Regional brain glucose metabolism is differentially affected by ketogenic diet: A human semiquantitative positron emission tomography

Author:

Horowitz tatiana1ORCID,Doche Emilie2,Phlip Mary2,Cammilleri Serge2,Suissa Laurent2,GUEDJ Eric1

Affiliation:

1. Aix Marseille Univ, APHM, CNRS, Central Marseille, Institut Fresnel, Timone Hospital, CERIMED, Nuclear Medicine Department, Marseille, France

2. AP-HM: Assistance Publique Hopitaux de Marseille

Abstract

Abstract Purpose Ketogenic diet (KD) is recommended to avoid intense [18F]FDG myocardial physiologic uptake in PET imaging. Neuroprotective and anti-seizure effects of KD have been suggested, but their mechanisms remain to be elucidated. This [18F]FDG PET study aims to evaluate the effect of KD on glucose brain metabolism. Method Subjects who underwent KD prior to whole-body and brain [18F]FDG PET in our department for suspected endocarditis were retrospectively included. Myocardial glucose suppression (MGS) on whole-body PET was analysed. The main exclusion criteria were brain abnormalities. Thirty-four subjects with MGS were considered the KD population, and 14 subjects without MGS were considered a KD failure. Brain SUVmax of these groups was compared. Second, the KD population (n = 34, mean age: 61.8 ± 17.2 years) was compared to a control group of 27 healthy subjects fasting for at least 6 h (mean age of 62.4 ± 10.9 years). A semiquantitative voxel-based intergroup statistical analysis was conducted using SPM. Results A 20% lower brain SUVmax was found in subjects under KD with MGS in comparison to those without MGS, p = 0.02. Whole-brain voxel-based intergroup analysis revealed that patients under KD had relative hypermetabolism of limbic regions including medial temporal cortices and cerebellum lobes and relative hypometabolism of bilateral posterior regions (occipito-parietal). Conclusion KD globally reduces brain glucose metabolism but with regional differences. These results have a clinical implication, since the realization of a KD could lead to misinterpretation of these regions, and a pathophysiological perspective as it could help understand underlying neurological effects of KD through possible decrease of oxidative stress in posterior regions, and functional compensation in the limbic regions.

Publisher

Research Square Platform LLC

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