Energy‑dense diet triggers changes in gut microbiota, reorganization of gut‑brain vagal communication and increases body fat accumulation
Open accessAbstract
Obesity is associated with consumption of energy-dense diets and development of systemic inflammation. Gut microbiota play a role in energy harvest and inflammation and can influence the change from lean to obese phenotypes. The nucleus of the solitary tract (NTS) is a brain target for gastrointestinal signals modulating satiety and alterations in gut-brain vagal pathway may promote overeating and obesity. Therefore, we tested the hypothesis that high-fat diet‑induced changes in gut microbiota alter vagal gut-brain communication associated with increased body fat accumulation. Sprague-Dawley rats consumed a low energy‑dense rodent diet (LFD; 3.1 kcal/g) or high energy‑dense diet (HFD, 5.24 kcal/g). Minocycline was used to manipulate gut microbiota composition. 16S Sequencing was used to determine microbiota composition. Immunofluorescence against IB4 and Iba1 was used to determine NTS reorganization and microglia activation. Nodose ganglia from LFD rats were isolated and co-cultured with different bacteria strains to determine neurotoxicity. HFD altered gut microbiota with increases in Firmicutes/Bacteriodetes ratio and in pro-inflammatory Proteobacteria proliferation. HFD triggered reorganization of vagal afferents and microglia activation in the NTS, associated with weight gain. Minocycline-treated HFD rats exhibited microbiota profile comparable to LFD animals. Minocycline suppressed HFD‑induced reorganization of vagal afferents and microglia activation in the NTS, and reduced body fat accumulation. Proteobacteria isolated from cecum of HFD rats were toxic to vagal afferent neurons in culture. Our findings show that diet‑induced shift in gut microbiome may disrupt vagal gut‑brain communication resulting in microglia activation and increased body fat accumulation.
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In rats, a high-energy dense diet rapidly alters the gut microbiota, increasing the Firmicutes/Bacteroidetes ratio and pro-inflammatory Proteobacteria proliferation compared to a low-energy diet.
“rats fed a high-energy dense diet rapidly altered their gut microbiota with increases in Firmicutes/Bacteroidetes ratio and in pro-inflammatory Proteobacteria proliferation compared to those consuming a low-energy diet [154].”
From The athletic gut microbiota (2020) · cites this paper as [154]
The high-energy diet increased circulating pro-inflammatory LPS in rats.
“Moreover, the high-energy diet increased circulating pro-inflammatory LPS.”
From The athletic gut microbiota (2020) · cites this paper as [154]
In a rat model of obesity, changes in the gut microbiota induced by an energy-dense diet were associated with alterations in brain-gut vagal (NTS) communication.
“In a rat model of obesity, changes in the gut microbiota induced by an energy-dense diet were associated with alterations in brain-gut vagal (NTS) communication53, which may alter vagal satiety signalling and stimulate energy intake and adiposity54.”
From The gut microbiota and the brain–gut–kidney axis in hypertension and chronic kidney disease (2018) · cites this paper as [53]
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Mechanosensation of the heart and gut elicits hypometabolism and vigilance in mice
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Microbiota, a New Playground for the Omega-3 Polyunsaturated Fatty Acids in Cardiovascular Diseases
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A neuroscience perspective of the gut theory of Parkinson's disease
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- Authors
- C. Vaughn, A., M. Cooper, E., M. DiLorenzo, P., J. O’Loughlin, L., E. Konkel, M., H. Peters, J., Hajnal, A., Sen, T., Hye Lee, S., B. de La Serre, C., & Czaja, K.
- Affiliations
- University of Georgia (US)
- Venue
- Acta Neurobiologiae Experimentalis
- Published
- 2017
- Volume
- 77
- Issue
- 1
- Pages
- 18-30
- ISSN
- 0065-1400 (ISSN-L)
- 1689-0035
- PMC
- PMC5382806
- OpenAlex
- W2606717595
- Cited by
- 166
- References
- 51
- Citations by year
- 2026: 10 · 2025: 19 · 2024: 14 · 2023: 11 · 2022: 18 · 2021: 19 · 2020: 28 · 2019: 16 · 2018: 22 · 2017: 9
- FWCI
- 8.38
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by
- Locations
- Acta Neurobiologiae Experimentalis (publishedVersion, cc-by)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Zenodo (CERN European Organization for Nuclear Research) (submittedVersion, cc-by)
- Funders
- National Institute on Deafness and Other Communication Disorders (R01DC013904)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK092651, R21DK110511)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- energy-dense diet, high-fat diet, gut microbiota, nucleus tractus solitarius, vagal afferents, microglial activation, body fat accumulation, obesity, minocycline, Proteobacteria, Firmicutes/Bacteroidetes ratio, neurotoxicity, nodose ganglion, satiety
- MeSH terms
- Gastrointestinal Microbiome, Adipose Tissue, Afferent Pathways, Animals, Anti-Bacterial Agents, Body Weight, Eating, Feces, Gram-Negative Bacteria, Lipopolysaccharides, Male, Minocycline, Nodose Ganglion, RNA, Ribosomal, 16S, Time Factors, Vagus Nerve, Rats, Sprague-Dawley, Solitary Nucleus, Microglia, Lectins, Rats, Diet, High-Fat
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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