Comparison Log
2025-12-15 03:28:31.611440
mwtab Python Library Version: 2.0.0
Source:      https://www.metabolomicsworkbench.org/rest/study/analysis_id/AN007153/mwtab/...
Study ID:    ST004300
Analysis ID: AN007153
Status:      Inconsistent

Sections "PROJECT" contain missmatched items: {'PROJECT_SUMMARY': ["Alcohol-associated liver disease (ALD) involves profound systemic lipid disruption. Using comprehensive 2DLC-MS-based untargeted lipidomics, we characterized the hepatic and cerebral lipidomes in wild-type and fat-1 transgenic (endogenous omega-3 PUFA-producing) mice subjected to a chronic-plus-binge ethanol model. Compared to fat-1 gene, ethanol intake was the dominant factor that induced 228 lipids in the liver and 316 in the brain with significant abundance changes. . Those significantly changed lipids were consistent across wild-type and fat-1 genotypes but highly tissue-specific. Furthermore, fat-1 genotype significantly modulated ethanol's impact and even reversed the regulation of some lipids, including sphingolipids and monosaturated and saturated fatty acyl-containing lipids. Four lipids in the liver and seven lipids in the brain were co-regulated by ethanol, genotype, and their interaction, with excellent discriminatory power in linear discriminant analysis. The odd-chain lipids of those 11 lipids suggest gut microbiome contributions. While ethanol effects were tissue-specific, fat-1 induced consistent responses in the two tissues, indicating conserved protective pathways. Our findings revealed complex lipid network remodeling in ALD through a multi-factorial affecting the liver-brain axis, highlighting the potential of fat-1 gene to mitigate tissue-specific metabolic dysfunction and informing future therapeutic strategies.", "Alcohol-associated liver disease (ALD) involves profound systemic lipid disruption. Using comprehensive 2DLC-MS-based untargeted lipidomics, we characterized the hepatic and cerebral lipidomes in wild-type and fat-1 transgenic (endogenous omega-3 PUFA-producing) mice subjected to a chronic-plus-binge ethanol model. Compared to fat-1 gene, ethanol intake was the dominant factor that induced 228 lipids in the liver and 316 in the brain with significant abundance changes. . Those significantly changed lipids were consistent across wild-type and fat-1 genotypes but highly tissue-specific. Furthermore, fat-1 genotype significantly modulated ethanol''s impact and even reversed the regulation of some lipids, including sphingolipids and monosaturated and saturated fatty acyl-containing lipids. Four lipids in the liver and seven lipids in the brain were co-regulated by ethanol, genotype, and their interaction, with excellent discriminatory power in linear discriminant analysis. The odd-chain lipids of those 11 lipids suggest gut microbiome contributions. While ethanol effects were tissue-specific, fat-1 induced consistent responses in the two tissues, indicating conserved protective pathways. Our findings revealed complex lipid network remodeling in ALD through a multi-factorial affecting the liver-brain axis, highlighting the potential of fat-1 gene to mitigate tissue-specific metabolic dysfunction and informing future therapeutic strategies."]}