Dietary restriction normalizes glucose metabolism and BDNF levels, slows disease progression, and increases survival in huntingtin mutant mice
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In addition to neurological deficits, Huntington's disease (HD) patients and transgenic mice expressing mutant human huntingtin exhibit reduced levels of brain-derived neurotrophic factor, hyperglycemia, and tissue wasting. We show that the progression of neuropathological (formation of huntingtin inclusions and apoptotic protease activation), behavioral (motor dysfunction), and metabolic (glucose intolerance and tissue wasting) abnormalities in huntingtin mutant mice, an animal model of HD, are retarded when the mice are maintained on a dietary restriction (DR) feeding regimen resulting in an extension of their life span. DR increases levels of brain-derived neurotrophic factor and the protein chaperone heat-shock protein-70 in the striatum and cortex, which are depleted in HD mice fed a normal diet. The suppression of the pathogenic processes by DR in HD mice suggests that mutant huntingtin promotes neuronal degeneration by impairing cellular stress resistance, and that the body wasting in HD is driven by the neurodegenerative process. Our findings suggest a dietary intervention that may suppress the disease process and increase the life span of humans that carry the mutant huntingtin gene.
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Dietary restriction or addition of supplementary substances such as omega-3 fatty acids or resveratrol can induce an increase in BDNF levels and reduce cognitive impairment in animal models.
“dietary restriction (i.e., the maintenance of a balanced diet) or addition of supplementary substances (e.g., omega-3 fatty acids; resveratrol) can induce an increase in BDNF levels and reduce cognitive impairment in animal models [224–226].”
From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [225]
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Self-citation
- Authors
- Duan, W., Guo, Z., Jiang, H., Ware, M., Li, X.-J., & Mattson, M. P.
- Affiliations
- Johns Hopkins University (US)
- National Institutes of Health (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2003-02-14
- Volume
- 100
- Issue
- 5
- Pages
- 2911-2916
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC151440
- OpenAlex
- W1997887740
- Cited by
- 428
- References
- 59
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 14 · 2023: 8 · 2022: 17 · 2021: 13 · 2020: 18 · 2019: 19 · 2018: 18 · 2017: 22 · 2016: 13 · 2015: 18 · 2014: 26 · 2013: 18 · 2012: 16
- FWCI
- 10.16
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
- Keywords
- Huntington's disease, dietary restriction, brain-derived neurotrophic factor, HSP70, impaired glucose tolerance, hyperglycemia, tissue wasting, motor impairment, apoptosis, neurodegeneration, cellular stress resistance, lifespan extension, striatum, cortex
- MeSH terms
- Huntingtin Protein, Animals, Behavior, Animal, Blood Glucose, Brain, Cell Survival, Enzyme Activation, Enzyme-Linked Immunosorbent Assay, Glucose, Insulin, Male, Mice, Transgenic, Mutation, Nerve Tissue Proteins, Nuclear Proteins, Time Factors, Immunoblotting, Up-Regulation, Disease Progression, Brain-Derived Neurotrophic Factor, Neurodegenerative Diseases, Caspases, Leptin, Mice
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