Evidence map›Paper›PMID 28034722›Full record

ArticleBrain research2017

Specific regions of the brain are capable of fructose metabolism.

Sarah A Oppelt, Wanming Zhang, Dean R Tolan

Open access · greenAbstract read
In one paragraph

Article in Brain research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Brain Proteomic Responses to Glucocorticoids and Their Relationship With Transcriptome: A Systematic Meta-Analysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. GLUT5-overexpression-related tumorigenic implications.Molecular medicine (Cambridge, Mass.) · 2024
    Review
  9. Article
  10. Fructose: A New Variable to Consider in SIADH and the Hyponatremia Associated With Long-Distance Running?American journal of kidney diseases : the official journal of the National Kidney Foundation · 2023
    Article
  11. Review
  12. Article
  13. Observational
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Sarah A OppeltProgram in Molecular Biology, Cell Biology, and Biochemistry, Boston University, 5 Cummington Mall, Boston, MA, USA.
Wanming ZhangDepartment of Biology, Boston University, 5 Cummington Mall, Boston, MA, USA. Electronic address: wanming.zhang1@gmail.com.
Dean R TolanProgram in Molecular Biology, Cell Biology, and Biochemistry, Boston University, 5 Cummington Mall, Boston, MA, USA; Department of Biology, Boston University, 5 Cummington Mall, Boston, MA, USA. Electronic address: tolan@bu.edu.
Boston University · US

Funding

Metabolic Pathways and Defects in Fructose MetabolismR01DK065089 · NIDDK · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI TOLAN, DEAN R. · 2004 to 2009
$1.5M
NIDDK NIH HHS R01 DK065089
6 · The paper itself

Abstract

High fructose consumption in the Western diet correlates with disease states such as obesity and metabolic syndrome complications, including type II diabetes, chronic kidney disease, and non-alcoholic fatty acid liver disease. Liver and kidneys are responsible for metabolism of 40-60% of ingested fructose, while the physiological fate of the remaining fructose remains poorly understood. The primary metabolic pathway for fructose includes the fructose-transporting solute-like carrier transport proteins 2a (SLC2a or GLUT), including GLUT5 and GLUT9, ketohexokinase (KHK), and aldolase. Bioinformatic analysis of gene expression encoding these proteins (glut5, glut9, khk, and aldoC, respectively) identifies other organs capable of this fructose metabolism. This analysis predicts brain, lymphoreticular tissue, placenta, and reproductive tissues as possible additional organs for fructose metabolism. While expression of these genes is highest in liver, the brain is predicted to have expression levels of these genes similar to kidney. RNA in situ hybridization of coronal slices of adult mouse brains validate the in silico expression of glut5, glut9, khk, and aldoC, and show expression across many regions of the brain, with the most notable expression in the cerebellum, hippocampus, cortex, and olfactory bulb. Dissected samples of these brain regions show KHK and aldolase enzyme activity 5-10 times the concentration of that in liver. Furthermore, rates of fructose oxidation in these brain regions are 15-150 times that of liver slices, confirming the bioinformatics prediction and in situ hybridization data. This suggests that previously unappreciated regions across the brain can use fructose, in addition to glucose, for energy production.

Indexed as

Analysis of VarianceAnimalsBlotting, WesternBrainComputational BiologyFructokinasesFructoseFructose-Bisphosphate AldolaseGene ExpressionGlucose Transporter Type 5Glucose Transport Proteins, FacilitativeHexokinaseIn Situ HybridizationLiverMaleMice, Inbred C57BLFructokinasesFructoseFructose-Bisphosphate AldolaseGlucose Transporter Type 5Glucose Transport Proteins, FacilitativeHexokinaseketohexokinaseSlc2a5 protein, mouseSlc2a9 protein, mouseBrain energy metabolismFructose toxicityFructose transporters

Identifiers

PMID28034722
PMCPMC5420427
OpenAlexW2561271722

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.