Evidence map›Paper›PMID 30919933›Full record

ArticleClinical and experimental immunology2019

High fructose-induced metabolic changes enhance inflammation in human dendritic cells.

N Jaiswal, S Agrawal, A Agrawal

Abstract read
In one paragraph

Article in Clinical and experimental immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

34 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Microglial fructose metabolism is essential for glioblastoma growth.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  19. Dietary Fructose and Fructose-Induced Pathologies.Annual review of nutrition · 2022
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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.

N JaiswalDivision of Basic and Clinical Immunology, Department of Medicine, University of California, Irvine, Irvine, CA, USA.
S AgrawalDivision of Basic and Clinical Immunology, Department of Medicine, University of California, Irvine, Irvine, CA, USA.
A AgrawalDivision of Basic and Clinical Immunology, Department of Medicine, University of California, Irvine, Irvine, CA, USA.ORCID 0000-0002-3323-9152

Funding

University of California Health Participation in the National COVID Cohort Collaborative (N3C)UL1TR001414 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI COOPER, DAN M, VILAIN, ERIC J. · 2015 to 2023
$35.1M
Institute for Clinical and Translational ScienceUL1TR000153 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI COOPER, DAN M · 2012 to 2015
$12.1M
Impaired ability of aged human dendritic cells to maintain mucosal toleranceR01AG045216 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI AGRAWAL, ANSHU · 2014 to 2018
$1.6M
NCATS NIH HHS UL1 TR000153NCATS NIH HHS UL1 TR001414NIA NIH HHS R01 AG045216
6 · The paper itself

Abstract

Dendritic cells (DCs) are critical antigen-presenting cells which are the initiators and regulators of the immune response. Numerous studies support the idea that dietary sugars influence DC functions. Increased consumption of fructose has been thought to be the leading cause of metabolic disorders. Although evidence supports their association with immune dysfunction, the specific mechanisms are not well understood. Fructose is one of the main dietary sugars in our diet. Therefore, here we compared the effect of fructose and glucose on the functions of human DCs. High levels of D-fructose compared to D-glucose led to activation of DCs in vitro by promoting interleukin (IL)-6 and IL-1β production. Moreover, fructose exposed DCs also induced interferon (IFN)-γ secretion from T cells. Proinflammatory response of DCs in high fructose environment was found to be independent of the major known metabolic regulators or glycolytic control. Instead, DC activation on acute exposure to fructose was via activation of receptor for advanced glycation end product (RAGE) in response to increased accumulation of advanced glycation end products (AGE). However, chronic exposure of DCs to high fructose environment induced a shift towards glycolysis compared to glucose cultured DCs. Further investigations revealed that the AGEs formed by fructose induced increased levels of inflammatory cytokines in DCs compared to AGEs from glucose. In summary, understanding the link between metabolic changes and fructose-induced DC activation compared to glucose has broad implications for immune dysfunction associated with metabolic disorders.

Indexed as

AdultDendritic CellsDietary SugarsFructoseGlucoseGlycation End Products, AdvancedHumansImmune System DiseasesInflammationInterferon-gammaMuscle, SkeletalReactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsT-LymphocytesYoung AdultDietary SugarsFructoseGlucoseGlycation End Products, AdvancedIFNG protein, humanInterferon-gammaReactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsAGE-RAGEdendritic cellsfructoseglucoseinflammation

Identifiers

PMID30919933
PMCPMC6642875

What OpenQuestion holds

Textmetadata
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.