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Beta-hydroxybutyrate (BHB) elicits concentration-dependent anti-inflammatory effects on microglial cells which are reversible by blocking its monocarboxylate (MCT) importer

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Paper Summary

Paperzilla title
Keto Molecule BHB Calms Down Mouse Microglia's Inflammation (in a Dish)

This in vitro study found that beta-hydroxybutyrate (BHB), a molecule produced during ketosis, reduces inflammation in mouse microglia cells in a concentration-dependent manner, suggesting a possible mechanism for the ketogenic diet's benefits. The effects were partly reversed by blocking a transporter that BHB uses to enter cells, indicating BHB may act both inside and outside the cells. Further research is needed to confirm these findings in living organisms.

Explain Like I'm Five

In a lab setting, a molecule called BHB helped reduce inflammation in mouse brain immune cells (microglia), especially at levels found in people on a keto diet.

Possible Conflicts of Interest

None identified

Identified Limitations

BV2 Microglial cell model
The study used BV2 microglia, an immortalized cell line, which may not fully reflect the behavior of primary microglia in vivo.
In vitro study
The study was conducted in vitro, meaning it was done in a controlled lab setting rather than in living organisms.
Mouse microglial cells
The study focuses on mouse microglia and may not translate directly to humans.

Rating Explanation

This is an average in vitro study with limitations inherent to its methodology. It uses a mouse model to suggest relevance to human microglial behavior, but the findings need to be validated in more complex model systems like in vivo studies. The experimental design is generally sound, but the limitations of using cell lines and the in vitro setup cap the potential impact of the findings.

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File Information

Original Title: Beta-hydroxybutyrate (BHB) elicits concentration-dependent anti-inflammatory effects on microglial cells which are reversible by blocking its monocarboxylate (MCT) importer
Uploaded: August 14, 2025 at 04:51 PM
Privacy: Public