Evidence map›Paper›PMID 20217240›Full record

ArticleMolecular biology reports2010

Oxidative stress induced by high-glucose diet in liver of C57BL/6J mice and its underlying mechanism.

Dan Du, Yong-Hui Shi, Guo-Wei Le

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Article in Molecular biology reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

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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

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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

21 citing papers in PubMed, 32 citations in OpenAlex.

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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 at 2 institutions in 1 country.

Dan DuState Key Lab of Food Science and Technology, Jiangnan University, 1800 Lihu Road, Wuxi, 214122, Jiangsu Province, China.
Yong-Hui Shi
Guo-Wei Le
State Key Laboratory of Food Science and Technology · CNJiangnan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High glycemic index diet can induce multiple diseases. Many research indicated that oxidative stress played important role in many pathological conditions. However, the impact of gene expression and dietary habit on oxidation process are still less clear. We used high-glucose diet to feed C57BL/6J mice for 4 weeks, measured the redox status, physiological and biochemical changes related to diabetes and consequence of metabolic syndrome (nonalcoholic fatty liver, cardiovascular disease), and detected the expressions of 14,446 genes in liver of C57BL/6J mice with DNA microarray. The results showed high-glucose diet induced elevated fatty acid accumulation in liver, insulin resistance index and higher weight in C57BL/6J mice, which indicated high-glucose diet caused to the initiation and development of diabetes and consequence of metabolic syndrome. The results also showed high-glucose diet induced oxidative stress in liver of C57BL/6J mice, which might the cause of initiation and development of diabetes and consequence of metabolic syndrome. Microarray analysis found expressions of genes related to thiol redox, fatty acid oxidation in peroxisome and cytochrome P450 were significantly changed, indicating system in which non-enzyme antioxidant capacity was impaired and sources from which reactive oxygen species (ROS) generated, which revealed the molecular mechanism of oxidative stress induced by high-glucose diet. We validated our microarray findings by conducting real-time RT-PCR assays on selected genes.

Indexed as

DietAnimalsDiabetes MellitusFree Radical ScavengersGene Expression ProfilingGene Expression RegulationGlucoseLiverMetabolic SyndromeMiceMice, Inbred C57BLOligonucleotide Array Sequence AnalysisOxidation-ReductionOxidative StressReactive Oxygen SpeciesReproducibility of ResultsFree Radical ScavengersGlucoseReactive Oxygen SpeciesRNA, Messenger

Identifiers

PMID20217240
OpenAlexW2081281899

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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.