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

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

PROVIDER: PRJNA660435 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12554756_1.fastq.gz	Fastqsanger.gz
	SRR12554756_2.fastq.gz	Fastqsanger.gz
	SRR12554757_1.fastq.gz	Fastqsanger.gz
	SRR12554757_2.fastq.gz	Fastqsanger.gz
	SRR12554758_1.fastq.gz	Fastqsanger.gz

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Sex-specific roles of PKLR in NAFLD using 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.

2021-01-19 | GSE157201 | GEO

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

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

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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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Roles of PKLR in NAFLD

Project description:Roles of PKLR in NAFLD

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Project description:In this project, the gene expression profiles of commonly used murine models of NAFLD were compared to two publically available human datasets to assess proximity to human pathophysiology, focusing on differential expression and pathway enrichment. CCL4 was used as a positive control for fibrosis.

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Project description:The Salicaceae family is of growing interest in the study of dioecy in plants because the sex determination region (SDR) has been shown to be highly dynamic, with differing locations and heterogametic systems across taxa. Previous studies investigating the mechanisms regulating sex in the genus Salix have been limited to genome resequencing and differential expression, which are mostly descriptive in nature, and functional validation of candidate sex determination genes has not been conducted. Here we use functional analysis to test a suite of previously identified candidate genes involved in sex determination and sex dimorphism in the bioenergy shrub willow Salix purpurea. Six candidate master regulator genes for sex determination were overexpressed in Arabidopsis, followed by floral proteome analysis. Eleven transcription factors with predicted roles in mediating sex dimorphism downstream of the SDR were tested using DAP-Seq in both male and female S. purpurea DNA. The results of this study provide further evidence to support models for the roles of ARR17 and GATA15 as master regulator genes of sex determination in S. purpurea, contributing to a regulatory system that is notably different from that of the related genus Populus. Two transcription factors, an AP2/ERF family gene and a homeodomain-like transcription factor, have evidence supporting roles in downstream regulation of sex dimorphism.

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Project description:Non-alcoholic fatty liver disease (NAFLD) is a sexually dimorphic disease influenced by dietary factors. Here, we assess the metabolic and hepatic effects of dietary amino acid (AA) source in Western diet (WD)-induced NAFLD in male and female mice. The AA source was either casein or a free AA mixture mimicking the composition of casein. As expected, males fed a casein-based WD displayed glucose intolerance, fasting hyperglycemia, and insulin-resistance and developed NAFLD associated with changes in hepatic gene expression and dysbiosis. In contrast, males fed the AA-based WD showed no steatosis, a similar gene expression profile as males fed a control diet, and a distinct microbiota composition compared to males fed a casein-based WD. Females were protected against WD-induced liver damage, hepatic gene expression, and gut microbiota changes regardless of the AA source. Thus, free dietary AA intake prevents the unhealthy metabolic outcomes of a WD in a sex-specific manner.

2024-01-01 | GSE234591 | GEO

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