JFM42H], 1125 fish muscle [JFM45D]) were discarded for further analysis after performing cluster analysis (they were clustering in a different groups). Also their RIN values were not as high as those of the other samples, indicating lower quality of the RNA.
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Project description:The current study was designed to determine if dietary fatty acid concentration and composition affects the development and progression of nonalcoholic fatty liver disease. Male SD rats were overfed diets low (5%) or high (70%) fat diets via total enteral nutrition where the fat source was olive oil (monounsaturated), or corn oil (polyunsaturated). Overfeeding 5% corn oil produced little steatosis relative to feeding 5% olive oil. This was associated with lower fatty acid synthesis and reduced SREBP-c signaling in the 5% corn oil group. Overfeeding 70% fat diets increased steatosis and lead to increased liver necrosis in the 70% corn oil but not olive oil group. Increased injury after feeding polyunsaturated fat diets was linked to peroxidizability of hepatic free fatty acids and triglycerides and appearance of peroxidaized lipid products HETES and HODES previously linked to clinical nonalcoholic steatohepatitis.
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