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

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

doi:10.3390/nu14010126

Cited by 9 publications

(4 citation statements)

References 74 publications

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“…Since the c-Fos-IR cell levels of CTR-CAF rats were also not significantly different from CTR-chow rats in the PFC, we conclude that the PrL and IL of the PFC are not involved in this aspect of reward processing. This is in line with another study that also failed to detect changes in monoamine neurotransmitters in the PFC after CAF exposure [52].…”

Section: Discussionsupporting

confidence: 92%

Changes in reward-induced neural activity upon Cafeteria Diet consumption

Heijkoop,

Lalanza,

Solanas

et al. 2023

Preprint

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Excessive consumption of highly palatable foods rich in sugar and fat, often referred to as "junk" or "fast" foods, plays a central role in the development of obesity. The highly palatable characteristics of these foods activate hedonic and motivational mechanisms to promote food-seeking behavior and overeating, which is largely regulated by the brain reward system. Excessive junk food consumption can alter the functioning of this reward system, but exact mechanisms of these changes are still largely unknown. This study investigated whether long-term junk food consumption, in the form of Cafeteria (CAF) diet, can alter the reward system in female rats, and whether different regimes of CAF diet influence the extent of these changes. To this end, rats were exposed to a 6-week diet with either standard chow, or ad libitum daily access to CAF diet, 30% restricted but daily access to CAF diet, or one-day-a-week (intermittent) ad libitum access to CAF diet, after which c-Fos expression in the Nucleus Accumbens (NAc), Prefrontal Cortex (PFC), and Ventral Tegmental Area (VTA) following consumption of a CAF reward was examined. We found that all CAF diet regimes decreased c-Fos expression in the NAc-shell when presented with a CAF reward. While no changes in c-Fos expression upon the different diet regimes were found in the PFC, future research should reveal potential decreases in neural activity in the VTA. Our data suggests that long-term junk food exposure can affect the brain reward system, resulting in an attenuated activity of the NAc-shell.

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Section: Discussionsupporting

confidence: 92%

Changes in reward-induced neural activity upon Cafeteria Diet consumption

Heijkoop,

Lalanza,

Solanas

et al. 2023

Preprint

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“…Regarding the effects of an HFD on BDNF, the literature reports both increases and decreases in BDNF levels in the prefrontal cortex. For example, Virtuoso et al reported that a chronic cafeteria diet on a restricted schedule increases BDNF levels in the prefrontal cortex (PFC) of rats [38]. Nevertheless, Miao et al found that in pregnant female mice, HFD induced decreases in BDNF in the hippocampus and prefrontal cortex, but increases in the amygdala [39].…”

Section: Discussionmentioning

confidence: 99%

A Four-Week High-Fat Diet Induces Anxiolytic-like Behaviors through Mature BDNF in the mPFC of Mice

Huang,

et al. 2024

Brain Sciences

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The effect of a high-fat diet (HFD) on mood is a widely debated topic, with the underlying mechanisms being poorly understood. This study explores the anxiolytic effects of a four-week HFD in C57BL/6 mice. Five-week-old mice were exposed to either an HFD (60% calories from fat) or standard chow diet (CD) for four weeks, followed by cannula implantation, virus infusion, behavioral tests, and biochemical assays. Results revealed that four weeks of an HFD induced anxiolytic-like behaviors and increased the protein levels of mature brain-derived neurotrophic factor (mBDNF) and phosphorylated tyrosine kinase receptor B (p-TrkB) in the medial prefrontal cortex (mPFC). Administration of a BDNF-neutralizing antibody to the mPFC reversed HFD-induced anxiolytic-like behaviors. Elevated BDNF levels were observed in both neurons and astrocytes in the mPFC of HFD mice. Additionally, these mice exhibited a higher number of dendritic spines in the mPFC, as well as upregulation of postsynaptic density protein 95 (PSD95). Furthermore, mRNA levels of the N6-methyladenosine (m6A) demethylase, fat mass and obesity-associated protein (FTO), and the hydrolase matrix metalloproteinase-9 (MMP9), also increased in the mPFC. These findings suggest that an HFD may induce FTO and MMP9, which could potentially regulate BDNF processing, contributing to anxiolytic-like behaviors. This study proposes potential molecular mechanisms that may underlie HFD-induced anxiolytic behaviors.

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“…This model shows increased adiposity and hepatosteatosis, white fat, and more inflammation in the adipose tissue and liver [14,41]. A chronic CAF on a restricted schedule has also been shown to increase BDNF levels and its receptor TrkB in the prefrontal cortex of rats [139].…”

Section: Cafeteria Diet (Caf)mentioning

confidence: 90%

Murine Models of Obesity

et al. 2022

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Obesity, classified as an epidemic by the WHO, is a disease that continues to grow worldwide. Obesity results from abnormal or excessive accumulation of fat and usually leads to the development of other associated diseases, such as type 2 diabetes, hypertension, cancer, cardiovascular diseases, among others. In vitro and in vivo models have been crucial for studying the underlying mechanisms of obesity, discovering new therapeutic targets, and developing and validating new pharmacological therapies against obesity. Preclinical animal models of obesity comprise a variety of species: invertebrates, fishes, and mammals. However, small rodents are the most widely used due to their cost-effectiveness, physiology, and easy genetic manipulation. The induction of obesity in rats or mice can be achieved by the occurrence of spontaneous single-gene mutations or polygenic mutations, by genetic modifications, by surgical or chemical induction, and by ingestion of hypercaloric diets. In this review, we describe some of the most commonly used murine models in obesity research.

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

Cited by 9 publications

References 74 publications

Changes in reward-induced neural activity upon Cafeteria Diet consumption

Changes in reward-induced neural activity upon Cafeteria Diet consumption

A Four-Week High-Fat Diet Induces Anxiolytic-like Behaviors through Mature BDNF in the mPFC of Mice

Murine Models of Obesity

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