ArticleCell reports2016
Hepatic mTORC1 Opposes Impaired Insulin Action to Control Mitochondrial Metabolism in Obesity.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- mTORC1-TFEB/TFE3 signaling is associated with bile acid diversification during hepatic metabolic adaptation.Science advances · 2026Article
- Mammalian aging involves genome-wide splicing degeneration leading to functional decline.bioRxiv : the preprint server for biology · 2026Article
- Hepatic malonyl-CoA synthesis restrains gluconeogenesis by suppressing fat oxidation, pyruvate carboxylation, and amino acid availability.Cell metabolism · 2024Article
- mTORC1 controls murine postprandial hepatic glycogen synthesis via Ppp1r3b.The Journal of clinical investigation · 2024Article
- S100A9 exerts insulin-independent antidiabetic and anti-inflammatory effects.Science advances · 2024Article
- Persistent fasting lipogenesis links impaired ketogenesis with citrate synthesis in humans with nonalcoholic fatty liver.The Journal of clinical investigation · 2023Observational
- Role of NLRP3 inflammasome and oxidative stress in hepatic insulin resistance and the ameliorative effect of phytochemical intervention.Frontiers in pharmacology · 2023Review
- Pharmacological inhibition of Lin28 promotes ketogenesis and restores lipid homeostasis in models of non-alcoholic fatty liver disease.Nature communications · 2022Article
- Hepatic non-parenchymal S100A9-TLR4-mTORC1 axis normalizes diabetic ketogenesis.Nature communications · 2022Article
- Emerging Role of Hepatic Ketogenesis in Fatty Liver Disease.Frontiers in physiology · 2022Review
- Rheb Promotes Triglyceride Secretion and Ameliorates Diet-Induced Steatosis in the Liver.Frontiers in cell and developmental biology · 2022Article
- Crosstalk between beta-adrenergic and insulin signaling mediates mechanistic target of rapamycin hyperactivation in liver of high-fat diet-fed male mice.Physiological reports · 2021Article
- In Vivo Estimation of Ketogenesis Using Metabolic Flux Analysis-Technical Aspects and Model Interpretation.Metabolites · 2021Article
- Role of exercise and rapamycin on the expression of energy metabolism genes in liver tissues of rats fed a high‑fat diet.Molecular medicine reports · 2020Article
- Partial impairment of insulin receptor expression mimics fasting to prevent diet-induced fatty liver disease.Nature communications · 2020Article
- Amyloid-beta impairs insulin signaling by accelerating autophagy-lysosomal degradation of LRP-1 and IR-β in blood-brain barrier endothelial cells in vitro and in 3XTg-AD mice.Molecular and cellular neurosciences · 2019Article
- Impaired ketogenesis and increased acetyl-CoA oxidation promote hyperglycemia in human fatty liver.JCI insight · 2019Observational
- Concurrent activation of growth factor and nutrient arms of mTORC1 induces oxidative liver injury.Cell discovery · 2019Article
- Inactivating hepatic follistatin alleviates hyperglycemia.Nature medicine · 2018Article
- DEPTOR at the Nexus of Cancer, Metabolism, and Immunity.Physiological reviews · 2018Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Dysregulated mitochondrial metabolism during hepatic insulin resistance may contribute to pathophysiologies ranging from elevated glucose production to hepatocellular oxidative stress and inflammation. Given that obesity impairs insulin action but paradoxically activates mTORC1, we tested whether insulin action and mammalian target of rapamycin complex 1 (mTORC1) contribute to altered in vivo hepatic mitochondrial metabolism. Loss of hepatic insulin action for 2 weeks caused increased gluconeogenesis, mitochondrial anaplerosis, tricarboxylic acid (TCA) cycle oxidation, and ketogenesis. However, activation of mTORC1, induced by the loss of hepatic Tsc1, suppressed these fluxes. Only glycogen synthesis was impaired by both loss of insulin receptor and mTORC1 activation. Mice with a double knockout of the insulin receptor and Tsc1 had larger livers, hyperglycemia, severely impaired glycogen storage, and suppressed ketogenesis, as compared to those with loss of the liver insulin receptor alone. Thus, activation of hepatic mTORC1 opposes the catabolic effects of impaired insulin action under some nutritional states.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.