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Ketogenic diet induces an inflammatory reactive astrocytes phenotype reducing glioma growth

Maria Rosito1,2, Javeria Maqbool3, Alice Reccagni3

  • 1Department of Physiology and Pharmacology, Sapienza University, P.Le Aldo Moro 5, 00185, Rome, Italy. maria.rosito@gmail.com.

Cellular and Molecular Life Sciences : CMLS
|February 8, 2025
PubMed

Insights

The ketogenic diet (KD) and its product beta-hydroxybutyrate (β-HB) slow glioma growth by activating astrocytes. These activated glial cells reduce tumor proliferation and protect the brain from excitotoxicity.

Area of Science:

  • Neuro-oncology
  • Metabolic therapies
  • Cancer research

Background:

  • Glioma is a primary brain tumor with poor prognosis.
  • Ketogenic diet (KD) is explored as an adjuvant therapy for glioma.
  • Mechanisms of KD effects on glioma microenvironment are not fully understood.

Purpose of the Study:

  • Investigate glial cells' role in mediating KD effects on glioma.
  • Determine if beta-hydroxybutyrate (β-HB) influences glioma growth and survival.
  • Elucidate the impact of KD on astrocyte phenotype and function.

Main Methods:

  • Glioma-bearing mice were treated with KD or β-HB.
  • Assessed glioma growth and survival rates in vivo.
  • Analyzed astrocyte phenotype, glutamate transporter function, and intracellular calcium levels in glioma cells.

Main Results:

  • KD and β-HB significantly reduced glioma growth in mice.
  • β-HB induced a pro-inflammatory astrocyte phenotype and increased glutamate transporters.
  • Glioma cells showed increased intracellular calcium when treated with β-HB or co-cultured with astrocytes.

Conclusions:

  • Glial cells, particularly astrocytes, mediate beneficial effects of KD in glioma.
  • β-HB-induced pro-inflammatory astrocytes may inhibit glioma proliferation.
  • These findings suggest a protective role for astrocytes against glioma and excitotoxicity.
Keywords:
AstrocytesAstrogliosisGliomaKetogenic dietMicrogliaPro-inflammatory astrocytesβ-HB

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