Neuroinflammation and neurodegeneration in overnutrition-induced diseases
Open accessAbstract
Overnutrition-induced diseases such as obesity and type 2 diabetes (T2D) involve neural dysregulation of metabolic physiology. Recently, interdisciplinary research in neuroscience and immunology has linked overnutrition to a non-classical onset of inflammation in the brain, particularly in the hypothalamus. This neuroinflammation impairs central regulatory pathways of energy balance and nutrient metabolism, and leads to obesity, diabetes, and cardiovascular complications. This review describes recent findings on the roles of overnutrition-induced hypothalamic inflammation in neurodegeneration and defective adult neurogenesis, as well as in impaired neural stem cell regeneration, and their relevance to obesity and related diseases. In addition, commonalities in terms of neuroinflammation between neurodegenerative diseases and overnutrition-induced metabolic diseases are discussed. Targeting neuroinflammation and neurodegeneration will provide promising approaches for treating obesity and other overnutrition-related diseases.
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One mechanism of microglia activation is the increase in LPS levels in peripheral blood, due to poor diet.
“One mechanism of microglia activation is the increase in LPS levels in peripheral blood, due to poor diet [50,51].”
From Polyphenol Microbial Metabolites Exhibit Gut and Blood–Brain Barrier Permeability and Protect Murine Microglia against LPS-Induced Inflammation (2019) · cites this paper as [50]
The section on hypothalamic neurogenesis links chronic overnutrition to inflammation involving microglial cells, and the section on central NF-κB activation discusses diet-related neuroinflammation. Neither passage identifies increased LPS in peripheral blood as the mechanism of microglial activation; searches for LPS, lipopolysaccharide, and endotoxemia found no such statement in our copy. (LLM, conf=0.82)
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Self-citation
- Authors
- Cai, D.
- Affiliations
- Albert Einstein College of Medicine (US)
- Corresponding author
- Cai, Dongsheng
- ORCID
- Cai, Dongsheng
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2013-01
- Volume
- 24
- Issue
- 1
- Pages
- 40-47
- ISSN
- 1043-2760 (ISSN-L)
- PMC
- PMC3556486
- OpenAlex
- W2007225703
- Cited by
- 256
- References
- 110
- Citations by year
- 2026: 8 · 2025: 16 · 2024: 7 · 2023: 14 · 2022: 20 · 2021: 21 · 2020: 16 · 2019: 20 · 2018: 20 · 2017: 20 · 2016: 31 · 2015: 27 · 2014: 25 · 2013: 10 · 2012: 1
- FWCI
- 1.87
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Diabetes Association
- National Institutes of Health
- National Institute on Aging (R01AG031774)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK078750, R56DK078750)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- neuroinflammation, neurodegeneration, overnutrition, obesity, type 2 diabetes, hypothalamic inflammation, energy balance, nutrient metabolism, adult neurogenesis, neural stem cells, neurodegenerative diseases, cardiovascular complications
- MeSH terms
- Animals, Humans, Hypothalamus, Inflammation, Obesity, Neurodegenerative Diseases, Overnutrition, Neural Stem Cells
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