ArticleBMJ open diabetes research & care2020
Iron overload is related to elevated blood glucose levels in obese children and aggravates high glucose-induced endothelial cell dysfunction in vitro.
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 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Moderate iron restriction improves metabolism via epigenetic regulation of GDF15.The Journal of nutritional biochemistry · 2026Article
- Crosstalk between autophagy and ferroptosis in diabetes.Genes & diseases · 2026Review
- Proteomics-Based Exploration of the Hepatoprotective Mechanism of α-Lipoic Acid in Rats with Iron Overload-Induced Liver Injury.International journal of molecular sciences · 2025Article
- Repair and regeneration: ferroptosis in the process of remodeling and fibrosis in impaired organs.Cell death discovery · 2024Review
- Association between iron profile status and insulin resistance in patients with type 2 diabetes mellitus.Journal of diabetes and metabolic disorders · 2023Article
- Ferritin But Not Iron Increases in Retina Upon Systemic Iron Overload in Diabetic and Iron-Dextran Injected Mice.Investigative ophthalmology & visual science · 2023Article
- Pea protein hydrolysate reduces blood glucose in high-fat diet and streptozotocin-induced diabetic mice.Frontiers in nutrition · 2023Article
- Acute iron overload aggravates blood-brain barrier disruption and hemorrhagic transformation after transient focal ischemia in rats with hyperglycemia.IBRO neuroscience reports · 2022Article
- Oxidative Stress and Lipid Peroxidation: Prospective Associations Between Ferroptosis and Delayed Wound Healing in Diabetic Ulcers.Frontiers in cell and developmental biology · 2022Review
- Article
- Oxidative stress and programmed cell death in diabetic wounds: A comprehensive review.Science progressReview
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThis study was performed to investigate the role of iron overload in the early stage of hyperglycemia-induced vascular functional impairment. RESEARCH DESIGN AND
methodsA total of 196 obese children were enrolled, and data regarding ferritin levels, blood glucose levels, intima-media thickness of carotid arteries, liver function and fibrosis index, hemoglobin, blood pressure, blood lipids, and inflammation indicators were collected. Ferritin levels were compared with a control group, which consisted of 148 healthy non-obese children who were age-matched and gender-matched. Endothelial cells were cultured in high glucose medium and supplemented with ferric citrate with or without iron remover (deferoxamine), a reducing agent (N-acetyl-cysteine), or a nuclear factor-κB (NF-κB) inhibitor (BAY 11-7082). Apoptosis, oxidative stress, nitric oxide levels, and endothelin content were evaluated. DNA microarray analysis was performed to analyze the expression of genes in the NF-κB signaling pathway.
resultsObese children have significantly higher ferritin levels compared with the control group. Ferritin level was positively correlated with hemoglobin and was related to metabolic disorders, including impaired glucose tolerance, higher blood pressure, dyslipidemia, and impaired hepatic function. Endothelial cells treated with ferric citrate showed a significantly higher rate of apoptosis, higher levels of oxidative stress, and impaired vasomotor function under high glucose conditions. The above effects were rescued by treatment with an iron remover, reducing agent, or NF-κB inhibitor. Further, detection of phosphorylated-p65 distribution in cells confirmed activation of the NF-κB pathway. DNA microarrays and subsequent gene oncology enrichment analyses revealed the main processes activated in cells.
conclusionIncreased ferritin levels are related to impaired glucose tolerance and other metabolic disorders in obese children. At the cellular level, iron overload aggravated the endothelial cell dysfunction caused by high glucose.
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