ArticleNeurochemical research2016
Insulin Stimulates S100B Secretion and These Proteins Antagonistically Modulate Brain Glucose Metabolism.
Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- RAGE Axis in the Pathogenesis and Treatment of CNS Neurodegeneration in Long-Term Hyperglycemia.International journal of molecular sciences · 2026Review
- Sex-Associated Cerebellar and Hippocampal Volume Reduction in Alzheimer's Disease: Insights from the Clinical ADNI Cohort and STZ Animal Model.International journal of molecular sciences · 2025Article
- Application value of serum S100B combined with glucose metabolism indexes in predicting adverse pregnancy outcomes of patients with severe preeclampsia.Journal of human hypertension · 2024Article
- S100B Secretion in Astrocytes, Unlike C6 Glioma Cells, Is Downregulated by Lactate.Metabolites · 2023Article
- Review
- Potential Glioprotective Strategies Against Diabetes-Induced Brain Toxicity.Neurotoxicity research · 2021Review
- The Impact of High Glucose or Insulin Exposure on S100B Protein Levels, Oxidative and Nitrosative Stress and DNA Damage in Neuron-Like Cells.International journal of molecular sciences · 2021Article
- Ammonia-Induced Glial-Inflammaging.Molecular neurobiology · 2020Article
- Levels of serum S100B are associated with cognitive dysfunction in patients with type 2 diabetes.Aging · 2020Article
- Short-Term Protocols to Obtain Insulin-Producing Cells from Rat Adipose Tissue: Signaling Pathways and In Vivo Effect.International journal of molecular sciences · 2019Article
- GABANeurochemical research · 2019Article
- Receptor for Advanced Glycation End Products (RAGE) in Type 1 Diabetes Pathogenesis.Current diabetes reports · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain metabolism is highly dependent on glucose, which is derived from the blood circulation and metabolized by the astrocytes and other neural cells via several pathways. Glucose uptake in the brain does not involve insulin-dependent glucose transporters; however, this hormone affects the glucose influx to the brain. Changes in cerebrospinal fluid levels of S100B (an astrocyte-derived protein) have been associated with alterations in glucose metabolism; however, there is no evidence whether insulin modulates glucose metabolism and S100B secretion. Herein, we investigated the effect of S100B on glucose metabolism, measuring D-(3)H-glucose incorporation in two preparations, C6 glioma cells and acute hippocampal slices, and we also investigated the effect of insulin on S100B secretion. Our results showed that: (a) S100B at physiological levels decreases glucose uptake, through the multiligand receptor RAGE and mitogen-activated protein kinase/ERK signaling, and (b) insulin stimulated S100B secretion via PI3K signaling. Our findings indicate the existence of insulin-S100B modulation of glucose utilization in the brain tissue, and may improve our understanding of glucose metabolism in several conditions such as ketosis, streptozotocin-induced dementia and pharmacological exposure to antipsychotics, situations that lead to changes in insulin signaling and extracellular levels of S100B.
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Registered trials
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