ArticleThe Journal of nutrition2006
Rapamycin inhibits liver growth during refeeding in rats via control of ribosomal protein translation but not cap-dependent translation initiation.
Article in The Journal of nutrition, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 44 citations in OpenAlex.
- Mitochondrial ATP concentration decreases immediately after glucose administration to glucose-deprived hepatocytes.FEBS open bio · 2024Article
- Genome-Wide Identification, Evolution and Expression of the Complete Set of Cytoplasmic Ribosomal Protein Genes in Nile Tilapia.International journal of molecular sciences · 2020Article
- Regulation of fetal liver growth in a model of diet restriction in the pregnant rat.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Persistent effect of mTOR inhibition on preneoplastic foci progression and gene expression in a rat model of hepatocellular carcinoma.Carcinogenesis · 2016Article
- Profiling of the fetal and adult rat liver transcriptome and translatome reveals discordant regulation by the mechanistic target of rapamycin (mTOR).American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
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- Postnatal liver growth and regeneration are independent of c-myc in a mouse model of conditional hepatic c-myc deletion.BMC physiology · 2012Article
- Phosphoproteomic analysis of liver homogenates.Methods in molecular biology (Clifton, N.J.) · 2012Article
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- The physiology and pathophysiology of rapamycin resistance: implications for cancer.Cell cycle (Georgetown, Tex.) · 2011Article
- Resveratrol inhibits protein translation in hepatic cells.PloS one · 2011Article
- Phosphoproteomic profiling of in vivo signaling in liver by the mammalian target of rapamycin complex 1 (mTORC1).PloS one · 2011Article
- Rapamycin inhibits postprandial-mediated X-box-binding protein-1 splicing in rat liver.The Journal of nutrition · 2010Article
- Article
- The alpha4-containing form of protein phosphatase 2A in liver and hepatic cells.Journal of cellular biochemistry · 2008Article
- Hepatic translation control in the late-gestation fetal rat.American journal of physiology. Regulatory, integrative and comparative physiology · 2008Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We examined the role of the mammalian target of rapamycin (mTOR) in hepatic cell growth. To dissociate cell growth from cell proliferation, we employed an in vivo model of nonproliferative liver growth in rats, refeeding after 48 h of food deprivation. Starvation resulted in a decrease in liver mass, liver protein, and cell size, all of which were largely restored after 24 h of refeeding. Administration of the mTOR inhibitor, rapamycin, before the refeeding period partially inhibited the restoration of liver protein content. Refeeding was also associated with an increase in ribosomal protein S6 phosphorylation and phosphorylation of the eukaryotic initiation factor (eIF) 4E binding protein 1 (4E-BP1). 4E-BP1 phosphorylation was accompanied by a decrease in the abundance of the complex containing 4E-BP1 with eIF4E. These changes were prevented by rapamycin administration. However, association of eIF4E and eIF4G and eIF2alpha phosphorylation, both of which are stimulated by refeeding, were insensitive to rapamycin. The functional importance of these observations was confirmed by polysome fractionation, which showed that translation initiation of 5' oligopyrimidine tract-containing mRNAs, which encode ribosomal proteins, was inhibited by rapamycin, whereas translation of signal transducer and activator of transcription 1 (STAT1), a cap-dependent mRNA, was unaffected. The abundance of ribosomal proteins paralleled total protein content during refeeding in both control and rapamycin-injected rats. We conclude that accretion of liver protein during refeeding is dependent on mTOR-mediated activation of the translation of ribosomal proteins but not dependent on mTOR-mediated activation of cap-dependent translation initiation.
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