ArticleThe Journal of biological chemistry2015
Conditional knock-out reveals a requirement for O-linked N-Acetylglucosaminase (O-GlcNAcase) in metabolic homeostasis.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.
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Who cites it
95 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The human O-GlcNAcome database and meta-analysis.Scientific data · 2021Pooled it
- PerturbingCells · 2026Article
- O-GlcNAcase promotes dendritic spine morphogenesis while downregulating their GluA2-containing AMPA receptors.The Journal of biological chemistry · 2026Article
- Discovery of Sennoside A as a NaturalResearch (Washington, D.C.) · 2026Article
- Human O-GlcNAcase catalytic-stalk dimer anchors flexible histone binding domains.Communications chemistry · 2025Article
- Zscan4 as a Candidate Conveyor of Early Developmental Defects in O-GlcNAc Transferase Intellectual Disability.Molecular & cellular proteomics : MCP · 2025Article
- Protein O-GlcNAcylation in reproductive biology and the impact of metabolic disease.Human reproduction update · 2025Review
- O-GlcNAcylation promotes angiogenic transdifferentiation to reverse vascular ischemia.Nature cardiovascular research · 2025Article
- Brain O-GlcNAcylation: Bridging physiological functions, disease mechanisms, and therapeutic applications.Molecular psychiatry · 2025Review
- HumanResearch square · 2025Article
- The post-translational modification O-GlcNAc is a sensor and regulator of metabolism.Open biology · 2024Review
- O-GlcNAcase regulates pluripotency states of human embryonic stem cells.Stem cell reports · 2024Article
- Article
- Neurodevelopmental defects in a mouse model of O-GlcNAc transferase intellectual disability.Disease models & mechanisms · 2024Article
- Understanding and exploiting the roles of O-GlcNAc in neurodegenerative diseases.The Journal of biological chemistry · 2023Review
- The O-GlcNAc dichotomy: when does adaptation become pathological?Clinical science (London, England : 1979) · 2023Review
- Article
- O-GlcNAcylation regulates neurofilament-light assembly and function and is perturbed by Charcot-Marie-Tooth disease mutations.Nature communications · 2023Article
- Sustained Increases in Cardiomyocyte ProteinJournal of the American Heart Association · 2023Article
- An O-GlcNAc transferase pathogenic variant linked to intellectual disability affects pluripotent stem cell self-renewal.Disease models & mechanisms · 2023Article
35 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors.
Funding
Abstract
O-GlcNAc cycling is maintained by the reciprocal activities of the O-GlcNAc transferase and the O-GlcNAcase (OGA) enzymes. O-GlcNAc transferase is responsible for O-GlcNAc addition to serine and threonine (Ser/Thr) residues and OGA for its removal. Although the Oga gene (MGEA5) is a documented human diabetes susceptibility locus, its role in maintaining insulin-glucose homeostasis is unclear. Here, we report a conditional disruption of the Oga gene in the mouse. The resulting homozygous Oga null (KO) animals lack OGA enzymatic activity and exhibit elevated levels of the O-GlcNAc modification. The Oga KO animals showed nearly complete perinatal lethality associated with low circulating glucose and low liver glycogen stores. Defective insulin-responsive GSK3β phosphorylation was observed in both heterozygous (HET) and KO Oga animals. Although Oga HET animals were viable, they exhibited alterations in both transcription and metabolism. Transcriptome analysis using mouse embryonic fibroblasts revealed deregulation in the transcripts of both HET and KO animals specifically in genes associated with metabolism and growth. Additionally, metabolic profiling showed increased fat accumulation in HET and KO animals compared with WT, which was increased by a high fat diet. Reduced insulin sensitivity, glucose tolerance, and hyperleptinemia were also observed in HET and KO female mice. Notably, the respiratory exchange ratio of the HET animals was higher than that observed in WT animals, indicating the preferential utilization of glucose as an energy source. These results suggest that the loss of mouse OGA leads to defects in metabolic homeostasis culminating in obesity and insulin resistance.
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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.