Evidence map›Paper›PMID 31541119›Full record

ArticleScientific reports2019

2-Aminoadipic acid (2-AAA) as a potential biomarker for insulin resistance in childhood obesity.

Hyo Jung Lee, Han Byul Jang, Won-Ho Kim, Keon Jae Park, Kwang Youl Kim, Sang Ick Park, Hye- Ja Lee

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.

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  10. Hepatic CBP/p300 Orchestrate Amino Acid-Driven Gluconeogenesis through Histone Crotonylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

7 authors at 3 institutions in 1 country.

Hyo Jung LeeCenter for Biomedical Sciences, National Institute of Health, Osong Health Technology Administration Complex, Chungcheongbuk-do, South Korea.
Han Byul JangCenter for Biomedical Sciences, National Institute of Health, Osong Health Technology Administration Complex, Chungcheongbuk-do, South Korea.
Won-Ho KimCenter for Biomedical Sciences, National Institute of Health, Osong Health Technology Administration Complex, Chungcheongbuk-do, South Korea.
Keon Jae ParkCenter for Biomedical Sciences, National Institute of Health, Osong Health Technology Administration Complex, Chungcheongbuk-do, South Korea.
Kwang Youl KimDepartment of Clinical Pharmacology, Inha University Hospital, Incheon, South Korea.
Sang Ick ParkCenter for Biomedical Sciences, National Institute of Health, Osong Health Technology Administration Complex, Chungcheongbuk-do, South Korea.
Hye- Ja LeeCenter for Biomedical Sciences, National Institute of Health, Osong Health Technology Administration Complex, Chungcheongbuk-do, South Korea. hyejalee@yahoo.co.kr.
Korea National Institute of Health · KRChungbuk National University · KRInha University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance is an important clinical feature of metabolic syndrome, which includes obesity and type 2 diabetes. Increased adipose energy storage in obesity promote insulin resistance and other metabolic adverse effects. To identify a new link between adipocyte and insulin resistance, we performed targeted metabolite profiling of differentiated adipocytes and studied the association between adipogenic metabolites and insulin resistance. We found a correlation between 2-aminoadipic acid (2-AAA) and adipogenic differentiation. Also, circulatory 2-AAA was positively associated with obesity-related factors (fat mass, fat percent, waist circumference, BMI, BMI z-score, triglycerides, insulin, and HOMA-IR) at baseline and after 2 years in the children cohort study. Of these factors, increased BMI z-score and HOMA-IR were the primary independent factors associated with higher 2-AAA levels, and the baseline 2-AAA level was an indicator of the BMI z-score after 2 years. To validate the relationship between 2-AAA and obesity-related factors, we analyzed changes in 2-AAA levels following obesity intervention programs in two independent studies. In both studies, changes in 2-AAA levels during the intervention period were positively correlated with changes in the BMI z-score and HOMA-IR after adjusting for confounders. Moreover, the 2-AAA levels were increased in cell and mouse models of obesity-related insulin resistance. Excess 2-AAA levels led to impaired insulin signaling in insulin-sensitive cells (liver, skeletal muscle and adipose cells) and caused abnormal gluconeogenesis. Our results demonstrate that 2-AAA is associated with adipogenesis and insulin resistance. In this regard, 2-AAA could be a potential biomarker of obesity and obesity-related metabolic disorders.

Indexed as

2-Aminoadipic AcidAdipocytesAdipogenesisAdipose TissueAdiposityAdolescentAnimalsBiomarkersBlood GlucoseBody Mass IndexCell DifferentiationChildCohort StudiesDiabetes Mellitus, Type 2FemaleFollow-Up Studies2-Aminoadipic AcidBiomarkersBlood GlucoseInsulinLeptinTriglycerides

Identifiers

PMID31541119
PMCPMC6754510
OpenAlexW2974607223

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.