Evidence map›Paper›PMID 34354464›Full record

ArticleSaudi journal of biological sciences2021

A metabolomics approach to investigate the proceedings of mitochondrial dysfunction in rats from prediabetes to diabetes.

Chun-Feng Huang, Ann Chen, Siao-Yun Lin, Mei-Ling Cheng, Ming-Shi Shiao, Tso-Yen Mao

Open access · hybridAbstract read
In one paragraph

Article in Saudi journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

3 citing papers in PubMed, 6 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

6 authors at 3 institutions in 1 country.

Chun-Feng HuangDepartment of Family Medicine, National Yang Ming Chiao Tung University Hospital, No.152, Xinmin Rd., Yilan City, 260 Yilan County, Taiwan, ROC.
Ann ChenDepartment of Biomedical Sciences, Chang Gung University, No.259, Wenhua 1st Rd, Guishan Dist, 33302 Taoyuan City, Taiwan, ROC.
Siao-Yun LinDepartment of Family Medicine, National Yang Ming Chiao Tung University Hospital, No.152, Xinmin Rd., Yilan City, 260 Yilan County, Taiwan, ROC.
Mei-Ling ChengDepartment of Biomedical Sciences, Chang Gung University, No.259, Wenhua 1st Rd, Guishan Dist, 33302 Taoyuan City, Taiwan, ROC.
Ming-Shi ShiaoDepartment of Biomedical Sciences, Chang Gung University, No.259, Wenhua 1st Rd, Guishan Dist, 33302 Taoyuan City, Taiwan, ROC.
Tso-Yen MaoDepartment of Leisure Services Management, Chaoyang University of Technology, No.168, Jifeng E. Rd, Wufeng District, 413 Taichung City, Taiwan, ROC.
Chang Gung University · TWChaoyang University of Technology · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus (DM) is a leading cause of preventable cardiovascular disease, but the metabolic changes from prediabetes to diabetes have not been fully clarified. This study implemented a metabolomics profiling platform to investigate the variations of metabolites and to elucidate their global profiling from metabolic syndrome to DM.

methodsMale Sprague-Dawley rats (n = 44) were divided into four groups. Three groups were separately fed with a normal diet, a high-fructose diet (HF), or a high-fat (HL) diet while one group was treated with streptozotocin. The HF and HL diet were meant to induce insulin resistance, obesity, and dyslipidemia, which known to induce DM.

resultsThe most significant metabolic variations in the DM group's urine samples were the reduced release of citric acid cycle intermediates, the increase in acylcarnitines, and the decrease in urea excretion, all of which indicated energy metabolism abnormalities and mitochondrial dysfunction. Overall, the metabolic analysis revealed tryptophan metabolic pathway variations in the prediabetic phase, even though the mitochondrial function remains unaffected.

conclusionThis study show that widespread methylations and impaired tryptophan metabolism occur in metabolic syndrome and are then followed by a decline in citric acid cycle intermediates, indicating mitochondrial dysfunction in diabetes.

Indexed as

CAN, acetonitrileDiabetesDM, diabetes mellitusGOT, glutamate oxaloacetate transaminaseGPT, glutamate pyruvate transaminaseHF, high-fructoseHL, high-fatHMDB, human metabolome databaseKEGG, kyoto encyclopedia of genes and genomesLC-MS, liquid chromatography–mass spectrometryMetabolic syndromeMetabolomicsMethylationMitochondrial dysfunctionPCA, principal component analysisPrediabetesSTZ, streptozotocinTC, total cholesterolTG, triacylglycerolTryptophan

Identifiers

PMID34354464
PMCPMC8324946
OpenAlexW3158791987

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.