Circulating progranulin in human infants: relation to prenatal growth and early postnatal nutrition.


Journal

Pediatric research
ISSN: 1530-0447
Titre abrégé: Pediatr Res
Pays: United States
ID NLM: 0100714

Informations de publication

Date de publication:
09 2023
Historique:
received: 16 12 2022
accepted: 15 03 2023
revised: 04 03 2023
medline: 24 8 2023
pubmed: 9 4 2023
entrez: 8 4 2023
Statut: ppublish

Résumé

Progranulin (PGRN) displays pleiotropic biological functions and has been proposed as a biomarker for metabolic diseases. We longitudinally assessed PGRN concentrations in infants born appropriate (AGA) or small for gestational age (SGA), the latter being at risk for obesity and type 2 diabetes, especially if they experience an excessive postnatal catch-up in weight and are formula-fed (FF). The study population consisted of 183 infants who were exclusively breast-fed [(BF), AGA, n = 66; SGA, n = 40], or FF (AGA, n = 31; SGA, n = 46) over the first 4 months. Assessments included auxology, fasting glucose, insulin, IGF-1, high-molecular-weight adiponectin, PGRN and body composition (by DXA), at birth, and at age 4 and 12 months. PGRN levels were low at birth and unaffected by prenatal growth. PGRN increased at 4 and 12 months, although to a lesser extent in SGA infants, and was unrelated to the mode of feeding. PGRN correlated with markers of adiposity, inflammation and insulin resistance in both AGA and SGA infants, especially in those FF. The attenuated increase of PGRN levels in SGA infants over the first year of life, along with the association to markers of unhealthy metabolic profile, might point to a role of PGRN in future disease risks. Progranulin (PGRN) displays pleiotropic biological functions and has been proposed as a biomarker for metabolic diseases. In healthy infants, PGRN concentrations are low at birth and experience a significant and progressive increase up to age 12 months, which is less marked in infants born small for gestational age (SGA) and is unrelated to the mode of feeding. Circulating PGRN is related to markers of adiposity, inflammation, and insulin sensitivity, especially in formula-fed SGA infants. PGRN may play a role in the metabolic adaptations of SGA infants during early life, potentially contributing to the risk for obesity and type 2 diabetes in this population.

Sections du résumé

BACKGROUND
Progranulin (PGRN) displays pleiotropic biological functions and has been proposed as a biomarker for metabolic diseases. We longitudinally assessed PGRN concentrations in infants born appropriate (AGA) or small for gestational age (SGA), the latter being at risk for obesity and type 2 diabetes, especially if they experience an excessive postnatal catch-up in weight and are formula-fed (FF).
METHODS
The study population consisted of 183 infants who were exclusively breast-fed [(BF), AGA, n = 66; SGA, n = 40], or FF (AGA, n = 31; SGA, n = 46) over the first 4 months. Assessments included auxology, fasting glucose, insulin, IGF-1, high-molecular-weight adiponectin, PGRN and body composition (by DXA), at birth, and at age 4 and 12 months.
RESULTS
PGRN levels were low at birth and unaffected by prenatal growth. PGRN increased at 4 and 12 months, although to a lesser extent in SGA infants, and was unrelated to the mode of feeding. PGRN correlated with markers of adiposity, inflammation and insulin resistance in both AGA and SGA infants, especially in those FF.
CONCLUSIONS
The attenuated increase of PGRN levels in SGA infants over the first year of life, along with the association to markers of unhealthy metabolic profile, might point to a role of PGRN in future disease risks.
IMPACT
Progranulin (PGRN) displays pleiotropic biological functions and has been proposed as a biomarker for metabolic diseases. In healthy infants, PGRN concentrations are low at birth and experience a significant and progressive increase up to age 12 months, which is less marked in infants born small for gestational age (SGA) and is unrelated to the mode of feeding. Circulating PGRN is related to markers of adiposity, inflammation, and insulin sensitivity, especially in formula-fed SGA infants. PGRN may play a role in the metabolic adaptations of SGA infants during early life, potentially contributing to the risk for obesity and type 2 diabetes in this population.

Identifiants

pubmed: 37031297
doi: 10.1038/s41390-023-02595-1
pii: 10.1038/s41390-023-02595-1
doi:

Substances chimiques

Progranulins 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1189-1194

Informations de copyright

© 2023. The Author(s), under exclusive licence to the International Pediatric Research Foundation, Inc.

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Auteurs

Marta Díaz (M)

Pediatric Research Institute Sant Joan de Déu, University of Barcelona, 08950, Esplugues, Barcelona, Spain.
Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Health Institute Carlos III, Madrid, Spain.

Alberto Mestres-Arenas (A)

Biochemistry and Molecular Biomedicine Department, Biomedicine Institute, University of Barcelona, 08028, Barcelona, Spain.
Network Biomedical Research Center of Physiopathology of Obesity and Nutrition (CIBEROBN), Health Institute Carlos III, 28029, Madrid, Spain.

Carles Lerin (C)

Pediatric Research Institute Sant Joan de Déu, University of Barcelona, 08950, Esplugues, Barcelona, Spain.
Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Health Institute Carlos III, Madrid, Spain.

Rubén Cereijo (R)

Biochemistry and Molecular Biomedicine Department, Biomedicine Institute, University of Barcelona, 08028, Barcelona, Spain.
Research Institute, Hospital de la Santa Creu i de Sant Pau, Barcelona, Spain.

Abel López-Bermejo (A)

Department of Pediatrics, Dr. Josep Trueta Hospital, 17007, Girona, Spain.
Girona Institute forBiomedical Research, 17007, Girona, Spain.

Francis de Zegher (F)

University of Leuven, 3000, Leuven, Belgium.

Francesc Villarroya (F)

Biochemistry and Molecular Biomedicine Department, Biomedicine Institute, University of Barcelona, 08028, Barcelona, Spain. fvillarroya@ub.edu.
Network Biomedical Research Center of Physiopathology of Obesity and Nutrition (CIBEROBN), Health Institute Carlos III, 28029, Madrid, Spain. fvillarroya@ub.edu.

Lourdes Ibáñez (L)

Pediatric Research Institute Sant Joan de Déu, University of Barcelona, 08950, Esplugues, Barcelona, Spain. libanez@hsjdbcn.org.
Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Health Institute Carlos III, Madrid, Spain. libanez@hsjdbcn.org.

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