ArticleiScience2025
Insulin acts on astrocytes to shift their substrate preference to fatty acids.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Enhanced Energy Metabolism and Developmental Signaling in Neonatal Brains of Female Piglets Parenterally Fed with 18-Carbon n-3 Fatty Acid-Based Vegaven Compared with Fish Oil-Containing Lipid Emulsion.Current developments in nutrition · 2026Article
- Astrocytes in systemic regulation of blood glucose and the development of type 2 diabetes.Frontiers in cellular neuroscience · 2026Review
- One-month early time-restricted eating enhances cognition via white matter-cortical pathways in males with metabolic syndrome: evidence from TBSS and SBM analyses.Frontiers in nutrition · 2026Article
- Central cytometabolic functional vascular coupling in health and disease.npj metabolic health and disease · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
It is increasingly recognized that brain can β-oxidize fatty acids for use as an energy substrate. However, mechanism(s) by which neural cells switch their preference from glucose to fatty acids are not fully elucidated. Here we provide evidence that insulin acts directly on astrocytes to promote the uptake of glucose and fatty acids while modifying their substrate preference through a sequential shift in the expression of genes associated with fatty acid uptake, synthesis, transport, and metabolism. Under these conditions, fatty acids are converted into TCA cycle intermediates to satisfy astrocyte energy demands, allowing pyruvate derived from glucose to be directed toward the production of lactate; a preferred fuel for neurons. This shift in astrocyte energy substrate preference is required for insulin to enhance long-term potentiation in the Schaffer collateral. These findings establish a homeostatic mechanism where insulin promotes LTP by switching the energy substrate preference of astrocytes to fatty acids.
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What Socratic holds
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 Socratic graph.