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Glucagon contributes to liver zonation in mice [Gcg infusion]

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

PROVIDER: PRJNA434235 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6729560.fastq.gz	Fastqsanger.gz
	SRR6729570.fastq.gz	Fastqsanger.gz
	SRR6729561.fastq.gz	Fastqsanger.gz
	SRR6729571.fastq.gz	Fastqsanger.gz
	SRR6729562.fastq.gz	Fastqsanger.gz

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Glucagon contributes to liver zonation in mice [Gcg KO]

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

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Glucagon contributes to liver zonation in mice [Gcg infusion]

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.

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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.

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

A Metabolomic Signature of Glucagon Action in Healthy Individuals with Overweight/Obesity Humans

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.

2020-10-26 | ST001515 | MetabolomicsWorkbench

Glucagon contributes to liver zonation in mice

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

2018-03-01 | GSE110674 | GEO

RNA-Sequence of the liver after administration of adenovirus associated with metabolic liver zonation

Project description:Metabolic zonation in the liver is broadly defined as spatiotemporal variability in the intra-hepatic distribution of nutrients. R-spondin3 (Rspo3) regulates metabolic features around hepatic central veins. Herein, we demonstrate that altered hepatic metabolic zonation due to Rspo3 contributes to maintaining systemic glucose metabolism and body composition via inter-organ communication mechanism. Hepatic Rspo3 induction in obesity improves obesity-associated features by restoring insulin sensitivity, reversing adipose tissue enlargement and reversing overstimulated adaptive thermogenesis. These remote effects partly consist of neuronal communication via the afferent vagus from the liver. In contrast, hepatic Rspo3 suppression exacerbates diabetes due to insulin resistance and develops fatty liver.

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RNAseq liver Glucagon+T3

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Glucagon receptor blocked liver gene signature

Project description:Liver RNA-seq in lean or diet-induced obese mice administered with glucagon receptor blocking antibody

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