Brain glucose metabolism in health, obesity, and cognitive decline-does insulin have anything to do with it? A narrative review
Open accessAbstract
Imaging brain glucose metabolism with fluorine-labelled fluorodeoxyglucose ([18F]-FDG) positron emission tomography (PET) has long been utilized to aid the diagnosis of memory disorders, in particular in differentiating Alzheimer’s disease (AD) from other neurological conditions causing cognitive decline. The interest for studying brain glucose metabolism in the context of metabolic disorders has arisen more recently. Obesity and type 2 diabetes—two diseases characterized by systemic insulin resistance—are associated with an increased risk for AD. Along with the well-defined patterns of fasting [18F]-FDG-PET changes that occur in AD, recent evidence has shown alterations in fasting and insulin-stimulated brain glucose metabolism also in obesity and systemic insulin resistance. Thus, it is important to clarify whether changes in brain glucose metabolism are just an epiphenomenon of the pathophysiology of the metabolic and neurologic disorders, or a crucial determinant of their pathophysiologic cascade. In this review, we discuss the current knowledge regarding alterations in brain glucose metabolism, studied with [18F]-FDG-PET from metabolic disorders to AD, with a special focus on how manipulation of insulin levels affects brain glucose metabolism in health and in systemic insulin resistance. A better understanding of alterations in brain glucose metabolism in health, obesity, and neurodegeneration, and the relationships between insulin resistance and central nervous system glucose metabolism may be an important step for the battle against metabolic and cognitive disorders.
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Brain glucose transport and metabolism can be both increased or decreased by obesity, depending upon the structure under investigation.
“Brain glucose transport and metabolism can be both increased or decreased by obesity, depending upon the structure under investigation [59].”
From The menace of obesity to depression and anxiety prevalence (2022) · cites this paper as [59]
Reductions in glucose uptake in the hippocampus have been connected to cognitive deficits in obesity.
“Reductions in glucose uptake in the hippocampus have been connected to cognitive deficits in obesity [59].”
From The menace of obesity to depression and anxiety prevalence (2022) · cites this paper as [59]
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Self-citation
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The menace of obesity to depression and anxiety prevalence
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“Reductions in glucose uptake in the hippocampus have been connected to cognitive deficits in obesity [59].”
Background
- Authors
- Rebelos, E., Rinne, J. O., Nuutila, P., & Ekblad, L. L.
- Affiliations
- University of Turku (FI)
- Corresponding author
- Ekblad, Laura L.
- Venue
- Journal of Clinical Medicine
- Publisher
- MDPI AG
- Published
- 2021-04-06
- Volume
- 10
- Issue
- 7
- Pages
- 1532
- ISSN
- 2077-0383 (ISSN-L)
- PMC
- PMC8038699
- OpenAlex
- W3141113378
- Cited by
- 66
- References
- 114
- Citations by year
- 2026: 11 · 2025: 9 · 2024: 13 · 2023: 16 · 2022: 13 · 2021: 4
- FWCI
- 2.05
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Clinical Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UTUPub (University of Turku) (submittedVersion, cc-by)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- European Foundation for the Study of Diabetes
- Suomen Kulttuurirahasto
- Emil Aaltosen Säätiö
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- brain glucose metabolism, insulin resistance, obesity, type 2 diabetes, Alzheimer's disease, cognitive decline, 18F-FDG PET, insulin-stimulated glucose metabolism, metabolic disorders, neurodegeneration
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.
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