Evidence map›Paper›PMID 32856048›Full record

ArticleThe Journal of nutrition2020

Host Genetic Background and Gut Microbiota Contribute to Differential Metabolic Responses to Fructose Consumption in Mice.

In Sook Ahn, Jennifer M Lang, Christine A Olson, Graciel Diamante, Guanglin Zhang, Zhe Ying, Hyae Ran Byun, Ingrid Cely, Jessica Ding, Peter Cohn and 5 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of nutrition, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  11. Article
  12. Review
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  14. Diets, Gut Microbiota and Metabolites.Phenomics (Cham, Switzerland) · 2023
    Review
  15. Dietary Fructose and Fructose-Induced Pathologies.Annual review of nutrition · 2022
    Review
  16. Article
  17. Frontiers in immunology · 2022
    Review
  18. Article
  19. Article
  20. Review
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

15 authors at 1 institution in 1 country.

In Sook AhnDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.
Jennifer M LangDepartment of Medicine, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Christine A OlsonDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.
Graciel DiamanteDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.
Guanglin ZhangDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.
Zhe YingDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.
Hyae Ran ByunDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.
Ingrid CelyDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.
Jessica DingDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.
Peter CohnDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.
Ira KurtzDepartment of Medicine, Division of Nephrology, University of California, Los Angeles, CA, USA.
Fernando Gomez-PinillaDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.
Aldons J LusisDepartment of Medicine, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Elaine Y HsiaoDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.
Xia YangDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, USA.
University of California, Los Angeles · US

Funding

ULTRASTRUCTURE OF THE INTIMA IN EARLY LESION FORMATIONP01HL030568 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 1985 to 2019
$55.2M
Training in Molecular ToxicologyT32ES015457 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ALLARD, PATRICK, HANKINSON, OLIVER NMN · 2008 to 2025
$4.0M
NEPHROLOGY SCIENTIST TRAINING GRANTT32DK007789 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KURTZ, IRA · 2000 to 2017
$1.5M
Dissecting gut microbiota-based effects on aging-associated cognitive deficitsF31AG064844 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI OLSON, CHRISTINE · 2019 to 2020
$79k
Functional Role of IL-6 in Fetal Brain Development and Abnormal BehaviorF31MH090749 · NIMH · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI HSIAO, ELAINE · 2011 to 2012
$64k
NHLBI NIH HHS P01 HL030568NIA NIH HHS F31 AG064844NIDDK NIH HHS T32 DK007789NIEHS NIH HHS T32 ES015457NIMH NIH HHS F31 MH090749
6 · The paper itself

Abstract

backgroundIt is unclear how high fructose consumption induces disparate metabolic responses in genetically diverse mouse strains.

objectiveWe aimed to investigate whether the gut microbiota contributes to differential metabolic responses to fructose.

methodsEight-week-old male C57BL/6J (B6), DBA/2J (DBA), and FVB/NJ (FVB) mice were given 8% fructose solution or regular water (control) for 12 wk. The gut microbiota composition in cecum and feces was analyzed using 16S ribosomal DNA sequencing, and permutational multivariate ANOVA (PERMANOVA) was used to compare community across mouse strains, treatments, and time points. Microbiota abundance was correlated with metabolic phenotypes and host gene expression in hypothalamus, liver, and adipose tissues using Biweight midcorrelation. To test the causal role of the gut microbiota in determining fructose response, we conducted fecal transplants from B6 to DBA mice and vice versa for 4 wk, as well as gavaged antibiotic-treated DBA mice with Akkermansia for 9 wk, accompanied with or without fructose treatment.

resultsCompared with B6 and FVB, DBA mice had significantly higher Firmicutes to Bacteroidetes ratio and lower baseline abundance of Akkermansia and S24-7 (P < 0.05), accompanied by metabolic dysregulation after fructose consumption. Fructose altered specific microbial taxa in individual mouse strains, such as a 7.27-fold increase in Akkermansia in B6 and 0.374-fold change in Rikenellaceae in DBA (false discovery rate <5%), which demonstrated strain-specific correlations with host metabolic and transcriptomic phenotypes. Fecal transplant experiments indicated that B6 microbes conferred resistance to fructose-induced weight gain in DBA mice (F = 43.1, P < 0.001), and Akkermansia colonization abrogated the fructose-induced weight gain (F = 17.8, P < 0.001) and glycemic dysfunctions (F = 11.8, P = 0.004) in DBA mice.

conclusionsOur findings support that differential microbiota composition between mouse strains is partially responsible for host metabolic sensitivity to fructose, and that Akkermansia is a key bacterium that confers resistance to fructose-induced metabolic dysregulation.

Indexed as

AnimalsBacteriaCecumEnergy MetabolismFecal Microbiota TransplantationFecesFructoseGastrointestinal MicrobiomeMaleMiceMice, Inbred StrainsRandom AllocationFructoseAkkermansiafecal transplantfructosegene by diet interactiongut microbiotametabolic syndromemicrobiota-host interaction

Identifiers

PMID32856048
PMCPMC7549307
OpenAlexW3082343303

What Socratic 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 Socratic graph.