Evidence map›Paper›PMID 29899272›Full record

ArticleNutrients2018

High-Glucose or -Fructose Diet Cause Changes of the Gut Microbiota and Metabolic Disorders in Mice without Body Weight Change.

Moon Ho Do, Eunjung Lee, Mi-Jin Oh, Yoonsook Kim, Ho-Young Park

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 244 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
244citing papers in PubMed, 3 pooled it
14.6field-weighted citation impact, top 1% 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

244 citing papers in PubMed, 3 syntheses or guidelines pooled it, 419 citations in OpenAlex.

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  18. A conserved peptidase governs glucose homeostasis inbioRxiv : the preprint server for biology · 2026
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184 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Moon Ho DoResearch Division of Food Functionality, Korea Food Research Institute, Jeollabuk-do 55365, Korea. Do.Moon-ho@kfri.re.kr.
Eunjung LeeResearch Division of Strategic Food Technology, Korea Food Research Institute, Jeollabuk-do 55365, Korea. ejlee@kfri.re.kr.
Mi-Jin OhResearch Division of Food Functionality, Korea Food Research Institute, Jeollabuk-do 55365, Korea. Oh.Mi-jin@kfri.re.kr.
Yoonsook KimResearch Division of Food Functionality, Korea Food Research Institute, Jeollabuk-do 55365, Korea. kimyus@kfri.re.kr.
Ho-Young ParkResearch Division of Food Functionality, Korea Food Research Institute, Jeollabuk-do 55365, Korea. hypark@kfri.re.kr.ORCID 0000-0002-9966-9059
Korea Food Research Institute · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High fat diet-induced changes in gut microbiota have been linked to intestinal permeability and metabolic endotoxemia, which is related to metabolic disorders. However, the influence of a high-glucose (HGD) or high-fructose (HFrD) diet on gut microbiota is largely unknown. We performed changes of gut microbiota in HGD- or HFrD-fed C57BL/6J mice by 16S rRNA analysis. Gut microbiota-derived endotoxin-induced metabolic disorders were evaluated by glucose and insulin tolerance test, gut permeability, Western blot and histological analysis. We found that the HGD and HFrD groups had comparatively higher blood glucose and endotoxin levels, fat mass, dyslipidemia, and glucose intolerance without changes in bodyweight. The HGD- and HFrD-fed mice lost gut microbial diversity, characterized by a lower proportion of Bacteroidetes and a markedly increased proportion of Proteobacteria. Moreover, the HGD and HFrD groups had increased gut permeability due to alterations to the tight junction proteins caused by gut inflammation. Hepatic inflammation and lipid accumulation were also markedly increased in the HGD and HFrD groups. High levels of glucose or fructose in the diet regulate the gut microbiota and increase intestinal permeability, which precedes the development of metabolic endotoxemia, inflammation, and lipid accumulation, ultimately leading to hepatic steatosis and normal-weight obesity.

Indexed as

Dietary SugarsFructoseGastrointestinal MicrobiomeGlucoseAdiposityAnimalsBacteriaBiomarkersBlood GlucoseBody WeightDisease Models, AnimalDyslipidemiasEndotoxinsGlucose IntoleranceInflammationInsulin ResistanceBiomarkersBlood GlucoseDietary SugarsEndotoxinsFructoseGlucoseLipidsgut microbiotahigh fructose diethigh glucose dietinflammationlipid metabolism

Identifiers

PMID29899272
PMCPMC6024874
OpenAlexW2807848689

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.