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Glucagon contributes to liver zonation in mice [Gcg KO]

ABSTRACT: Glucagon contributes to liver zonation in mice [Gcg KO]

PROVIDER: PRJNA434234 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6729590.fastq.gz	Fastqsanger.gz
	SRR6729591.fastq.gz	Fastqsanger.gz
	SRR6729592.fastq.gz	Fastqsanger.gz
	SRR6729593.fastq.gz	Fastqsanger.gz
	SRR6729594.fastq.gz	Fastqsanger.gz

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Glucagon contributes to liver zonation in mice [Gcg infusion]

Project description:Glucagon contributes to liver zonation in mice [Gcg infusion]

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Glucagon contributes to liver zonation in mice [Gcg KO]

Project description:Liver zonation characterizes the separation of metabolic pathways along the lobules and is required for optimal function. Wnt/beta-catenin signaling controls metabolic zonation by activating genes in the perivenous hepatocytes, while suppressing genes in the periportal counterparts. We now demonstrate that glucagon opposes the actions of Wnt/beta-catenin signaling on gene expression and metabolic zonation pattern. The effects were more pronounced in the periportal hepatocytes where 28% of all genes were activated by glucagon and inhibited by Wnt/beta-catenin. The glucagon and Wnt/beta-catenin receptors and their signaling pathways are uniformly distributed in periportal and perivenous hepatocytes and the expression is not regulated by the opposing signal. Collectively, our results show that glucagon controls gene expression and metabolic zonation in the liver through a counter play with the Wnt/beta-catenin signaling pathway.

2018-03-01 | GSE110672 | GEO

Glucagon contributes to liver zonation in mice

Project description:Glucagon contributes to liver zonation in mice

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Glucagon contributes to liver zonation in mice [Gcg infusion]

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Glucagon contributes to liver zonation.

Project description:Liver zonation characterizes the separation of metabolic pathways along the lobules and is required for optimal function. Wnt/β-catenin signaling controls metabolic zonation by activating genes in the perivenous hepatocytes, while suppressing genes in the periportal counterparts. We now demonstrate that glucagon opposes the actions of Wnt/β-catenin signaling on gene expression and metabolic zonation pattern. The effects were more pronounced in the periportal hepatocytes where 28% of all genes were activated by glucagon and inhibited by Wnt/β-catenin. The glucagon and Wnt/β-catenin receptors and their signaling pathways are uniformly distributed in periportal and perivenous hepatocytes and the expression is not regulated by the opposing signal. Collectively, our results show that glucagon controls gene expression and metabolic zonation in the liver through a counterplay with the Wnt/β-catenin signaling pathway.

| S-EPMC5924920 | biostudies-literature

Glucagon receptor signaling in GCGR KO mice

Project description:GCGR wt and ko mice Glucagon receptor signaling in GCGR KO mice: fig 2a in Solloway et al.

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Glucagon contributes to liver zonation in mice

Project description:This SuperSeries is composed of the SubSeries listed below.

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Glucagon receptor deficient liver during postnatal development

Project description:Glucagon receptor deficient liver during postnatal development: fig S5a-S5c in Solloway et al. livers from ko and wt GCGR mice at various developmental stages

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Project description:Objective: We sought to identify the circulating metabolites that would serve as markers of glucagon action. Design: In this study, we performed a continuous 72-hour glucagon infusion in healthy individuals with overweight/obesity. Participants were randomized to either glucagon (12.5 ng/kg/min) (GCG 12.5) or glucagon (25 ng/kg/min) GCG 25 or a placebo control were included. A comprehensive metabolomics analysis was then performed from plasma isolated at several time points during the infusion to identify markers of glucagon activity.

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