ArticleCellular signalling2016
Glucosamine induces REDD1 to suppress insulin action in retinal Müller cells.
Article in Cellular signalling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Excessive glycosylation drives thoracic aortic aneurysm formation through integrated stress response.European heart journal · 2025Article
- DDIT4 participates in high glucose-induced fibroblast-like synoviocytes overactivation and cartilage injury by regulating glycolysis.Regenerative therapy · 2025Article
- Therapeutic targets in diabetic peripheral neuropathy: heat shock proteins.Frontiers in endocrinology · 2025Review
- A genome-wide scan of non-coding RNAs and enhancers for refractive error and myopia.Human genetics · 2025Article
- Hyperglycemia and Oxidative Stress: An Integral, Updated and Critical Overview of Their Metabolic Interconnections.International journal of molecular sciences · 2023Review
- Review
- Pathogenesis and Molecular Treatment Strategies of Diabetic Neuropathy Collateral Glucose-Utilizing Pathways in Diabetic Polyneuropathy.International journal of molecular sciences · 2020Review
- Role of glucosamine in development of diabetic neuropathy independent of the aldose reductase pathway.Brain communications · 2020Article
- Glucosamine inhibits IL-1β expression by preserving mitochondrial integrity and disrupting assembly of the NLRP3 inflammasome.Scientific reports · 2019Article
- Is REDD1 a Metabolic Éminence Grise?Trends in endocrinology and metabolism: TEM · 2016Review
- NGBR is required to ameliorate type 2 diabetes in mice by enhancing insulin sensitivity.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Resistance to insulin action is a key cause of diabetic complications, yet much remains unknown about the molecular mechanisms that contribute to the defect. Glucose-induced insulin resistance in peripheral tissues such as the retina is mediated in part by the hexosamine biosynthetic pathway (HBP). Glucosamine (GAM), a leading dietary supplement marketed to relieve the discomfort of osteoarthritis, is metabolized by the HBP, and in doing so bypasses the rate-limiting enzyme of the pathway. Thus, exogenous GAM consumption potentially exacerbates the resistance to insulin action observed with diabetes-induced hyperglycemia. In the present study, we evaluated the effect of GAM on insulin action in retinal Müller cells in culture. Addition of GAM to Müller cell culture repressed insulin-induced activation of the Akt/mTORC1 signaling pathway. However, the effect was not recapitulated by chemical inhibition to promote protein O-GlcNAcylation, nor was blockade of O-GlcNAcylation sufficient to prevent the effects of GAM. Instead, GAM induced ER stress and subsequent expression of the protein Regulated in DNA Damage and Development (REDD1), which was necessary for GAM to repress insulin-stimulated phosphorylation of Akt on Thr308. Overall, the findings support a model whereby GAM promotes ER stress in retinal Müller cells, resulting in elevated REDD1 expression and thus resistance to insulin action.
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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.