ArticleScientific reports2015
Paradoxical effect of rapamycin on inflammatory stress-induced insulin resistance in vitro and in vivo.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
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- Mechanism of TNFα-induced downregulation of salt-inducible kinase 2 in adipocytes.Scientific reports · 2023Article
- The Role of mTOR Inhibitors after Liver Transplantation for Hepatocellular Carcinoma.Current oncology (Toronto, Ont.) · 2023Review
- AMPK hyperactivation promotes dendrite retraction, synaptic loss, and neuronal dysfunction in glaucoma.Molecular neurodegeneration · 2021Article
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- In vitro toxicity model: Upgrades to bridge the gap between preclinical and clinical research.Bosnian journal of basic medical sciences · 2020Review
- Nutrient Sensor mTOR and OGT: Orchestrators of Organelle Homeostasis in PancreaticJournal of diabetes research · 2020Review
- Article
- Bidirectional modulation of insulin action by reactive oxygen species in 3T3‑L1 adipocytes.Molecular medicine reports · 2018Article
- mTOR complexes differentially orchestrates eosinophil development in allergy.Scientific reports · 2018Article
- Airborne PMInternational journal of environmental research and public health · 2017Article
- Cancer, obesity, diabetes, and antidiabetic drugs: is the fog clearing?Nature reviews. Clinical oncology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin resistance is closely related to inflammatory stress and the mammalian target of rapamycin/S6 kinase (mTOR/S6K) pathway. The present study investigated whether rapamycin, a specific inhibitor of mTOR, ameliorates inflammatory stress-induced insulin resistance in vitro and in vivo. We used tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) stimulation in HepG2 hepatocytes, C2C12 myoblasts and 3T3-L1 adipocytes and casein injection in C57BL/6J mice to induce inflammatory stress. Our results showed that inflammatory stress impairs insulin signaling by reducing the expression of total IRS-1, p-IRS-1 (tyr632), and p-AKT (ser473); it also activates the mTOR/S6K signaling pathway both in vitro and in vivo. In vitro, rapamycin treatment reversed inflammatory cytokine-stimulated IRS-1 serine phosphorylation, increased insulin signaling to AKT and enhanced glucose utilization. In vivo, rapamycin treatment also ameliorated the impaired insulin signaling induced by inflammatory stress, but it induced pancreatic β-cell apoptosis, reduced pancreatic β-cell function and enhanced hepatic gluconeogenesis, thereby resulting in hyperglycemia and glucose intolerance in casein-injected mice. Our results indicate a paradoxical effect of rapamycin on insulin resistance between the in vitro and in vivo environments under inflammatory stress and provide additional insight into the clinical application of rapamycin.
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