ArticleLife sciences2012
Chronic ingestion of a Western diet increases O-linked-β-N-acetylglucosamine (O-GlcNAc) protein modification in the rat heart.
Article in Life sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 47 citations in OpenAlex.
- Exploring the metabolic signaling network of GFPT in cancer.Cell death discovery · 2025Review
- Human Pulmonary Artery Endothelial Cells Increased Glycolysis and Decreased Nitric Oxide Synthase O-GlcNAcylation in Pulmonary Arterial Hypertension.International journal of translational medicine (Basel, Switzerland) · 2024Article
- Diet-inducing hypercholesterolemia show decreased O-GlcNAcylation of liver proteins through modulation of AMPK.Journal of physiology and biochemistry · 2024Article
- An O-GlcNAc transferase pathogenic variant linked to intellectual disability affects pluripotent stem cell self-renewal.Disease models & mechanisms · 2023Article
- The O-GlcNAc cycling in neurodevelopment and associated diseases.Biochemical Society transactions · 2022Review
- The dual role of the hexosamine biosynthetic pathway in cardiac physiology and pathophysiology.Frontiers in endocrinology · 2022Review
- Laminar Flow on Endothelial Cells Suppresses eNOS O-GlcNAcylation to Promote eNOS Activity.Circulation research · 2021Article
- CaMKII Inhibition is a Novel Therapeutic Strategy to Prevent Diabetic Cardiomyopathy.Frontiers in pharmacology · 2021Review
- Article
- Islet O-GlcNAcylation Is Required for Lipid Potentiation of Insulin Secretion through SERCA2.Cell reports · 2020Article
- Regulatory Effects of O-GlcNAcylation in Vascular Smooth Muscle Cells on Diabetic Vasculopathy.Journal of lipid and atherosclerosis · 2020Review
- Temporal Measures in Cardiac Structure and Function During the Development of Obesity Induced by Different Types of Western Diet in a Rat Model.Nutrients · 2019Article
- Metabolic Stress and Cardiovascular Disease in Diabetes Mellitus: The Role of ProteinArteriosclerosis, thrombosis, and vascular biology · 2019Review
- O-GlcNAc Transferase Promotes Compensated Cardiac Function and Protein Kinase A O-GlcNAcylation During Early and Established Pathological Hypertrophy From Pressure Overload.Journal of the American Heart Association · 2019Article
- Hyper-O-GlcNAcylation promotes epithelial-mesenchymal transition in endometrial cancer cells.Oncotarget · 2019Article
- Article
- Consumption of a high fat diet promotes protein O-GlcNAcylation in mouse retina via NR4A1-dependent GFAT2 expression.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
- A Crude 1-DNJ Extract from Home Made Bombyx Batryticatus Inhibits Diabetic Cardiomyopathy-Associated Fibrosis in db/db Mice and Reduces ProteinInternational journal of molecular sciences · 2018Article
- IncreasedFrontiers in physiology · 2018Article
- Chronic O-GlcNAcylation and Diabetic Cardiomyopathy: The Bitterness of Glucose.Frontiers in endocrinology · 2018Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
aimsProtein O-GlcNAcylation is both a nutrient sensing and cellular stress response that mediates signal transduction in the heart. Chronically elevated O-GlcNAc has been associated with the development of cardiac dysfunction at both the cellular and organ levels in obesity, insulin resistance and diabetes. Development of these pathologies is often attributed to diets high in saturated fat and sugar (a "Western" diet; WES) but a role for O-GlcNAc in diet-induced cardiac dysfunction has not been established. The aims of this study were to examine the effect of chronic consumption of WES on cardiac O-GlcNAcylation and investigate associations of O-GlcNAc with cardiac function and markers of cellular stress. MAIN
methodsYoung male rats received either a control diet (CON; n=9) or WES (n=8) diet for 52 weeks. KEY
findingsThere was no evidence of cardiac dysfunction, advanced glycation endproduct (AGE) accumulation, pathological cardiac hypertrophy, calcium handling impairment, fibrosis or endoplasmic reticulum stress in WES hearts. However, cardiac O-GlcNAc protein, particularly in the higher molecular weight range, was significantly higher in WES hearts compared to CON (P<0.05). Protein levels of the enzymes that regulate O-GlcNAc attachment were not different between groups; thus, the increased O-GlcNAcylation in WES hearts appears to be due to increased nutrient availability rather than enzymatic regulation of cellular stress. SIGNIFICANCE: These data suggest that diets high in saturated fat and sugar may contribute to the adverse effects of metabolic syndrome and diabetes by an O-GlcNAc-mediated process and that this may occur in the absence of overt cellular stress.
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Registered trials
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