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Identifying the role of Acox1 in metabolism and inflammation in non-alcoholic fatty liver disease through mRNA-sequencing.

ABSTRACT: Purpose: To identify the impact of Acox1 on cellular metabolism and inflammation related to non-alcoholic fatty liver disease, within the context of obesogenic dietary stress. Methods: Hepatic mRNA profiles were obtained in triplicate for control and Acox1Lampe1 mice on chow diet or obesogenic diet. Profiles were generated using the Illumina HiSeq2000, reads that passed quality inspection were processed through the TopHap/Cufflinks pipeline. Results: Approximately 20million reads per sample were aligned to the mm8 mouse genome, using annotations provided by Ensembl. Testing between control and Acox1Lampe1 mice on control and obesogenic diets was performed using a 2-way ANOVA, with a p-value cutoff of 0.05 and FC of 1.5. We observed a significant alteration of hepatic gene expression in Acox1Lampe1 mutant mice, a pattern that was exacerbated by the obesogenic diet. Among significant genes, we observed an enrichment of those known to teb associated with inflammatory responses, leukocyte activation and adhesion, and abnormal liver physiology, regeneration, and development. Conclusion: Through next generation sequencing of hepatic tissues from control and Acox1Lampe1 mutant mice on control and obesogenic diets, we demonstrate that Acox1 regulates both metabolism and inflammation, the interplay of which correlates with increased hepatocellular damage and impared hepatic mitochondrial function.

ORGANISM(S): Mus musculus

PROVIDER: GSE89626 | GEO | 2018/05/09

REPOSITORIES: GEO

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Project description:This dataset contains proteomic data from mice with high or low weight gain in response to a high fat diet. Both host and microbial proteins are present. In the supplemental, there are also tables and supplementary files that can be used for replicating the bioinformatic analysis. Abstract: Consumption of refined high-fat, low-fiber diets promotes development of obesity and its associated consequences. While genetics play an important role in dictating susceptibility to such obesogenic diets, mice with nearly uniform genetics exhibit marked heterogeneity in their extent of obesity in response to such diets. This suggests non-genetic determinants play a role in diet-induced obesity. Hence, we sought to identify parameters that predict, and/or correlate with, development of obesity in response to an obesogenic diet. We assayed behavior, metabolic parameters, inflammatory markers/cytokines, microbiota composition, and the fecal metaproteome, in a cohort of mice (n=50) prior to, and the 8 weeks following, administration of an obesogenic high-fat low-fiber diet. Neither behavioral testing nor quantitation of inflammatory markers broadly predicted severity of diet-induced obesity. Although, the small subset of mice that exhibited basal elevations in serum IL-6 (n=5) were among the more obese mice in the cohort. While fecal microbiota composition changed markedly in response to the obesogenic diet, it lacked the ability to predict which mice were relative prone or resistant to obesity. In contrast, fecal metaproteome analysis revealed functional and taxonomic differences among the proteins associated with proneness to obesity. Targeted interrogation of microbiota composition data successfully validated the taxonomic differences seen in the metaproteome. While future work will be needed to determine the breadth of applicability of these associations to other cohorts of animals and humans, this study nonetheless highlights the potential power of gut microbial proteins to predict and perhaps impact development of obesity.

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Identifying the role of Acox1 in metabolism and inflammation in non-alcoholic fatty liver disease through mRNA-sequencing.

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