Minocycline inhibits microglial activation and mitigates compulsive and anxiety-like behaviors induced by a high-refined carbohydrate diet in male BALB/c mice.
Level 5 - mechanism / opinion, no new human data
Preclinical animal model study (CEBM Level 5).
PubMed 41117867 · doi:10.1007/s11011-025-01731-6
What was done
Male BALB/c mice were fed either a standard chow control diet or a high-refined carbohydrate (HC) diet for 12 weeks. Mice received minocycline (50 mg/kg) either intraperitoneally for 7 days or orally by gavage for 15 days prior to the conclusion of the dietary protocol. Behavioral outcomes were evaluated 24 hours post-diet using the Marble Burying and Novelty Suppressed Feeding tests. Morphological and biochemical analyses were conducted on serum, adipose tissue, and brain specimens (prefrontal cortex and hippocampus).
What was found
The abstract reports no numerical values. Minocycline administered orally for 15 days—but not intraperitoneally for 7 days—reversed HC diet-induced compulsive and anxiety-like behaviors. The 15-day regimen also decreased microglial activation in both the prefrontal cortex and the hippocampus, while exerting limited effects on diet-altered peripheral metabolic parameters.
Why it matters
The study suggests that neuroinflammation driven by microglial activation contributes to behavioral alterations caused by a high-carbohydrate diet, and that targeting central inflammation with minocycline can mitigate these behaviors independent of peripheral metabolic improvements.
Limits
Total sample size and specific group sizes are omitted from the abstract. The study was conducted exclusively in male BALB/c mice, limiting generalizability to females and humans. The abstract does not provide quantitative data, effect sizes, or confidence intervals, and the differing administration routes (intraperitoneal vs. oral) confound direct comparison between the 7-day and 15-day regimens.
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