Evidence map›Paper›PMID 39082260›Full record

ArticleLiver international : official journal of the International Association for the Study of the Liver2024

Dynamic pattern of postprandial bile acids in paediatric non-alcoholic fatty liver disease.

Jiating Huang, Hu Lin, A-Na Liu, Wei Wu, Anna Alisi, Rohit Loomba, Cuifang Xu, Wenqin Xiang, Jie Shao, Guanping Dong and 3 more

Abstract read
In one paragraph

Article in Liver international : official journal of the International Association for the Study of the Liver, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Lipid metabolism in homeostasis and disease.Signal transduction and targeted therapy · 2026
    Review
  3. Article
  4. Article
  5. Review
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

13 authors.

Jiating HuangDepartment of Endocrinology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Hu LinDepartment of Endocrinology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
A-Na LiuDepartment of Endocrinology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Wei WuDepartment of Endocrinology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Anna AlisiResearch Unit of Genetics of Complex Phenotypes, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.ORCID 0000-0001-7241-6329
Rohit LoombaNAFLD Research Center, Division of Gastroenterology, University of California, San Diego, La Jolla, California, USA.ORCID 0000-0002-4845-9991
Cuifang XuDepartment of Endocrinology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Wenqin XiangDepartment of Clinical Laboratory, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Jie ShaoDepartment of Child Healthcare, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Guanping DongDepartment of Endocrinology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Ming-Hua ZhengMAFLD Research Center, Department of Hepatology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID 0000-0003-4984-2631
Junfen FuDepartment of Endocrinology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Yan NiDepartment of Endocrinology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.ORCID 0000-0003-1779-7266

Funding

UC San Diego Clinical and Translational Research InstituteUL1TR001442 · NCATS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FIRESTEIN, GARY S, HOGARTH, MICHAEL · 2015 to 2024
$88.3M
Pediatric Trials in Non-Alcoholic Steatohepatitis (NASH)U01DK061734 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROHIT LOOMBA · 2002 to 2026
$24.4M
Tissue-specific roles of FXR in CVD and NASHP01HL147835 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI EVANS, RONALD M · 2020 to 2024
$12.2M
San Diego Digestive Diseases Research CenterP30DK120515 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Bernd G. Schnabl · 2019 to 2026
$10.8M
HIV MASLD Clinical Research Network (HCRN)R01DK121378 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI NAGA P CHALASANI, ROHIT LOOMBA · 2020 to 2026
$8.7M
Novel IL-23 inhibitor for the treatment of alcohol associated liver diseaseU01AA029019 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KISSELEVA, TATIANA, LOOMBA, ROHIT · 2020 to 2024
$3.7M
QUS Technology for Diagnosis and Grading of Hepatic Steatosis in NAFLDR01DK106419 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LOOMBA, ROHIT, SIRLIN, CLAUDE B · 2015 to 2019
$3.4M
San Diego Cirrhosis Clinical Research NetworkU01DK130190 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROHIT LOOMBA · 2021 to 2026
$2.3M
Non-invasive screening of diabetics for advanced fibrosis due to NAFLDR01DK124318 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LOOMBA, ROHIT · 2020 to 2022
$1.7M
Key Research & Development Program of Zhejiang 2023C03047National Key Research and Development Program of China 2021YFC2701901National Key Research and Development Program of China 2021YFC2701904National Natural Science Foundation of China 81900510National Natural Science Foundation of China 82170583NCATS NIH HHS 5UL1TR001442NCATS NIH HHS UL1 TR001442NHLBI NIH HHS P01 HL147835NHLBI NIH HHS P01HL147835NIAAA NIH HHS U01 AA029019NIAAA NIH HHS U01AA029019NIDDK NIH HHS P30 DK120515NIDDK NIH HHS P30DK120515NIDDK NIH HHS R01 DK106419NIDDK NIH HHS R01DK106419NIDDK NIH HHS R01 DK121378NIDDK NIH HHS R01DK121378NIDDK NIH HHS R01 DK124318NIDDK NIH HHS R01DK124318NIDDK NIH HHS U01 DK061734NIDDK NIH HHS U01DK061734NIDDK NIH HHS U01 DK130190NIDDK NIH HHS U01DK130190
6 · The paper itself

Abstract

backgroundDysregulation of bile acids (BAs), as important signalling molecules in regulating lipid and glucose metabolism, contributes to the development of non-alcoholic fatty liver disease (NAFLD). However, static BA profiles during fasting may obscure certain pathogenetic aspects. In this study, we investigate the dynamic alterations of BAs in response to an oral glucose tolerance test (OGTT) among children with NAFLD.

methodsWe recruited 230 subjects, including children with overweight/obesity, or complicated with NAFLD, and healthy controls. Serum BAs, 7-hydroxy-4-cholesten-3-one (C4) and fibroblast growth factor 19 (FGF19) were quantified during OGTT. Clinical markers related to liver function, lipid metabolism and glucose metabolism were assessed at baseline or during OGTT.

findingsConjugated BAs increased while unconjugated ones decreased after glucose uptake. Most BAs were blunted in response to glucose in NAFLD (p > .05); only glycine and taurine-conjugated chenodeoxycholic acid (CDCA) and cholic acid (CA) were responsive (p < .05). Primary BAs were significantly increased while secondary BAs were decreased in NAFLD. C4 and FGF19 were significantly increased while their ratio FGF19/C4 ratio was decreased in NAFLD. The dynamic pattern of CDCA and taurine-conjugated hyocholic acid (THCA) species was closely correlated with glucose (correlation coefficient r = .175 and -.233, p < .05), insulin (r = .327 and -.236, p < .05) and c-peptide (r = .318 and -.238, p < .05). Among which, CDCA was positively associated with liver fat content in NAFLD (r = .438, p < .05). Additionally, glycochenodeoxycholic acid (GCDCA), CDCA and THCA were potential biomarkers to discriminate paediatric NAFLD from healthy controls and children with obesity.

interpretationThis study provides novel insights into the dynamics of BAs during OGTT in paediatric NAFLD. The observed variations in CDCA and HCA species were associated with liver dysfunction, dyslipidaemia and dysglycaemia, highlighting their potential roles as promising diagnostic and therapeutic targets in NAFLD.

Indexed as

Bile Acids and SaltsCholestenonesFibroblast Growth FactorsGlucose Tolerance TestNon-alcoholic Fatty Liver DiseasePostprandial PeriodAdolescentBiomarkersBlood GlucoseCase-Control StudiesChildFemaleHumansLipid MetabolismMalePediatric Obesity7 alpha-hydroxy-4-cholesten-3-oneBile Acids and SaltsBiomarkersBlood GlucoseCholestenonesFGF19 protein, humanFibroblast Growth Factorsbile acidsblunted responsedynamic patternnon‐alcoholic fatty liver diseaseoral glucose tolerance test

Identifiers

PMID39082260
PMCPMC12393223

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