ArticleBMJ open diabetes research & care2020
Acute and chronic neuroinflammation is triggered by diabetic ketoacidosis in a rat model.
Article in BMJ open diabetes research & care, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Effects of diabetes on microglial physiology: a systematic review of in vitro, preclinical and clinical studies.Journal of neuroinflammation · 2023Pooled it
- The Impact of Diabetes on Brain Health in Childhood.Biomedicines · 2026Review
- Association of cerebrovascular disease with adverse outcomes in patients with diabetic ketoacidosis.Endocrine connections · 2026Article
- Sex Differences in the Association Between Disease Complications and Markers of Oxidative Stress in Type 2 Diabetes Mellitus: A Cross-Sectional Study.Health science reports · 2026Article
- Extracellular(Serum) Levels of Matrix Metalloproteinases in Pediatric Type 1 Diabetes Mellitus and Association with Diabetic Ketoacidosis and Cerebral Edema.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Systemic Inflammatory Response Index (SIRI) as a Predictive Marker for Adverse Outcomes in Children with New-Onset Type 1 Diabetes Mellitus.Journal of clinical medicine · 2024Article
- Article
- Correlation between Neutrophil-to-Lymphocyte Ratio and Cerebral Edema in Children with Severe Diabetic Ketoacidosis.Biomedicines · 2023Article
- Diabetes and associated cognitive disorders: Role of the Hypothalamic-Pituitary Adrenal axis.Metabolism open · 2022Review
- Corresponding risk factors between cognitive impairment and type 1 diabetes mellitus: A narrative review.Heliyon · 2022Review
- The Importance of CXCL1 in the Physiological State and in Noncancer Diseases of the Oral Cavity and Abdominal Organs.International journal of molecular sciences · 2022Review
- Effects of TRAM-34 and minocycline on neuroinflammation caused by diabetic ketoacidosis in a rat model.BMJ open diabetes research & care · 2022Article
- Diabetic ketoacidosis causes chronic elevation in renal C-C motif chemokine ligand 5.Endocrine · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionCognitive decline is common in patients with type 1 diabetes and has been attributed to the effects of chronic hyperglycemia and severe hypoglycemia. Diabetic ketoacidosis (DKA) has only recently been suspected to be involved in causing cognitive decline. We hypothesized that DKA triggers both acute and chronic neuroinflammation, contributing to brain injury. RESEARCH METHODS AND
designWe measured concentrations of cytokines, chemokines and matrix metalloproteinases (MMP) in serum and brain tissue lysates in juvenile rats during and after DKA (during acute DKA, 24 hours and 7 days after DKA), and compared these to healthy controls and hyperglycemic controls. We also measured cytokine, chemokine and MMP concentrations in serum and brain tissue of adult rats (70 days) that had experienced DKA as juveniles and compared these measurements to those of adult diabetic rats without exposure to DKA.
resultsDuring acute DKA in the juvenile rats, serum concentrations of CCL3, tumor necrosis factor (TNF)-α, interleukin (IL)-1ß and MMP-9 were significantly increased. Serum concentrations of IL-2 and IL-17A increased 7 days after DKA recovery. In brain tissue lysates, concentrations of CCL3, CCL5, interferon (IFN)-γ and MMP-9 were significantly elevated during acute DKA. In adult rats that had DKA as juveniles (28 days previously), serum concentrations of IL-1ß and brain concentrations of IL-10 and IL-12p70 were elevated in comparison to diabetic rats without prior DKA. Composite scores for highly correlated cytokines and chemokines (mean z-scores for IL-10, IL-1ß, TNF-α, IL-17A, IFN-γ, CXCL-1 and CCL5) were also significantly elevated in adult rats with prior DKA.
conclusionsThese data confirm that DKA causes acute systemic inflammation and neuroinflammation in a rat model. Importantly, the neuroinflammatory response triggered by DKA is long-lasting, suggesting the possibility that DKA-induced chronic neuroinflammation could contribute to long-term cognitive decline in individuals with diabetes.
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