ArticleThe Journal of biological chemistry2019
Inhibition of mitochondrial complex 1 by the S6K1 inhibitor PF-4708671 partly contributes to its glucose metabolic effects in muscle and liver cells.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Metabolic checkpoints in the regulation of Th17 cells: implications for uveitis pathogenesis and therapy.Frontiers in immunology · 2026Review
- Article
- Camel milk exosomes regulate glucose metabolism by inhibiting mitochondrial complex I in hepatocytes.BMC veterinary research · 2025Article
- Characterization of novel anoikis-related genes as prognostic biomarkers and key determinants of the immune microenvironment in esophageal cancer.Frontiers in immunology · 2025Article
- The Influence of Metabolism on Immune Response: A Journey to Understand Immunometabolism in the Context of Viral Infection.Viruses · 2023Review
- Breast adipose tissue-derived extracellular vesicles from obese women alter tumor cell metabolism.EMBO reports · 2023Article
- PPM1H is down-regulated by ATF6 and dephosphorylates p-RPS6KB1 to inhibit progression of hepatocellular carcinoma.Molecular therapy. Nucleic acids · 2023Article
- Common Genetic Aberrations Associated with Metabolic Interferences in Human Type-2 Diabetes and Acute Myeloid Leukemia: A Bioinformatics Approach.International journal of molecular sciences · 2021Article
- Inhibition of Mitochondrial Respiration Impairs Nutrient Consumption and Metabolite Transport in Human Retinal Pigment Epithelium.Journal of proteome research · 2021Article
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
mTOR complex 1 (mTORC1) and p70 S6 kinase (S6K1) are both involved in the development of obesity-linked insulin resistance. Recently, we showed that the S6K1 inhibitor PF-4708671 (PF) increases insulin sensitivity. However, we also reported that PF can increase glucose metabolism even in the absence of insulin in muscle and hepatic cells. Here we further explored the potential mechanisms by which PF increases glucose metabolism in muscle and liver cells independent of insulin. Time course experiments revealed that PF induces AMP-activated protein kinase (AMPK) activation before inhibiting S6K1. However, PF-induced glucose uptake was not prevented in primary muscle cells from AMPK α1/2 double KO (dKO) mice. Moreover, PF-mediated suppression of hepatic glucose production was maintained in hepatocytes derived from AMPK α1/2-dKO mice. Remarkably, PF could still reduce glucose production and activate AMPK in hepatocytes from S6K1/2 dKO mice. Mechanistically, bioenergetics experiments revealed that PF reduces mitochondrial complex I activity in both muscle and hepatic cells. The stimulatory effect of PF on glucose uptake was partially reduced by expression of the
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