Cited by 64Neuroinflammation and Neurodegeneration MechanismsTryptophan and brain disordersNeurological Disease Mechanisms and Treatments

Microglial Function during Glucose Deprivation: Inflammatory and Neuropsychiatric Implications

Open access
Churchward, Matthew A., Tchir, Devan R., Todd, Kathryn G.·2018·Molecular Neurobiology

Abstract

Inflammation is increasingly recognized as a contributor to the pathophysiology of neuropsychiatric disorders, including depression, anxiety disorders and autism, though the factors leading to contextually inappropriate or sustained inflammation in pathological conditions are yet to be elucidated. Microglia, as the key mediators of inflammation in the CNS, serve as likely candidates in initiating pathological inflammation and as an ideal point of therapeutic intervention. Glucose deprivation, as a component of the pathophysiology of ischemia or occurring transiently in diabetes, may serve to modify microglial function contributing to inflammatory injury. To this end, primary microglia were cultured from postnatal rat brain and subject to glucose deprivation in vitro. Microglia were characterized for their proliferation, phagocytic function and secretion of inflammatory factors, and tested for their capacity to respond to a potent inflammatory stimulus. In the absence of glucose, microglia remained capable of proliferation, phagocytosis and inflammatory activation and showed increased release of inflammatory factors after presentation of an inflammatory stimulus. Glucose-deprived microglia demonstrated increased phagocytic activity and decreased accumulation of lipids in lipid droplets over a 48-h timecourse, suggesting they may use scavenged lipids as a key alternate energy source during metabolic stress. In the present manuscript, we present novel findings that glucose deprivation may sensitize microglial release of inflammatory mediators and prime microglial functions for both survival and inflammatory roles, which may contribute to psychiatric comorbidities of ischemia, diabetes and/or metabolic disorder.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1007/s12035-017-0422-9

Cites

121 of 121 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Certain metabolic states such as glucose starvation in microglia lead to lipid redistribution rather than de novo fatty acid synthesis.

    “Additionally, certain metabolic states such as glucose starvation in microglia lead to lipid redistribution rather than de novo FA synthesis [74].”

    From Lipoprotein Lipase Regulates Microglial Lipid Droplet Accumulation (2021) · cites this paper as [74]

    The Results and Discussion propose lipid redistribution rather than de novo fatty acid synthesis as a possible explanation for lipid-droplet increases after LPS stimulation, including in glucose-deprived microglia. They do not establish that glucose deprivation itself causes redistribution, and the explanation is explicitly tentative. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Churchward, M. A., Tchir, D. R., & Todd, K. G.
Affiliations
University of Alberta (CA)
Corresponding author
Todd, Kathryn G.
Venue
Molecular Neurobiology
Published
2017-02-07
Volume
55
Issue
2
Pages
1477-1487
ISSN
  • 0893-7648 (ISSN-L)
  • 1559-1182
OpenAlex
W2586839353
Cited by
63
References
121
Citations by year
2026: 2 · 2025: 8 · 2024: 11 · 2023: 11 · 2022: 6 · 2021: 10 · 2020: 7 · 2019: 6 · 2018: 2
FWCI
2.04
Type
journal article
Language
en
Open access
Locations
  • Molecular Neurobiology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
Alberta Health Services
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
microglia, glucose deprivation, neuroinflammation, phagocytosis, microglial proliferation, inflammatory mediators, lipid droplets, metabolic stress, ischemia, diabetes mellitus, neuropsychiatric disorders, depression, anxiety disorders, autism spectrum disorder
MeSH terms
Animals, Brain, Cells, Cultured, Hypoglycemia, Inflammation, Phagocytosis, Microglia, Cell Proliferation, Rats

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 ›

Are you an author, or do you see a problem with this page? Request a review