A Long-Term Energy-Rich Diet Increases Prefrontal BDNF in Sprague-Dawley Rats.

Alessandro Virtuoso,Pernille Tveden-Nyborg,Anne Marie Voigt Schou-Pedersen,Dorte Bratbo Sørensen,Betina Elfving,Heidi Kaastrup Müller,Jens Lykkesfeldt

doi:10.3390/nu14010126

Alessandro Virtuoso, Pernille Tveden-Nyborg + Show 5 more

Open Access

https://doi.org/10.3390/nu14010126

Copy DOI

Journal: Nutrients	Publication Date: Dec 28, 2021
Citations: 9	License type: CC BY 4.0

Affiliation: University of Copenhagen, Aarhus University

Abstract

Findings of the effect of high-fat feeding including “Cafeteria Diets” (CAF) on brain-derived neurotrophic factor (BDNF) in the hippocampus (HIP) and prefrontal cortex (PFC) in rodents are conflicting. CAF is a non-standardized, highly palatable energy-rich diet composed by everyday food items for human consumption and is known to induce metabolic syndrome and obesity in rats. However, the highly palatable nature of CAF may counteract a negative effect of chronic stress on anticipatory behavior and synaptic plasticity in the hippocampus, hence represent a confounding factor (e.g., when evaluating functional effects on the brain). This study investigated the effects of a chronic, restricted access to CAF on BDNF, monoamine neurotransmitters, and redox imbalance in HIP and PFC in male rats. Our results show that CAF induced BDNF and its receptor TrkB in PFC compared to the controls (p < 0.0005). No differences in monoamine neurotransmitters were detected in either PFC or HIP. CAF increased dehydroascorbic acid and decreased malondialdehyde in PFC (p < 0.05), suggesting an early redox imbalance insufficient to induce lipid peroxidation. This study supports that a chronic CAF on a restricted schedule increases BDNF levels in the PFC of rats, highlighting that this may be a suboptimal feeding regime when investigating the effects of diet-induced obesity in the brain and emphasizing this as a point of attention when comparing the findings.

Highlights

The effect of diets rich in fat and sugar have been extensively studied in rodent models regarding their effects on physiology [1,2,3] and behavior, both in cognitive [4,5] and non-cognitive models [6,7]
Our results suggest an induction of the brain-derived neurotrophic factor (BDNF)-tropomyosin receptor kinase B (TrkB) signaling pathway in the prefrontal cortex (PFC) of rats fed a Cafeteria Diet (CAF)
One study involving behavioral trials did not find any effect on the levels of BDNF in the PFC of rats fed a diet rich in fat and sucrose, but found a negative effect in rats fed fat and dextrose, suggesting a role of dietary sources on the BDNF metabolism [42]

Summary

Introduction

The effect of diets rich in fat and sugar have been extensively studied in rodent models regarding their effects on physiology [1,2,3] and behavior, both in cognitive [4,5] and non-cognitive models [6,7]. BDNF is a member of the protein family neurotrophins, which has been shown to promote neuronal development in the cortex and HIP [12] It is involved in learning and memory, especially in HIP [13], and has been shown to be reduced during high-fat feeding regimens in rats and mice with subsequent reduced cognitive performance [9,10,14]. All these effects are mediated by the BDNF receptor tropomyosin receptor kinase B (TrkB) [15], whose fully glycosylated form is considered to be the mature and active form of the receptor [16,17]. Assessing the effects on BDNF, TrkB, and Y817 provides information on the potentially involved regulatory pathways as well as the putative biological significance (i.e., active vs. inactive forms)

Objectives

Methods

Results

Conclusion