ArticleThe Journal of clinical investigation2024
mTORC1 controls murine postprandial hepatic glycogen synthesis via Ppp1r3b.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 9 citations in OpenAlex.
- mTORC1-TFEB/TFE3 signaling is associated with bile acid diversification during hepatic metabolic adaptation.Science advances · 2026Article
- Acute high-protein feeding induces hepatic amino acid accumulation in diabetic male mice prior to transcriptional adaptation.Physiological reports · 2026Article
- Acute AKT signaling increases glucose phosphorylation and contribution to glycogen in hepatocytes.iScience · 2026Article
- SUCNR1 coordinates metabolic flux, mitochondrial function, and nutrient-dependent adaptation in hepatocytes.Science advances · 2026Article
- Article
- Hepatocyte nuclear factors dynamically regulate triglyceride metabolic reprogramming in metabolic dysfunction-associated steatotic liver disease: Mechanisms and implications.World journal of hepatology · 2025Review
- Promoter H3K4me3 and Gene Expression Involved in Systemic Metabolism Are Altered in Fetal Calf Liver of Nutrient-Restricted Dams.International journal of molecular sciences · 2025Article
- Review
- Transcriptomic and epigenomic signatures of liver metabolism and insulin sensitivity in aging mice.Mechanisms of ageing and development · 2025Article
- Article
- Article
- LRP1 facilitates hepatic glycogenesis by improving the insulin signaling pathway in HFD-fed mice.Animal models and experimental medicine · 2024Article
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Authors and funding
13 authors at 5 institutions in 7 countries.
Funding
Abstract
In response to a meal, insulin drives hepatic glycogen synthesis to help regulate systemic glucose homeostasis. The mechanistic target of rapamycin complex 1 (mTORC1) is a well-established insulin target and contributes to the postprandial control of liver lipid metabolism, autophagy, and protein synthesis. However, its role in hepatic glucose metabolism is less understood. Here, we used metabolomics, isotope tracing, and mouse genetics to define a role for liver mTORC1 signaling in the control of postprandial glycolytic intermediates and glycogen deposition. We show that mTORC1 is required for glycogen synthase activity and glycogenesis. Mechanistically, hepatic mTORC1 activity promotes the feeding-dependent induction of Ppp1r3b, a gene encoding a phosphatase important for glycogen synthase activity whose polymorphisms are linked to human diabetes. Reexpression of Ppp1r3b in livers lacking mTORC1 signaling enhances glycogen synthase activity and restores postprandial glycogen content. mTORC1-dependent transcriptional control of Ppp1r3b is facilitated by FOXO1, a well characterized transcriptional regulator involved in the hepatic response to nutrient intake. Collectively, we identify a role for mTORC1 signaling in the transcriptional regulation of Ppp1r3b and the subsequent induction of postprandial hepatic glycogen synthesis.
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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.