Evidence map›Paper›PMID 29506909›Full record

ArticleMolecular metabolism2018

VEGF and GLUT1 are highly heritable, inversely correlated and affected by dietary fat intake: Consequences for cognitive function in humans.

Rita Schüler, Nicole Seebeck, Martin A Osterhoff, Veronica Witte, Agnes Flöel, Andreas Busjahn, Alexander Jais, Jens C Brüning, Turid Frahnow, Stefan Kabisch and 4 more

Registry-linked trialOpen access · goldAbstract readControlled Clinical TrialTwin Study
In one paragraph

Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01631123 (Genetic Determinants of Metabolic Responses to Isocaloric Carbohydrate and Fat Diet Strategies), which is not on this map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.4field-weighted citation impact, top 11% 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.

NCT01631123 nacompletednot on this map

Genetic Determinants of Metabolic Responses to Isocaloric Carbohydrate and Fat Diet Strategies

TypeinterventionalSponsorGerman Institute of Human NutritionRan2009 to 2012Enrolled120ConditionsMetabolic Response to Dietary ModificationArmsIsocaloric high carbohydrate diet intervention, Isocaloric high fat diet intervention
3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 64 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Neurovascular plasticity as a modulator of hypothalamic function.Reviews in endocrine & metabolic disorders · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Alterations of the blood-brain barrier during aging.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Review
  10. Review
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  12. Syndecan-1 as a predictor of vulnerable atherosclerotic plaques.Frontiers in cell and developmental biology · 2024
    Article
  13. Article
  14. Review
  15. Article
  16. Article
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  18. Variation inFrontiers in cardiovascular medicine · 2023
    Article
  19. The Role of VEGF Family in Lipid Metabolism.Current pharmaceutical biotechnology · 2023
    Article
  20. Article
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

14 authors at 5 institutions in 1 country.

Rita SchülerDepartment of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), Nuthetal 14558, Germany; German Center for Diabetes Research (DZD), München-Neuherberg 85764, Germany. Electronic address: Rita.Schueler@dife.de.
Nicole SeebeckDepartment of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), Nuthetal 14558, Germany.
Martin A OsterhoffDepartment of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), Nuthetal 14558, Germany; German Center for Diabetes Research (DZD), München-Neuherberg 85764, Germany; Department of Endocrinology, Diabetes and Nutrition, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin 12200, Germany.
Veronica WitteDepartment of Neurology, Charité-Universitätsmedizin Berlin, Berlin 10117, Germany; NeuroCure Cluster of Excellence, Charité-Universitätsmedizin Berlin, Berlin 10117, Germany; Department of Neurology, Max Planck Institute of Human Cognitive and Brain Sciences, SFB 1052 Obesity Mechanism subproject A1, University of Leipzig, Leipzig 04103, Germany.
Agnes FlöelDepartment of Neurology, Charité-Universitätsmedizin Berlin, Berlin 10117, Germany; NeuroCure Cluster of Excellence, Charité-Universitätsmedizin Berlin, Berlin 10117, Germany; Department of Neurology, University Medicine Greifswald, Greifswald 17475, Germany.
Andreas BusjahnHealthTwiSt GmbH, Berlin 13125, Germany.
Alexander JaisDepartment of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Cologne 50931, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Cologne 50924, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne 50931, Germany.
Jens C BrüningGerman Center for Diabetes Research (DZD), München-Neuherberg 85764, Germany; Department of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Cologne 50931, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Cologne 50924, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Center of Molecular Medicine Cologne (CMMC), University of Cologne, Cologne 50931, Germany.
Turid FrahnowDepartment of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), Nuthetal 14558, Germany.
Stefan KabischDepartment of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), Nuthetal 14558, Germany; German Center for Diabetes Research (DZD), München-Neuherberg 85764, Germany; Department of Endocrinology, Diabetes and Nutrition, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin 12200, Germany.
Olga PivovarovaDepartment of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), Nuthetal 14558, Germany; German Center for Diabetes Research (DZD), München-Neuherberg 85764, Germany; Department of Endocrinology, Diabetes and Nutrition, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin 12200, Germany.
Silke HornemannDepartment of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), Nuthetal 14558, Germany.
Michael KruseDepartment of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), Nuthetal 14558, Germany; Department of Endocrinology, Diabetes and Nutrition, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin 12200, Germany.
Andreas F H PfeifferDepartment of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), Nuthetal 14558, Germany; German Center for Diabetes Research (DZD), München-Neuherberg 85764, Germany; Department of Endocrinology, Diabetes and Nutrition, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin 12200, Germany.
Deutsches Diabetes-Zentrum e.V. · DEGerman Institute of Human Nutrition · DEUniversity of Cologne · DEMax Planck Institute for Human Cognitive and Brain Sciences · DEUniversitätsmedizin Greifswald · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveReduction of brain glucose transporter GLUT1 results in severe neurological dysfunction. VEGF is required to restore and maintain brain glucose uptake across the blood brain barrier via GLUT1, which was shown to be acutely diminished in response to a high fat diet (HFD) in mice. The genetic and HFD-related regulation and association of VEGF and GLUT1 (SLC2A1) in humans was investigated in the NUtriGenomic Analysis in Twins (NUGAT) study.

methods92 healthy and non-obese twins were standardized to a high-carbohydrate low-fat diet for 6 weeks before switched to a 6-week HFD under isocaloric conditions. Three clinical investigation days were conducted: after 6 weeks of low-fat diet and after 1 and 6 weeks of HFD. Serum VEGF and other cytokine levels were measured using ELISA. Gene expression in subcutaneous adipose tissue was assessed by quantitative Real-Time PCR. Genotyping was performed using microarray. The Auditory Verbal Learning Task was conducted to measure cognitive performance.

resultsIn this human study, we showed that the environmental regulation of SLC2A1 expression and serum VEGF by HFD was inversely correlated and both factors showed strong heritability (>90%). In response to the HFD containing 45% fat, serum VEGF levels increased (P = 0.002) while SLC2A1 mRNA expression in adipose tissue decreased (P = 0.001). Higher BMI was additionally associated with lower SLC2A1 expression. AA-genotypes of the rs9472159 polymorphism, which explained ∼39% of the variation in circulating VEGF concentrations, showed significantly reduced serum VEGF levels (P = 6.4 × 10

conclusionsThe results provide evidence to suggest the translatability of the dietary regulation of VEGF and GLUT1 from mouse models to humans. Our data demonstrate that HFD induces a genetically determined and correlated decrease of GLUT1 and increase of VEGF which may affect memory performance. CLINICAL TRIAL REGISTRATION NUMBER: NCT01631123.

Indexed as

CognitionAdipose TissueAdolescentAdultDietary FatsDiet, High-FatFemaleGlucose Transporter Type 1HumansMaleMiddle AgedPolymorphism, Single NucleotideTwins, DizygoticTwins, MonozygoticVascular Endothelial Growth Factor ADietary FatsGlucose Transporter Type 1SLC2A1 protein, humanVascular Endothelial Growth Factor AVEGFA protein, humanCognitionGLUT1High fat dietVEGF

Identifiers

PMID29506909
PMCPMC6001408
OpenAlexW2791999377

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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.