Dataset Information

Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-seq2]

ABSTRACT: Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-seq2]

PROVIDER: PRJNA768332 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16183319_1.fastq.gz	Fastqsanger.gz
	SRR16183319_2.fastq.gz	Fastqsanger.gz
	SRR16183320_1.fastq.gz	Fastqsanger.gz
	SRR16183320_2.fastq.gz	Fastqsanger.gz
	SRR16183321_1.fastq.gz	Fastqsanger.gz

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Project description:High Fructose Corn Syrup (HFCS), a sweetener rich in glucose and fructose, is nowadays widely used in beverages and processed foods, and its consumption has been correlated to the emergence and progression of Non-Alcoholic Fatty Liver Disease (NAFLD). Nevertheless, the exact molecular mechanisms by which HFCS impacts hepatic metabolism are still unclear, especially in the context of obesity. In contrast, the vast majority of current studies in the field focus either on the detrimental role of fructose on NAFLD or compare the additive impact of fructose versus glucose in this process. Besides, studies elaborating on the role of fructose in NAFLD utilize molecular fructose, rather than HFCS, thus lacking simulation of human NAFLD in a more realistic way. Herein, by engaging combined omic approaches, we sought to characterize the additive impact of HFCS on NAFLD during obesity and recognize candidate pathways and molecules which could mediate the exaggeration of steatosis under these conditions. To achieve this goal, C57BL/6 male mice were fed a normal-fat (ND), a high-fat (HFD) or a HFD supplemented with HFCS (HFD-HFCS) and upon examination of their metabolic and NAFLD phenotype, proteomic and lipidomic analyses were conducted and utilized separately or in an integrated mode to identify HFCS-related molecular alterations of the hepatic metabolic landscape. Although HFD and HFD-HFCS mice displayed comparable obesity, HFD-HFCS mice showed greater aggravation of hepatic steatosis. Importantly, the HFD-HFCS hepatic proteome was characterized by an upregulation of the enzymes implicated in de novo lipogenesis (DNL), while palmitic-acid containing diglycerides were significantly increased in the HFD-HFCS hepatic lipidome, as compared to the HFD group. Integrated omic analysis further suggested that TCA cycle overstimulation, is likely contributing towards the intensification of steatosis in the HFD-HFCS dietary theme. Overall, our results imply that HFCS may significantly contribute to NAFLD aggravation during obesity, with its fructose-rich properties being the main suspect.

Dataset Information

Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-seq2]

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