ArticleNature communications2020
O-GlcNAc transferase inhibits visceral fat lipolysis and promotes diet-induced obesity.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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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
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Who cites it
53 citing papers in PubMed, 97 citations in OpenAlex.
- Sweetening the bonds: how O-GlcNAcylation modulates cell adhesion.Acta pharmacologica Sinica · 2026Review
- Chemical biology tools for the O-GlcNAc modification: Determining systems-level functions and druggability.Current opinion in chemical biology · 2026Review
- Glycosylation modification: a trigger for obesity and its complications?Molecular medicine (Cambridge, Mass.) · 2026Review
- Dammarenediol II enhances etoposide-induced apoptosis by targeting O-GlcNAc transferase and Akt/GSK3β/mTOR signaling in liver cancer.Molecular oncology · 2026Article
- PKCβ II antagonizes O-GlcNAcylated FOXO4 and inhibits lipid synthesis.Apoptosis : an international journal on programmed cell death · 2026Article
- O-GlcNAcylation regulates PPAR-driven metabolic programming in intestinal stem cells.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic Changes Associated With Obesity-related Metabolic Comorbidities.Journal of the Endocrine Society · 2025Review
- Protein O-GlcNAcylation in reproductive biology and the impact of metabolic disease.Human reproduction update · 2025Review
- Crosstalk between O-GlcNAcylation and phosphorylation in metabolism: regulation and mechanism.Cell death and differentiation · 2025Review
- Increased O-GlcNAcylation in Leukocytes from Overweight Pediatric Subjects: A Pilot Study.International journal of molecular sciences · 2025Article
- Adipocytes regulate monocyte development through the OGT-NEFA-CD36/FABP4 pathway in high-fat diet-induced obesity.Cell death & disease · 2025Article
- Unraveling the Link Between Obesity and Keratoconus Risk Based on Genetic Evidence.Translational vision science & technology · 2025Article
- Association between O-GlcNAc transferase activity and major adverse cardiovascular events: findings from the China PEACE-MPP cohort.BMC cardiovascular disorders · 2025Article
- Structural glycobiology - from enzymes to organelles.Biochemical Society transactions · 2025Review
- O-linked β-N-acetylglucosamine modification in diabetic foot ulcer pathogenesis.Burns & trauma · 2025Review
- Male Wistar Rats Chronically Fed with a High-Fat Diet Develop Inflammatory and Ionic Transport Angiotensin-(3-4)-Sensitive Myocardial Lesions but Preserve Echocardiographic Parameters.International journal of molecular sciences · 2024Article
- Protein O-GlcNAcylation coupled to Hippo signaling drives vascular dysfunction in diabetic retinopathy.Nature communications · 2024Article
- Glycosylation: mechanisms, biological functions and clinical implications.Signal transduction and targeted therapy · 2024Review
- Association between serum vitamin C and body mass index in adolescents aged 12-19 years.BMC public health · 2024Article
- Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Excessive visceral fat accumulation is a primary risk factor for metabolically unhealthy obesity and related diseases. The visceral fat is highly susceptible to the availability of external nutrients. Nutrient flux into the hexosamine biosynthetic pathway leads to protein posttranslational modification by O-linked β-N-acetylglucosamine (O-GlcNAc) moieties. O-GlcNAc transferase (OGT) is responsible for the addition of GlcNAc moieties to target proteins. Here, we report that inducible deletion of adipose OGT causes a rapid visceral fat loss by specifically promoting lipolysis in visceral fat. Mechanistically, visceral fat maintains a high level of O-GlcNAcylation during fasting. Loss of OGT decreases O-GlcNAcylation of lipid droplet-associated perilipin 1 (PLIN1), which leads to elevated PLIN1 phosphorylation and enhanced lipolysis. Moreover, adipose OGT overexpression inhibits lipolysis and promotes diet-induced obesity. These findings establish an essential role for OGT in adipose tissue homeostasis and indicate a unique potential for targeting O-GlcNAc signaling in the treatment of obesity.
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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.