ArticleDiabetologia2015
Obesity resistance and increased energy expenditure by white adipose tissue browning in Oga(+/-) mice.
Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed.
- Evaluation of high-fat diet-induced metabolic impairments in iBAT lipid metabolism usingMagma (New York, N.Y.) · 2026Article
- Elevated O-GlcNAcylation Enhances Metabolic Rate and Reduces the Excitability of Hypothalamic ARC Neurons in 10-month-old Male Mice.Experimental neurobiology · 2025Article
- O-GlcNAc Modification Is a Promising Therapeutic Target for Diabetic Retinopathy.International journal of molecular sciences · 2024Article
- Neurodevelopmental defects in a mouse model of O-GlcNAc transferase intellectual disability.Disease models & mechanisms · 2024Article
- Article
- GPR19 Coordinates Multiple Molecular Aspects of Stress Responses Associated with the Aging Process.International journal of molecular sciences · 2023Article
- Posttranslational modifications in diabetes: Mechanisms and functions.Reviews in endocrine & metabolic disorders · 2022Review
- Protein O-GlcNAcylation and the regulation of energy homeostasis: lessons from knock-out mouse models.Journal of biomedical science · 2022Review
- Review
- Upregulated integrin α11 in the stroma of cutaneous squamous cell carcinoma promotes skin carcinogenesis.Frontiers in oncology · 2022Article
- A nexus of lipid andFrontiers in endocrinology · 2022Review
- Pancreatic β-cell hyper-O-GlcNAcylation leads to impaired glucose homeostasisFrontiers in endocrinology · 2022Article
- [Precise identification ofSe pu = Chinese journal of chromatography · 2021Article
- PPARγ and Diabetes: Beyond the Genome and Towards Personalized Medicine.Current diabetes reports · 2021Review
- Role ofPhysiological reviews · 2021Review
- New Insights Into the Biology of Protein O-GlcNAcylation: Approaches and Observations.Frontiers in aging · 2020Article
- Asperlin Stimulates Energy Expenditure and Modulates Gut Microbiota in HFD-Fed Mice.Marine drugs · 2019Article
- Critical observations that shaped our understanding of the function(s) of intracellular glycosylation (O-GlcNAc).FEBS letters · 2018Review
- O-GlcNAcylation: key regulator of glycolytic pathways.Journal of bioenergetics and biomembranes · 2018Review
- O-GlcNAc cycling in the developing, adult and geriatric brain.Journal of bioenergetics and biomembranes · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisO-GlcNAcylation plays a role as a metabolic sensor regulating cellular signalling, transcription and metabolism. Transcription factors and signalling pathways related to metabolism are modulated by N-acetyl-glucosamine (O-GlcNAc) modification. Aberrant regulation of O-GlcNAcylation is closely linked to insulin resistance, type 2 diabetes and obesity. Current evidence shows that increased O-GlcNAcylation negatively regulates insulin signalling, which is associated with insulin resistance and type 2 diabetes. Here, we aimed to evaluate the effects of Oga (also known as Mgea5) haploinsufficiency, which causes hyper-O-GlcNAcylation, on metabolism.
methodsWe examined whether Oga(+/-) mice developed insulin resistance. Metabolic variables were determined including body weight, glucose and insulin tolerance, metabolic rate and thermogenesis.
resultsOga deficiency does not affect insulin signalling even at hyper-O-GlcNAc levels. Oga(+/-) mice are lean with reduced fat mass and improved glucose tolerance. Furthermore, Oga(+/-) mice resist high-fat diet-induced obesity with ameliorated hepatic steatosis and improved glucose metabolism. Oga haploinsufficiency potentiates energy expenditure through the enhancement of brown adipocyte differentiation from the stromal vascular fraction of subcutaneous white adipose tissue (WAT). CONCLUSIONS/
interpretationOur observations suggest that O-GlcNAcase (OGA) is essential for energy metabolism via regulation of the thermogenic WAT program.
Indexed as
Identifiers
26342595What OpenQuestion holds
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.