Evidence map›Paper›PMID 31908508›Full record

ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2019

Detection of Secondary Metabolites as Biomarkers for the Early Diagnosis and Prevention of Type 2 Diabetes.

Jumana Y Al-Aama, Hadiah B Al Mahdi, Mohammed A Salama, Khadija H Bakur, Amani Alhozali, Hala H Mosli, Suhad M Bahijri, Ahmed Bahieldin, Lothar Willmitzer, Sherif Edris

Open access · goldAbstract read
In one paragraph

Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  3. Nutrients · 2024
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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

10 authors at 3 institutions in 3 countries.

Jumana Y Al-AamaKing Abdulaziz University, Princess Al Jawhara Albrahim Centre of Excellence in Research of Hereditary Disorders, Jeddah, KSA.ORCID 0000-0003-0594-3078
Hadiah B Al MahdiKing Abdulaziz University, Princess Al Jawhara Albrahim Centre of Excellence in Research of Hereditary Disorders, Jeddah, KSA.
Mohammed A SalamaKing Abdulaziz University, Princess Al Jawhara Albrahim Centre of Excellence in Research of Hereditary Disorders, Jeddah, KSA.
Khadija H BakurKing Abdulaziz University, Princess Al Jawhara Albrahim Centre of Excellence in Research of Hereditary Disorders, Jeddah, KSA.ORCID 0000-0002-0668-1762
Amani AlhozaliKing Abdulaziz University, Faculty of Medicine, Department of Endocrinology and Metabolism, Jeddah, KSA.
Hala H MosliKing Abdulaziz University, Faculty of Medicine, Department of Endocrinology and Metabolism, Jeddah, KSA.ORCID 0000-0002-1227-5429
Suhad M BahijriKing Abdulaziz University, Faculty of Medicine, Department of Clinical Biochemistry, Jeddah, KSA.ORCID 0000-0001-6674-5409
Ahmed BahieldinKing Abdulaziz University, Faculty of Science, Biological Sciences Department, Jeddah, KSA.
Lothar WillmitzerMax-Planck-Institut Für Molekulare Pflanzenphysiologie, Molecular Physiology, Golm, DE, Germany.
Sherif EdrisKing Abdulaziz University, Princess Al Jawhara Albrahim Centre of Excellence in Research of Hereditary Disorders, Jeddah, KSA.ORCID 0000-0002-2810-3736
King Abdulaziz University · SAAin Shams University · EGMax Planck Institute of Molecular Plant Physiology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundType 2 diabetes, or T2D, is a metabolic disease that results in insulin resistance. In the present study, we hypothesize that metabolomic analysis in blood samples of T2D patients sharing the same ethnic background can recover new metabolic biomarkers and pathways that elucidate early diagnosis and predict the incidence of T2D.

methodsThe study included 34 T2D patients and 33 healthy volunteers recruited between the years 2012 and 2013; the secondary metabolites were extracted from blood samples and analyzed using HPLC.

resultsPrincipal coordinate analysis and hierarchical clustering patterns for the uncharacterized negatively and positively charged metabolites indicated that samples from healthy individuals and T2D patients were largely separated with only a few exceptions. The inspection of the top 10% secondary metabolites indicated an increase in fucose, tryptophan and choline levels in the T2D patients, while there was a reduction in carnitine, homoserine, allothreonine, serine and betaine as compared to healthy individuals. These metabolites participate mainly in three cross-talking pathways, namely "glucagon signaling", "glycine, serine and threonine" and "bile secretion". Reduced level of carnitine in T2D patients is known to participate in the impaired insulin-stimulated glucose utilization, while reduced betaine level in T2D patients is known as a common feature of this metabolic syndrome and can result in the reduced glycine production and the occurrence of insulin resistance. However, reduced levels of serine, homoserine and allothrionine, substrates for glycine production, indicate the depletion of glycine, thus possibly impair insulin sensitivity in T2D patients of the present study.

conclusionWe introduce serine, homoserine and allothrionine as new potential biomarkers of T2D.

Indexed as

bile secretionglucagon signalingglycine productioninsulin sensitivity/resistance

Identifiers

PMID31908508
PMCPMC6930579
OpenAlexW2996333634

What Socratic holds

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Registered trials

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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 Socratic graph.