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Transcriptomic analysis of hepatic genes in high-fat diet treated wild type and Sesn3 knockout mice

ABSTRACT: Transcriptomic analysis of hepatic genes in high-fat diet treated wild type and Sesn3 knockout mice

PROVIDER: PRJNA540851 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9004670_1.fastq.gz	Fastqsanger.gz
	SRR9004670_2.fastq.gz	Fastqsanger.gz
	SRR9004671_1.fastq.gz	Fastqsanger.gz
	SRR9004671_2.fastq.gz	Fastqsanger.gz
	SRR9004666_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of hepatic genes in high-fat diet treated wild type and Sesn3 knockout mice

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Project description:Pyruvate has two major fates upon entry into mitochondria, the oxidative decarboxylation to acetyl-CoA or the biotin-dependent carboxylation to oxaloacetate via pyruvate carboxylase (Pcx). Here we have generated mice with a liver specific knockout of pyruvate carboxylase (PcxL-/-) to understand the role of Pcx in hepatic mitochondrial metabolism under disparate physiological states. PcxL-/- mice exhibited a deficit in hepatic gluconeogenesis as expected but were able to maintain systemic euglycemia following a 24hr fast and enhanced ketogenesis. Feeding a high fat diet to PcxL-/- mice resulted in animals that were resistant to glucose intolerance without affecting body weight. However, PcxL-/- mice fed a ketogenic diet for 1 week became severely hypoglycemic, demonstrating a requirement for hepatic Pcx for long term glycemia under carbohydrate limited diets. Loss of Pcx was associated with an induction of protein acetylation in PcxL-/- mice regardless of physiologic state. Furthermore, liver acetyl-proteomics revealed a biased induction in mitochondrial lysine acetylation. These data show that Pcx is important for maintaining the proper balance of pyruvate metabolism between oxidative and anaplerotic pathways.

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