Dimethyl itaconate ameliorates cognitive impairment induced by a high-fat diet via the gut-brain axis in mice
Open accessAbstract
Background: Gut homeostasis, including intestinal immunity and microbiome, is essential for cognitive function via the gut-brain axis. This axis is altered in high-fat diet (HFD)-induced cognitive impairment and is closely associated with neurodegenerative diseases. Dimethyl itaconate (DI) is an itaconate derivative and has recently attracted extensive interest due to its anti-inflammatory effect. This study investigated whether intraperitoneal administration of DI improves the gut-brain axis and prevents cognitive deficits in HF diet-fed mice. Results: DI effectively attenuated HFD-induced cognitive decline in behavioral tests of object location, novel object recognition, and nesting building, concurrent with the improvement of hippocampal RNA transcription profiles of genes associated with cognition and synaptic plasticity. In agreement, DI reduced the damage of synaptic ultrastructure and deficit of proteins (BDNF, SYN, and PSD95), the microglial activation, and neuroinflammation in the HFD-fed mice. In the colon, DI significantly lowered macrophage infiltration and the expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) in mice on the HF diet, while upregulating the expression of immune homeostasis-related cytokines (IL-22, IL-23) and antimicrobial peptide Reg3γ. Moreover, DI alleviated HFD-induced gut barrier impairments, including elevation of colonic mucus thickness and expression of tight junction proteins (zonula occludens-1, occludin). Notably, HFD-induced microbiome alteration was improved by DI supplementation, characterized by the increase of propionate- and butyrate-producing bacteria. Correspondingly, DI increased the levels of propionate and butyrate in the serum of HFD mice. Intriguingly, fecal microbiome transplantation from DI-treated HF mice facilitated cognitive variables compared with HF mice, including higher cognitive indexes in behavior tests and optimization of hippocampal synaptic ultrastructure. These results highlight the gut microbiota is necessary for the effects of DI in improving cognitive impairment. Conclusions: The present study provides the first evidence that DI improves cognition and brain function with significant beneficial effects via the gut-brain axis, suggesting that DI may serve as a novel drug for treating obesity-associated neurodegenerative diseases.
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This is accompanied by alleviation of microglial activation, neuroinflammation, synaptic impairment, and cognitive impairment induced by HFD.
“This is accompanied by alleviation of microglial activation, neuroinflammation, synaptic impairment, and cognitive impairment induced by HFD.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [645]
Reshaping the gut microbiome of HFD-fed mice using dimethyl itaconate restores intestinal barrier integrity by increasing SCFAs-producing bacteria and restoring intestinal immune homeostasis.
“reshaping the gut microbiome of HFD-fed mice using dimethyl itaconate restores intestinal barrier integrity by increasing SCFAs-producing bacteria and restoring intestinal immune homeostasis.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [645]
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Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases
Loh, J. S., Mak, W. Q., Tan, L. K. S., Ng, C. X., Chan, H. H., Yeow, S. H., Foo, J. B., Ong, Y. S., How, C. W., & Khaw, K. Y. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01743-1 · Cited by 1,193 · see citing works
- Authors
- Pan, W., Zhao, J., Wu, J., Xu, D., Meng, X., Jiang, P., Shi, H., Ge, X., Yang, X., Hu, M., Zhang, P., Tang, R., Nagaratnam, N., Zheng, K., Huang, X.-F., & Yu, Y.
- Affiliations
- Xuzhou Medical College (CN)
- University of Wollongong (AU)
- Corresponding author
- Zheng, Kuiyang
- Huang, Xu-Feng
- Yu, Yinghua
- ORCID
- Venue
- Microbiome
- Published
- 2023-02-21
- Volume
- 11
- Issue
- 1
- Pages
- 30-30
- ISSN
- 2049-2618 (ISSN-L)
- PMC
- PMC9942412
- OpenAlex
- W4321459676
- Cited by
- 113
- References
- 73
- Citations by year
- 2026: 32 · 2025: 44 · 2024: 26 · 2023: 11
- FWCI
- 10.02
- Type
- journal article
- Language
- en
- Update notices
- correction (2023-03-20)
- Open access
- gold
- doi.org
- Locations
- Microbiome (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research Online (University of Wollongong) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion)
- Funders
- Natural Science Foundation of Jiangsu Province (BK20201459)
- National Natural Science Foundation of China (81871670, 82071184)
- the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD) in 2014
- Natural Science Foundation of the Jiangsu Higher Education Institutions of China (19KJA560003)
- Starting Foundation for Talents of Xuzhou Medical University (D2018003)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- dimethyl itaconate, high-fat diet, cognitive impairment, gut-brain axis, gut microbiota, neuroinflammation, microglial activation, synaptic plasticity, hippocampus, tight junctions, inflammatory cytokines, IL-22, IL-23, Reg3γ, butyrate, propionate, fecal microbiota transplantation, brain-derived neurotrophic factor, PSD-95
- MeSH terms
- Brain-Gut Axis, Animals, Butyrates, Mice, Inbred C57BL, Obesity, Propionates, Succinates, Cytokines, Mice, Diet, High-Fat, Cognitive Dysfunction
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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