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Spatial hepatocyte plasticity of gluconeogenic gene expression and gluconeogenic activity during the metabolic transitions between fed, fasted and starvation states [scRNA-Seq]

ABSTRACT: Spatial hepatocyte plasticity of gluconeogenic gene expression and gluconeogenic activity during the metabolic transitions between fed, fasted and starvation states [scRNA-Seq]

PROVIDER: PRJNA1097509 | ENA |

REPOSITORIES: ENA

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Spatial hepatocyte plasticity of gluconeogenic gene expression and gluconeogenic activity during the metabolic transitions between fed, fasted and starvation states [scRNA-Seq]

Project description:Single cell analyses of hepatocytes across the liver lobule demonstrated that gluconeogenic gene expression (Pck1 and G6pc) is relatively low in the fed state and gradually increase first in the periportal hepatocytes during the initial fasting period. As the time of fasting progresses, pericentral hepatocyte gluconeogenic gene expression increases and following entry into the starvation state the pericentral hepatocytes are not significantly different than the periportal hepatocytes. Similarly, pyruvate-dependent gluconeogenic activity is approximately 10-fold higher in the periportal hepatocytes during the initial fasting states but with only 1.5-fold different between the pericentral and periportal hepatocytes in the starvation state. In parallel, starvation induced a reduction of canonical beta-catenin signaling and redistribution of pericentral and periportal glutamine synthetase and glutaminase resulting in an enhanced pericentral glutamine-dependent gluconeogenesis. These data demonstrate that hepatocyte gluconeogenic gene expression and gluconeogenic activity are highly spatially and temporally plastic across the liver lobule and underscore the critical importance of using well-defined feeding and fasting times to define the basis of hepatic insulin resistance and glucose production.

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Spatial hepatocyte plasticity of gluconeogenic gene expression and gluconeogenic activity during the metabolic transitions between fed, fasted and starvation states [RNA-Seq]

Project description:Spatial hepatocyte plasticity of gluconeogenic gene expression and gluconeogenic activity during the metabolic transitions between fed, fasted and starvation states [RNA-Seq]

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Project description:Spatial hepatocyte plasticity of gluconeogenic gene expression and gluconeogenic activity during the metabolic transitions between fed, fasted and starvation states [targeted scRNA-seq]

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Spatial hepatocyte plasticity of gluconeogenesis during the metabolic transitions between fed, fasted and starvation states

Project description:The liver acts as a master regulator of metabolic homeostasis in part by performing gluconeogenesis. This process is dysregulated in type 2 diabetes, leading to elevated hepatic glucose output. The parenchymal cells of the liver (hepatocytes) are heterogeneous, existing on an axis between the portal triad and the central vein, and perform distinct functions depending on location in the lobule. Here, using single cell analysis of hepatocytes across the liver lobule, we demonstrate that gluconeogenic gene expression (Pck1 and G6pc) is relatively low in the fed state and gradually increases first in the periportal hepatocytes during the initial fasting period. As the time of fasting progresses, pericentral hepatocyte gluconeogenic gene expression increases, and following entry into the starvation state, the pericentral hepatocytes show similar gluconeogenic gene expression to the periportal hepatocytes. Similarly, pyruvate-dependent gluconeogenic activity is approximately 10-fold higher in the periportal hepatocytes during the initial fasting state but only 1.5-fold higher in the starvation state. In parallel, starvation suppresses canonical beta-catenin signaling and modulates expression of pericentral and periportal glutamine synthetase and glutaminase, resulting in an enhanced pericentral glutamine-dependent gluconeogenesis. These findings demonstrate that hepatocyte gluconeogenic gene expression and gluconeogenic activity are highly spatially and temporally plastic across the liver lobule, underscoring the critical importance of using well-defined feeding and fasting conditions to define the basis of hepatic insulin resistance and glucose production.

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