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Hepatocyte Smoothened Activity Controls Susceptibility to Insulin Resistance and Nonalcoholic Fatty Liver Disease [RNA-Seq]

ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) is strongly associated with insulin resistance (IR), but little is known about the key genetic driver that links these two disorders. We aimed to elucidate the mechanism by which Smoothened (Smo), a G-protein coupled receptor, contributes to pathogenesis of NAFLD and IR.

ORGANISM(S): Homo sapiens

PROVIDER: GSE213621 | GEO | 2023/03/01

REPOSITORIES: GEO

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Hepatocyte Smoothened Activity Controls Susceptibility to Insulin Resistance and Nonalcoholic Fatty Liver Disease [scRNA-Seq]

Project description:Nonalcoholic fatty liver disease (NAFLD) is strongly associated with insulin resistance (IR), but little is known about the key genetic driver that links these two disorders. We aimed to elucidate the mechanism by which Smoothened (Smo), a G-protein coupled receptor, contributes to pathogenesis of NAFLD and IR.

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Hepatocyte Smoothened Activity Controls Susceptibility to Insulin Resistance and Nonalcoholic Fatty Liver Disease [scRNA-Seq]

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Hepatocyte Smoothened Activity Controls Susceptibility to Insulin Resistance and Nonalcoholic Fatty Liver Disease.

Project description:Background & aimsNonalcoholic steatohepatitis (NASH), a leading cause of cirrhosis, strongly associates with the metabolic syndrome, an insulin-resistant proinflammatory state that disrupts energy balance and promotes progressive liver degeneration. We aimed to define the role of Smoothened (Smo), an obligatory component of the Hedgehog signaling pathway, in controlling hepatocyte metabolic homeostasis and, thereby, susceptibility to NASH.MethodsWe conditionally deleted Smo in hepatocytes of healthy chow-fed mice and performed metabolic phenotyping, coupled with single-cell RNA sequencing (RNA-seq), to characterize the role of hepatocyte Smo in regulating basal hepatic and systemic metabolic homeostasis. Liver RNA-seq datasets from 2 large human cohorts were also analyzed to define the relationship between Smo and NASH susceptibility in people.ResultsHepatocyte Smo deletion inhibited the Hedgehog pathway and promoted fatty liver, hyperinsulinemia, and insulin resistance. We identified a plausible mechanism whereby inactivation of Smo stimulated the mTORC1-SREBP1c signaling axis, which promoted lipogenesis while inhibiting the hepatic insulin cascade. Transcriptomics of bulk and single Smo-deficient hepatocytes supported suppression of insulin signaling and also revealed molecular abnormalities associated with oxidative stress and mitochondrial dysfunction. Analysis of human bulk RNA-seq data revealed that Smo expression was (1) highest in healthy livers, (2) lower in livers with NASH than in those with simple steatosis, (3) negatively correlated with markers of insulin resistance and liver injury, and (4) declined progressively as fibrosis severity worsened.ConclusionsThe Hedgehog pathway controls insulin sensitivity and energy homeostasis in adult livers. Loss of hepatocyte Hedgehog activity induces hepatic and systemic metabolic stress and enhances susceptibility to NASH by promoting hepatic lipoxicity and insulin resistance.

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Whole transcriptome profiling of Japanese nonalcoholic fatty liver disease cohort.

Project description:Nonalcoholic steatohepatitis (NASH) is a severe form of nonalcoholic fatty liver disease (NAFLD) that is characterized by hepatic steatosis, inflammation, hepatocellular injury, and fibrosis, which lead to progressed cirrhosis and hepatocellular carcinoma. Despite its increasing prevalence on a global scale, the pathogenesis of NASH progression is not well understood. To elucidate the underlying mechanisms of NASH progression, we conducted transcriptome analyses of Japanese NAFLD cohort in our facility.

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