Testing the role of myeloid cell glucose flux in inflammation and atherosclerosis
Open accessAbstract
Inflammatory activation of myeloid cells is accompanied by increased glycolysis, which is required for the surge in cytokine production. Although in vitro studies suggest that increased macrophage glucose metabolism is sufficient for cytokine induction, the proinflammatory effects of increased myeloid cell glucose flux in vivo and the impact on atherosclerosis, a major complication of diabetes, are unknown. We therefore tested the hypothesis that increased glucose uptake in myeloid cells stimulates cytokine production and atherosclerosis. Overexpression of the glucose transporter GLUT1 in myeloid cells caused increased glycolysis and flux through the pentose phosphate pathway but did not induce cytokines. Moreover, myeloid-cell-specific overexpression of GLUT1 in LDL receptor-deficient mice was ineffective in promoting atherosclerosis. Thus, increased glucose flux is insufficient for inflammatory myeloid cell activation and atherogenesis. If glucose promotes atherosclerosis by increasing cellular glucose flux, myeloid cells do not appear to be the key targets.
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Hexokinase 3 catalyzes the first committed step of glycolysis, while PFKFB3 catalyzes both the synthesis and degradation of fructose-2,6-bisphosphate (F2,6BP), a regulatory molecule that controls glycolysis in eukaryotes.
“Hexokinase 3 catalyzes the first committed step of glycolysis (Nishizawa et al., 2014), while PFKFB3 catalyzes both the synthesis and degradation of fructose-2,6-bisphosphate (F2,6BP), a regulatory molecule that controls glycolysis in eukaryotes.”
From TET2 Regulates the Neuroinflammatory Response in Microglia (2019) · cites this paper as Nishizawa et al., 2014
The Results and Discussion identify Hk3 as one of the hexokinases that catalyze the first, irreversible reaction in glycolysis, converting glucose to glucose-6-phosphate. The passage does not call that reaction the first committed step, so it supports the enzyme and reaction but not that qualifier. The PFKFB3 clause follows the citation and is not attributed to this source. (LLM, conf=0.85)
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- Authors
- Nishizawa, T., Kanter, J. E., Kramer, F., Barnhart, S., Shen, X., Vivekanandan-Giri, A., Wall, V. Z., Kowitz, J., Devaraj, S., O’Brien, K. D., Pennathur, S., Tang, J., Miyaoka, R. S., Raines, E. W., & Bornfeldt, K. E.
- Affiliations
- University of Washington (US)
- Baylor College of Medicine (US)
- University of Michigan (US)
- Corresponding author
- Bornfeldt, Karin E.
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2014-04
- Volume
- 7
- Issue
- 2
- Pages
- 356-365
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC4021396
- OpenAlex
- W2076336338
- Cited by
- 87
- References
- 20
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 5 · 2023: 8 · 2022: 8 · 2021: 8 · 2020: 13 · 2019: 7 · 2018: 9 · 2017: 8 · 2016: 8 · 2015: 5
- FWCI
- 3.20
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Daiichi-Sankyo
- National Institutes of Health
- National Heart, Lung, and Blood Institute (P01HL092969, R01HL067267, R01HL097365, R01HL081795, R01HL062887, P01HL018645)
- National Institute of Diabetes and Digestive and Kidney Diseases (U24DK097153, R33DK069801, P30DK020572, P30DK035816, P30DK017047, P30DK089503)
- Michigan Nutrition Obesity Research Center, Medical School, University of Michigan
- Daiichi Sankyo Europe
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- myeloid cells, glucose metabolism, glycolysis, GLUT1, glucose transporters, pentose phosphate pathway, macrophage activation, cytokine production, inflammation, atherosclerosis, LDL receptor deficiency, diabetes mellitus
- MeSH terms
- Animals, Biological Transport, Active, Glucose, Glycolysis, Inflammation, Pentose Phosphate Pathway, Receptors, LDL, Cytokines, Myeloid Cells, Atherosclerosis, Glucose Transporter Type 1, Mice
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