Association of Bright Liver With the PNPLA3 I148M Gene Variant in 1-Year-Old Toddlers.


Journal

The Journal of clinical endocrinology and metabolism
ISSN: 1945-7197
Titre abrégé: J Clin Endocrinol Metab
Pays: United States
ID NLM: 0375362

Informations de publication

Date de publication:
01 06 2019
Historique:
received: 14 09 2018
accepted: 09 01 2019
pubmed: 17 1 2019
medline: 28 4 2020
entrez: 17 1 2019
Statut: ppublish

Résumé

Nonalcoholic fatty liver disease (NAFLD) is being increasingly diagnosed at younger ages, pointing toward an early-life origin. To evaluate the frequency and risk factors for bright liver (BL) in 1-year-old toddlers. Secondary analysis of the 1-year follow-up of the Feeding Study. Exposures were child PNPLA3 and TM6SF2 gene variants; child anthropometry at birth and at 1 year of follow-up; child subcutaneous, visceral, and epicardial adipose tissue at 1 year of follow-up; maternal anthropometry at the start and at the end of pregnancy; and maternal red blood cell fatty-acid composition at the third trimester of pregnancy. General population. Among 505 mother-toddler pairs, 391 children (77%) underwent liver and abdominal ultrasonography at the 1-year follow-up. BL as diagnosed by ultrasonography. Seventeen (4%) of 391 toddlers had BL. Compared with the toddlers with the PNPLA 3 CC genotype, the odds (95% CI) of BL were 3.01 (1.05 to 8.64, P < 0.05) times higher in those with the PNAPLA3 CG genotype and 5.37 (1.12 to 25.77, P < 0.05) higher in those with the PNPLA3 CC genotype. We found no association between BL status and TM6SF2. Body weight, body mass index, and maternal weight gain during pregnancy were higher in BL+ than in BL- children. Visceral adipose tissue was higher but subcutaneous adipose tissue and epicardial adipose tissue were similar in BL+ and BL- children. Four percent of the Feeding Study children had BL at 1 year of age. In line with expectations, PNAPLA3 was already a predictor of BL at this early age.

Identifiants

pubmed: 30649436
pii: 5288753
doi: 10.1210/jc.2018-01998
doi:

Substances chimiques

Membrane Proteins 0
TM6SF2 protein, human 0
Lipase EC 3.1.1.3
adiponutrin, human EC 3.1.1.3

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2163-2170

Informations de copyright

Copyright © 2019 Endocrine Society.

Auteurs

Giorgio Bedogni (G)

Research Area for Multifactorial Disease, Children's Hospital Bambino Gesù, Rome, Italy.
Clinical Epidemiology Unit, Liver Research Center, Basovizza, Trieste, Italy.

Giuseppe De Matteis (G)

Research Area for Multifactorial Disease, Children's Hospital Bambino Gesù, Rome, Italy.
Department of Internal and Emergency Medicine, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.

Marta Fabrizi (M)

Research Area for Multifactorial Disease, Children's Hospital Bambino Gesù, Rome, Italy.

Anna Alisi (A)

Research Unit of Molecular Genetics of Complex Phenotypes, Bambino Gesù Children's Hospital, Rome, Italy.

Annalisa Crudele (A)

Research Unit of Molecular Genetics of Complex Phenotypes, Bambino Gesù Children's Hospital, Rome, Italy.

Fabrizio Pizzolante (F)

Department of Internal Medicine and Gastroenterology, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.

Fabrizio Signore (F)

Department of Obstetrics and Gynecology, Misericordia Hospital, Grosseto, Italy.

Bruno Dallapiccola (B)

Scientific Directorate, Bambino Gesù Children's Hospital, Rome, Italy.

Valerio Nobili (V)

Department of Pediatrics, University La Sapienza, Rome, Italy.
Hepatology Gastroenterology and Nutrition, Bambino Gesù Children's Hospital, Rome, Italy.

Melania Manco (M)

Research Area for Multifactorial Disease, Children's Hospital Bambino Gesù, Rome, Italy.

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Classifications MeSH