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Roles of PKLR in NAFLD using loss- and gain-of-function mouse models

ABSTRACT: Roles of PKLR in NAFLD using loss- and gain-of-function mouse models

PROVIDER: PRJNA635078 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11849318_1.fastq.gz	Fastqsanger.gz
	SRR11849318_2.fastq.gz	Fastqsanger.gz
	SRR11849319_1.fastq.gz	Fastqsanger.gz
	SRR11849319_2.fastq.gz	Fastqsanger.gz
	SRR11849320_1.fastq.gz	Fastqsanger.gz

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Roles of PKLR in NAFLD using loss- and gain-of-function mouse models

Project description:The etiology of non-alcoholic fatty liver disease (NAFLD) is poorly understood, with males and Mexican population exhibiting markedly increased susceptibility. Using a systems genetics approach, involving multi-omic analysis of ~100 inbred strains, we recently identified several candidate genes driving NAFLD. We investigated the role of one of these candidates, liver pyruvate kinase (L-PK or Pklr) in NAFLD using patient samples and mouse models. We examined L-PK expression in mice of both sexes and in a cohort of bariatric surgery patients. We used liver-specific loss- and gain-of-function strategies in independent animal models of diet-induced steatosis and fibrosis, involving both sexes. Following treatment, we measured several metabolic phenotypes associated with obesity, insulin resistance, dyslipidemia, liver steatosis and fibrosis. Furthermore, liver tissues were used for gene expression and western blots, and liver mitochondria for bioenergetics. Our results demonstrate that L-PK acts in a male-specific manner in the development of liver steatosis and fibrosis. Given that NAFLD/NASH exhibit sexual dimorphism, our results have important implications for the development of personalized therapeutics.

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Sex-specific roles of PKLR in NAFLD using gain-of-function mouse models

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Project description:The etiology of non-alcoholic fatty liver disease (NAFLD) is poorly understood, with males and Mexican population exhibiting markedly increased susceptibility. Using a systems genetics approach, involving multi-omic analysis of ~100 inbred strains, we recently identified several candidate genes driving NAFLD. We investigated the role of one of these candidates, liver pyruvate kinase (L-PK or Pklr) in NAFLD using patient samples and mouse models. We examined L-PK expression in mice of both sexes and in a cohort of bariatric surgery patients. We used liver-specific loss- and gain-of-function strategies in independent animal models of diet-induced steatosis and fibrosis, involving both sexes. Following treatment, we measured several metabolic phenotypes associated with obesity, insulin resistance, dyslipidemia, liver steatosis and fibrosis. Furthermore, liver tissues were used for gene expression and Western blots, and liver mitochondria for bioenergetics. Our results demonstrate that L-PK acts in a male-specific manner in the development of liver steatosis and fibrosis. Given that NAFLD/NASH exhibit sexual dimorphism, our results have important implications for the development of personalized therapeutics.

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