Intermittent Fasting serves as a Potential Intervention to counteract the High Fat Diet induced Neuronal Changes in Dentate Gyrus of Rats

Abdelfattah, Aya Abdelsattar; Abo-Elghit, Amal Taha; Kamel, Esam Omar; Abdellah, Tahany Abbass

doi:10.21608/svuijm.2025.388013.2180

Intermittent Fasting serves as a Potential Intervention to counteract the High Fat Diet induced Neuronal Changes in Dentate Gyrus of Rats

Document Type : Original research articles

Authors

¹ Department of Medical Histology, Faculty of Medicine, South Valley University, Qena, 83523, Egypt

² Department of Medical Histology, Faculty of Medicine, Assiut University, Assiut, 71511, Egypt

³ Department of Medical Histology, Faculty of Medicine, Al-Azhar University (Assiut Branch), Assiut, 71511, Egypt

10.21608/svuijm.2025.388013.2180

Abstract

Background: High-fat diet (HFD) consumed by adolescent mice is known to impede learning and memory processes within the dentate gyrus (DG) and implies that adolescence is especially susceptible to the detrimental effects of a HFD on hippocampal function.
Objectives: This study aims to examine the consequences of intermittent fasting (IF) on neuron changes resulting from HFD in the rat DG.
Materials and methods: 60 male Wistar albino rats, each weighing 150 ± 20 grams, at 12 weeks of age. Four groups of rats were established with equal numbers: Group I was provided with unrestricted access to water and a standard diet of rat chow for 24 weeks. Group II was fed High fat diet( HFD). Group III contained rats following IF regimen. Group IV contained rats initially fed HFD for 24 weeks, followed by 8 weeks of IF regimen. At the end of the experiment, rats from all groups were scarified, the brain was isolated, fixed, sectioned and then stained with hematoxylin and eosin (H&E) , Gallocyainine and immunohistochemical stains for glial fibrillary acidic protein (GFAP), Nuclear factor erythroid 2–related factor 2 (Nrf2) and tyrosine hydroxylase (TH) for light microscope examination.
Results: Histological examination of group II showed disruption of DG blades, widening in the subgranular area and vacuolization of granule cells. Restoring of granular layer normal structure was observed in Group IV. Astrocytes number was found to be significantly high in group II. Nrf2 was significantly high among group III. The level of TH expression was significantly low among group II.
Conclusion: HFD caused significant neuronal degeneration, disrupted DG architecture, and alterations in astrocyte activity and molecular markers. IF showed protective and restorative effects on DG integrity and function.

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