ArticleFrontiers in endocrinology2022
Sustained high glucose intake accelerates type 1 diabetes in NOD mice.
Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Diet, gut microbiome, and type 1 diabetes: from risk to translational opportunity.Gut microbes · 2026Review
- Experimental models in diabetes research.Laboratory animal research · 2026Review
- 3. Prevention or Delay of Diabetes and Associated Comorbidities: Standards of Care in Diabetes-2026.Diabetes care · 2026Review
- 3. Prevention or Delay of Diabetes and Associated Comorbidities: Standards of Care in Diabetes-2025.Diabetes care · 2025Review
- Autoimmune pathogenesis of gestational diabetes mellitus: the risk of progression to type 1 diabetes mellitus.Frontiers in endocrinology · 2025Review
- Immunopeptidome mining reveals a novel ERS-induced target in T1D.Cellular & molecular immunology · 2024Article
- 3. Prevention or Delay of Diabetes and Associated Comorbidities: Standards of Care in Diabetes-2024.Diabetes care · 2024Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Epidemiological studies have suggested that dietary factors, especially high consumption of high glycaemic index carbohydrates and sugars, may trigger or exacerbate the progression of type 1 diabetes. We aimed to provide experimental evidence to confirm this relevance and to explore the underlying mechanisms. Methods: NOD mice were given sustained high-glucose drinking or glucose-free water and observed for the incidence of type 1 diabetes and islet inflammation. RNAseq was performed to detect the transcriptome changes of the NOD islet beta cell line NIT-1 after high glucose treatment, and mass spectrometry was performed to detect the proteome changes of NIT-1-cells-derived sEVs. Results: Sustained high glucose drinking significantly aggravates islet inflammation and accelerates the onset of type 1 diabetes in NOD mice. Mechanistically, high glucose treatment induces aberrant ER stress and up-regulates the expression of autoantigens in islet beta cell. Moreover, high glucose treatment alters the proteome of beta-cells-derived sEVs, and significantly enhances the ability of sEVs to promote DC maturation and stimulate immune inflammatory response. Discussion: This study provides evidence for negative effect of high glucose intake as a dietary factor on the pathogenesis of type 1 diabetes in genetically predisposed individuals. Therefore, avoiding high sugar intake may be an effective disease prevention strategy for children or adults susceptible to type 1 diabetes.
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