ArticleMolecular endocrinology (Baltimore, Md.)2013
Activation of basal gluconeogenesis by coactivator p300 maintains hepatic glycogen storage.
Article in Molecular endocrinology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Review
- Blocking AMPKαS496 phosphorylation improves mitochondrial dynamics and hyperglycemia in aging and obesity.Cell chemical biology · 2023Article
- Regulation of Liver Glucose and Lipid Metabolism by Transcriptional Factors and Coactivators.Life (Basel, Switzerland) · 2023Review
- Hepatic transcriptional responses to fasting and feeding.Genes & development · 2021Review
- Glucagon's Metabolic Action in Health and Disease.Comprehensive Physiology · 2021Article
- Alterations of Gut Microbiota by Overnutrition Impact Gluconeogenic Gene Expression and Insulin Signaling.International journal of molecular sciences · 2021Review
- The importance of the AMPK gamma 1 subunit in metformin suppression of liver glucose production.Scientific reports · 2020Article
- Glucagon-Induced Acetylation of Energy-Sensing Factors in Control of Hepatic Metabolism.International journal of molecular sciences · 2019Review
- The depot-specific and essential roles of CBP/p300 in regulating adipose plasticity.The Journal of endocrinology · 2019Article
- p300/CBP as a Key Nutritional Sensor for Hepatic Energy Homeostasis and Liver Fibrosis.BioMed research international · 2018Review
- Article
- Endotoxemia-mediated activation of acetyltransferase P300 impairs insulin signaling in obesity.Nature communications · 2017Article
- Acetylation of glucokinase regulatory protein decreases glucose metabolism by suppressing glucokinase activity.Scientific reports · 2015Article
- Role of transcription factor acetylation in the regulation of metabolic homeostasis.Protein & cell · 2015Review
- p300 Regulates Liver Functions by Controlling p53 and C/EBP Family Proteins through Multiple Signaling Pathways.Molecular and cellular biology · 2015Article
- Metformin activates AMP-activated protein kinase by promoting formation of the αβγ heterotrimeric complex.The Journal of biological chemistry · 2015Article
- Low concentrations of metformin suppress glucose production in hepatocytes through AMP-activated protein kinase (AMPK).The Journal of biological chemistry · 2014Article
- Potential biomarker of metformin action.The Journal of endocrinology · 2014Article
- Control of Foxo1 gene expression by co-activator P300.The Journal of biological chemistry · 2014Article
- Genetic, epigenetic, and environmental contributions to neural tube closure.Annual review of genetics · 2014Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Because hepatic glycogenolysis maintains euglycemia during early fasting, proper hepatic glycogen synthesis in the fed/postprandial states is critical. It has been known for decades that gluconeogenesis is essential for hepatic glycogen synthesis; however, the molecular mechanism remains unknown. In this report, we show that depletion of hepatic p300 reduces glycogen synthesis, decreases hepatic glycogen storage, and leads to relative hypoglycemia. We previously reported that insulin suppressed gluconeogenesis by phosphorylating cAMP response element binding protein-binding protein (CBP) at S436 and disassembling the cAMP response element-binding protein-CBP complex. However, p300, which is closely related to CBP, lacks the corresponding S436 phosphorylation site found on CBP. In a phosphorylation-competent p300G422S knock-in mouse model, we found that mutant mice exhibited reduced hepatic glycogen content and produced significantly less glycogen in a tracer incorporation assay in the postprandial state. Our study demonstrates the important and unique role of p300 in glycogen synthesis through maintaining basal gluconeogenesis.
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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.