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Cited by 92Neurogenesis and neuroplasticity mechanismsNeuroscience and Neuropharmacology ResearchNeuroinflammation and Neurodegeneration Mechanisms

Hyperglycemia Alters Astrocyte Metabolism and Inhibits Astrocyte Proliferation

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Li, Wenjun, Roy Choudhury, Gourav, Winters, Ali, Prah, Jude, Lin, Wenping, Liu, Ran, Yang, Shao-Hua·2018·Aging and disease
DOI 10.14336/ad.2017.1208PMC PMC6065301
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Abstract

Diabetes milieu is a complex metabolic disease that has been known to associate with high risk of various neurological disorders. Hyperglycemia in diabetes could dramatically increase neuronal glucose levels which leads to neuronal damage, a phenomenon referred to as glucose neurotoxicity. On the other hand, the impact of hyperglycemia on astrocytes has been less explored. Astrocytes play important roles in brain energy metabolism through neuron-astrocyte coupling. As the component of blood brain barrier, glucose might be primarily transported into astrocytes, hence, impose direct impact on astrocyte metabolism and function. In the present study, we determined the effect of high glucose on the energy metabolism and function of primary astrocytes. Hyperglycemia level glucose (25 mM) induced cell cycle arrest and inhibited proliferation and migration of primary astrocytes. Consistently, high glucose decreased cyclin D1 and D3 expression. High glucose enhanced glycolytic metabolism, increased ATP and glycogen content in primary astrocytes. In addition, high glucose activated AMP-activated protein kinase (AMPK) signaling pathway in astrocytes. In summary, our in vitro study indicated that hyperglycemia might impact astrocyte energy metabolism and function phenotype. Our study provides a potential mechanism which may underlie the diabetic cerebral neuropathy and warrant further in vivo study to determine the effect of hyperglycemia on astrocyte metabolism and function.

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  • Primary astrocytes cultured under high concentrations of glucose presented cell cycle arrest and inhibited proliferation, migration, and metabolic changes.

    “However, primary astrocytes cultured under high concentrations of glucose presented cell cycle arrest and inhibited proliferation, migration, and metabolic changes [24].”

    From Proliferating Astrocytes in Primary Culture Do Not Depend upon Mitochondrial Respiratory Complex I Activity or Oxidative Phosphorylation (2023) · cites this paper as [24]

    The Results sections report G2/M cell-cycle arrest, inhibited proliferation, and inhibited migration in astrocytes cultured with high glucose. They also report metabolic changes, including increased ATP and glycogen, but do not say that metabolic changes were inhibited. (LLM, conf=0.86)

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Cited by

Sorted by citations

Authors
Li, W., Roy Choudhury, G., Winters, A., Prah, J., Lin, W., Liu, R., & Yang, S.-H.
Affiliations
  • University of North Texas Health Science Center (US)
  • Fujian Medical University (CN)
Corresponding author
Yang, Shao-Hua
ORCID
Venue
Aging and disease
Publisher
Aging and Disease
Published
2018
Volume
9
Issue
4
Pages
674
ISSN
2152-5250 (ISSN-L)
DOI
10.14336/ad.2017.1208
PMC
PMC6065301
OpenAlex
W2887577894
Cited by
92
References
2
Citations by year
2026: 10 · 2025: 16 · 2024: 20 · 2023: 17 · 2022: 8 · 2021: 10 · 2020: 6 · 2019: 5
FWCI
1.92
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Aging and Disease (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging (P01AG027956)
  • National Institute of Neurological Disorders and Stroke (R21NS087209, R01NS088596)
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
hyperglycemia, astrocytes, astrocyte energy metabolism, astrocyte proliferation, cell cycle arrest, cyclin D1, cyclin D3, glycolysis, glycogen, ATP, AMPK, diabetes mellitus

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