ArticleeNeuro
Glucocorticoids Mediate Short-Term High-Fat Diet Induction of Neuroinflammatory Priming, the NLRP3 Inflammasome, and the Danger Signal HMGB1.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 63 citations in OpenAlex.
- Balancing inflammation under stress: glucocorticoid regulation of innate immune pathways.Bioscience reports · 2026Review
- Proanthocyanidins Inhibit Neuroinflammation in High-Fat-Induced Obese Mice by Modulating Intestinal Flora and Their Metabolites.Nutrients · 2026Article
- Post-operative cognitive dysfunction is exacerbated by high-fat diet via TLR4 and prevented by dietary DHA supplementation.Brain, behavior, and immunity · 2024Article
- Adolescent high fat diet alters the transcriptional response of microglia in the prefrontal cortex in response to stressors in both male and female mice.Stress (Amsterdam, Netherlands) · 2024Article
- Short-term high-fat diet consumption impairs synaptic plasticity in the aged hippocampus via IL-1 signaling.NPJ science of food · 2023Article
- Young adult and aged female rats are vulnerable to amygdala-dependent, but not hippocampus-dependent, memory impairment following short-term high-fat diet.Brain research bulletin · 2023Review
- NLRP3 Inflammasome's Activation in Acute and Chronic Brain Diseases-An Update on Pathogenetic Mechanisms and Therapeutic Perspectives with Respect to Other Inflammasomes.Biomedicines · 2023Review
- Single-cell RNA sequencing identifies hippocampal microglial dysregulation in diet-induced obesity.iScience · 2023Article
- Blocking the Hormone Receptors Modulates NLRP3 in LPS-Primed Breast Cancer Cells.International journal of molecular sciences · 2023Article
- Pattern-recognition receptors in endometriosis: A narrative review.Frontiers in immunology · 2023Review
- MiR-124 Prevents the Microglial Proinflammatory Response by Inhibiting the Activities of TLR4 and Downstream NLRP3 in Palmitic Acid-Treated BV2 Cells.Journal of molecular neuroscience : MN · 2022Article
- cGAS/STING and innate brain inflammation following acute high-fat feeding.Frontiers in immunology · 2022Article
- Article
- Age-Related Cognitive Decline May Be Moderated by Frequency of Specific Food Products Consumption.Nutrients · 2021Article
- The Impact of Obesity on Microglial Function: Immune, Metabolic and Endocrine Perspectives.Cells · 2021Review
- Oxidative stress and neuroinflammation in a rat model of co-morbid obesity and psychogenic stress.Behavioural brain research · 2021Article
- The Effect of Short-Term Feeding of a High-Coconut Oil or High-Fat Diet on Neuroinflammation and the Performance of an Object-Place Task in Rats.Neurochemical research · 2021Article
- Evolution of the Human Diet and Its Impact on Gut Microbiota, Immune Responses, and Brain Health.Nutrients · 2021Review
- Age-Specific Modulation of Prefrontal Cortex LTP by Glucocorticoid Receptors Following Brief Exposure to HFD.Frontiers in synaptic neuroscience · 2021Article
- The Perfect Cytokine Storm: How Peripheral Immune Challenges Impact Brain Plasticity & Memory Function in Aging.Brain plasticity (Amsterdam, Netherlands) · 2021Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The impact of the foods we eat on metabolism and cardiac physiology has been studied for decades, yet less is known about the effects of foods on the CNS, or the behavioral manifestations that may result from these effects. Previous studies have shown that long-term consumption of high-fat foods leading to diet-induced obesity sensitizes the inflammatory response of the brain to subsequent challenging stimuli, causing deficits in the formation of long-term memories. The new findings reported here demonstrate that short-term consumption of a high-fat diet (HFD) produces the same outcomes, thus allowing the examination of mechanisms involved in this process long before obesity and associated comorbidities occur. Rats fed an HFD for 3 d exhibited increases in corticosterone, the inflammasome-associated protein NLRP3 (nod-like receptor protein 3), and the endogenous danger signal HMGB1 (high-mobility group box 1) in the hippocampus. A low-dose (10 μg/kg) lipopolysaccharide (LPS) immune challenge potentiated the neuroinflammatory response in the hippocampus of rats fed the HFD, and caused a deficit in the formation of long-term memory, effects not observed in rats fed regular chow. The blockade of corticosterone action with the glucocorticoid receptor antagonist mifepristone prevented the NLRP3 and HMGB1 increases in unchallenged animals, normalized the proinflammatory response to LPS, and prevented the memory impairment. These data suggest that short-term HFD consumption increases vulnerability to memory disruptions caused by an immune challenge by upregulating important neuroinflammatory priming and danger signals in the hippocampus, and that these effects are mediated by increases in hippocampal corticosterone.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.