Cerebral gluconeogenesis and diseases

Yip, James; Geng, Xiaokun; Shen, Jiamei; Ding, Yuchuan

doi:10.3389/fphar.2016.00521

Cited by 89Cancer, Hypoxia, and MetabolismGlycogen Storage Diseases and MyoclonusMetabolism, Diabetes, and Cancer

Cerebral gluconeogenesis and diseases

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Yip, James, Geng, Xiaokun, Shen, Jiamei, Ding, Yuchuan·2017·Frontiers in Pharmacology

DOI 10.3389/fphar.2016.00521PMC PMC5209353

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Abstract

The gluconeogenesis pathway, which has been known to normally present in the liver, kidney, intestine, or muscle, has four irreversible steps catalyzed by the enzymes: pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose 1,6-bisphosphatase, and glucose 6-phosphatase. Studies have also demonstrated evidence that gluconeogenesis exists in brain astrocytes but no convincing data have yet been found in neurons. Astrocytes exhibit significant 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 activity, a key mechanism for regulating glycolysis and gluconeogenesis. Astrocytes are unique in that they use glycolysis to produce lactate, which is then shuttled into neurons and used as gluconeogenic precursors for reduction. This gluconeogenesis pathway found in astrocytes is becoming more recognized as an important alternative glucose source for neurons, specifically in ischemic stroke and brain tumor. Further studies are needed to discover how the gluconeogenesis pathway is controlled in the brain, which may lead to the development of therapeutic targets to control energy levels and cellular survival in ischemic stroke patients, or inhibit gluconeogenesis in brain tumors to promote malignant cell death and tumor regression. While there are extensive studies on the mechanisms of cerebral glycolysis in ischemic stroke and brain tumors, studies on cerebral gluconeogenesis are limited. Here, we review studies done to date regarding gluconeogenesis to evaluate whether this metabolic pathway is beneficial or detrimental to the brain under these pathological conditions.

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Astrocytes express glucose-6-phosphatase-β (G6Pase-β) and are thus capable of gluconeogenesis.
“Astrocytes express glucose-6-phosphatase-β (G6Pase-β) and are thus capable of gluconeogenesis, or the synthesis of glucose from non-carbohydrate precursors such as aspartate, glutamate, alanine, and lactate [124].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [124]
The “Gluconeogenesis pathway” section states that astrocytes can perform gluconeogenesis using aspartate, glutamate, alanine, and lactate. The “Glycolysis and gluconeogenesis in the brain” section reports G6PC in a subset of astrocytes, but the paper identifies G6Pase-β (G6PC3) only as predominantly expressed in the brain, muscle, and kidney; it does not establish that astrocytes specifically express that isoform. Page numbers were not available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Glutamine is produced from glutamate by the activity of glutamine synthetase (GS).
“Glutamine is produced from glutamate by the activity of glutamine synthetase (GS) [124,131].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [124]
In “Glycolysis and gluconeogenesis in the brain” (page unavailable), the paper says astrocytes produce glutamine through transfer of an amino group to glutamate. In “Ischemic stroke” (page unavailable), it mentions glutamine synthetase as a glial enzyme, but does not explicitly identify it as the enzyme responsible for that production. (LLM, conf=0.82)
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The blood–brain barrier in systemic infection and inflammation
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Background
Glioblastoma Microenvironment and Cellular Interactions
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Authors: Yip, J., Geng, X., Shen, J., & Ding, Y.
Affiliations: Wayne State University (US)
Capital Medical University (CN)
Corresponding author: Geng, Xiaokun
Ding, Yuchuan
ORCID: Yip, James
Geng, Xiaokun
Ding, Yuchuan
Venue: Frontiers in Pharmacology
Publisher: Frontiers Media SA
Published: 2017-01-04
Volume: 7
Pages: 521-521
ISSN: 1663-9812 (ISSN-L)
DOI: 10.3389/fphar.2016.00521
PMC: PMC5209353
OpenAlex: W2561414178
Cited by: 89
References: 150
Citations by year: 2026: 8 · 2025: 10 · 2024: 9 · 2023: 5 · 2022: 18 · 2021: 13 · 2020: 9 · 2019: 9 · 2018: 5 · 2017: 2
FWCI: 0.70
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
Locations: Frontiers in Pharmacology (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: U.S. Department of Veterans Affairs (I01 RX001964, I01RX-001964-01)
American Heart Association (I01RX-001964-01, 14GRNT20460246)
National Natural Science Foundation of China (81501141)
Beijing Nova Program (xx2016061)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Health Sciences › Medicine › Rheumatology › Glycogen Storage Diseases and Myoclonus
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords: astrocytes, brain energy metabolism, ischemic stroke, brain tumors, lactate shuttle, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase, pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose-1,6-bisphosphatase, glucose-6-phosphatase, therapeutic target

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