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Obesity and microglial activation: potential for synergism in neurodegenerative diseases
Author(s) -
Sheridan Patricia A
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.326.4
Subject(s) - microglia , neuroinflammation , neurodegeneration , weanling , tlr4 , endocrinology , inflammation , medicine , population , receptor , immunology , biology , disease , environmental health
This study examines high fat diet feeding and obesity as a factor leading to the uncontrolled production of neuroinflammatory molecules by microglia, a hypothesized mechanism in the development of neurodegenerative diseases. We hypothesize that the inflammation resulting from a high fat diet and obesity activate microglia in the brain leading to increased neurodegeneration and will potentiate the neuroinflammation from a CNS insult. Weanling male mice were placed on a low fat (LF) or a high fat (HF) diet. After 4 weeks on the diet there is a modest, but significant, increase in leptin receptor expression on microglia from HF mice. In addition, there is a significant increase in the expression of toll‐like receptor (TLR) 2 on HF microglia. After 8 weeks, microglia from HF mice have significantly more TLR4/MD‐2 than LF microglia. MHC II is present on cells from both LF and HF mice at levels that are normally seen in young, healthy mice and there is no difference in MHCII expression between LF and HF microglia at these early time points. These data indicate that several cell surface proteins associated with microglial priming and activation are up‐regulated after only 4–8 weeks on a HF diet. As our population ages and becomes increasingly obese, the implications of diet on age related neurological conditions are a significant public health concern. This study was supported by the UNC NORC Grant DK56350.