Evidence map›Paper›PMID 29414685›Full record

ArticleCell metabolism2018

The Small Intestine Converts Dietary Fructose into Glucose and Organic Acids.

Cholsoon Jang, Sheng Hui, Wenyun Lu, Alexis J Cowan, Raphael J Morscher, Gina Lee, Wei Liu, Gregory J Tesz, Morris J Birnbaum, Joshua D Rabinowitz

Abstract read
In one paragraph

Article in Cell metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 333 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
333citing 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

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

  1. Pooled it
  2. Trial
  3. Ca:Mg ratio, medium-chain fatty acids, and the gut microbiome.Clinical nutrition (Edinburgh, Scotland) · 2022
    Trial
  4. Review
  5. Review
  6. Review
  7. Regional organization of nutrient absorption across the small intestine.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

273 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Cholsoon JangDepartment of Chemistry and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544, USA.
Sheng HuiDepartment of Chemistry and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544, USA.
Wenyun LuDepartment of Chemistry and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544, USA.
Alexis J CowanDepartment of Chemistry and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544, USA.
Raphael J MorscherDepartment of Chemistry and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544, USA.
Gina LeeDepartment of Pharmacology and Meyer Cancer Center, Weill Cornell Medical School, New York, NY 10065, USA.
Wei LiuPfizer Inc. Internal Medicine, Cambridge, MA 02139, USA.
Gregory J TeszPfizer Inc. Internal Medicine, Cambridge, MA 02139, USA.
Morris J BirnbaumPfizer Inc. Internal Medicine, Cambridge, MA 02139, USA.
Joshua D RabinowitzDepartment of Chemistry and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544, USA. Electronic address: joshr@princeton.edu.

Funding

VIRAL VECTOR COREP30DK019525 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI DOUGLAS J EPSTEIN · 1986 to 2026
$48.3M
PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM007388 · NIGMS · PRINCETON UNIVERSITY · PI CRISTEA, ILEANA M. · 1985 to 2022
$27.4M
Metabolism in Action: Quantitative Fluxes in MammalsDP1DK113643 · NIDDK · PRINCETON UNIVERSITY · PI RABINOWITZ, JOSHUA D · 2016 to 2020
$5.7M
NIDDK NIH HHS DP1 DK113643NIDDK NIH HHS P30 DK019525NIGMS NIH HHS T32 GM007388
6 · The paper itself

Abstract

Excessive consumption of sweets is a risk factor for metabolic syndrome. A major chemical feature of sweets is fructose. Despite strong ties between fructose and disease, the metabolic fate of fructose in mammals remains incompletely understood. Here we use isotope tracing and mass spectrometry to track the fate of glucose and fructose carbons in vivo, finding that dietary fructose is cleared by the small intestine. Clearance requires the fructose-phosphorylating enzyme ketohexokinase. Low doses of fructose are ∼90% cleared by the intestine, with only trace fructose but extensive fructose-derived glucose, lactate, and glycerate found in the portal blood. High doses of fructose (≥1 g/kg) overwhelm intestinal fructose absorption and clearance, resulting in fructose reaching both the liver and colonic microbiota. Intestinal fructose clearance is augmented both by prior exposure to fructose and by feeding. We propose that the small intestine shields the liver from otherwise toxic fructose exposure.

Indexed as

AnimalsCarboxylic AcidsDietary CarbohydratesFeeding BehaviorFructoseGlucoseIntestine, SmallIsotope LabelingLiverMetabolomeMice, Inbred C57BLMicrobiotaModels, BiologicalCarboxylic AcidsDietary CarbohydratesFructoseGlucosefluxfructosegutisotope tracingmetabolic diseasemetabolomicsmicrobiomesmall intestinesucrosesugar

Identifiers

PMID29414685
PMCPMC6032988

What OpenQuestion holds

Textmetadata
LicenceTDM
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.