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ß-Hydroxybutyrate Improves Mitochondrial Function After Transient Ischemia in the Mouse.

Alina Lehto1, Konrad Koch2, Johanna Barnstorf-Brandes1

  • 1Department of Pharmacology and Clinical Pharmacy, College of Pharmacy, Goethe University of Frankfurt, Max-von-Laue-Str. 9, 60438, Frankfurt, Germany.

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Summary

A single dose of beta-hydroxybutyrate (BHB), a ketone body, improved neurological scores and mitochondrial function in mice after brain ischemia. These neuroprotective effects were observed within 24 hours post-treatment.

Keywords:
Complex IComplex IIGlucoseMicrodialysisOxidative phosphorylationStroke

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Area of Science:

  • Neuroscience
  • Metabolic research
  • Mitochondrial biology

Background:

  • Ketone bodies, like beta-hydroxybutyrate (BHB), and ketogenic diets show potential neuroprotective effects in neurodegenerative diseases.
  • Ischemic stroke remains a leading cause of death and disability, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To investigate the neuroprotective effects of a single beta-hydroxybutyrate (BHB) administration following transient focal cerebral ischemia in a mouse model.
  • To assess the impact of BHB on mitochondrial function and neurological recovery after ischemic stroke.

Main Methods:

  • Transient focal cerebral ischemia was induced in mice by middle cerebral artery occlusion for 90 minutes.
  • Beta-hydroxybutyrate (BHB) was administered intraperitoneally (30 mg/kg) immediately after reperfusion.
  • Neurological scores were evaluated 24 hours post-ischemia. Mitochondrial oxygen consumption and activity of respiratory complexes (I, II, IV) were measured in brain tissue.

Main Results:

  • BHB administration significantly improved neurological scores 24 hours after ischemia.
  • Mitochondrial oxygen consumption, particularly for complexes I and II, was enhanced by BHB treatment at 24 hours post-ischemia.
  • Elevated plasma and brain BHB levels were observed 24 hours post-administration, without altering key mitochondrial intermediates.

Conclusions:

  • A single dose of BHB demonstrates acute neuroprotective effects and improves mitochondrial respiration following ischemic stroke in mice.
  • The beneficial effects of BHB on mitochondrial function appear transient, lasting approximately 1-2 days.
  • Endogenous BHB production may play a complementary role to exogenous administration in stroke recovery.