Associations of Obesity with Linear Growth and Puberty.


Journal

Hormone research in paediatrics
ISSN: 1663-2826
Titre abrégé: Horm Res Paediatr
Pays: Switzerland
ID NLM: 101525157

Informations de publication

Date de publication:
2022
Historique:
received: 19 02 2021
accepted: 27 03 2021
pubmed: 16 6 2021
medline: 24 6 2022
entrez: 15 6 2021
Statut: ppublish

Résumé

The prevalence of obesity in childhood has increased dramatically in recent decades with increased risk of developing cardiometabolic and other comorbidities. Childhood adiposity may also influence processes of growth and puberty. Growth patterns of obesity during childhood have been shown to be associated with increased linear growth in early childhood, leading to accelerated epiphyseal growth plate (EGP) maturation. Several hormones secreted by the adipose tissue may affect linear growth in the context of obesity, both via the growth hormone IGF-1 axis and via a direct effect on the EGP. The observation that children with obesity tend to mature earlier than lean children has led to the assumption that the degree of body fatness may trigger the neuroendocrine events that lead to pubertal onset. The most probable link between obesity and puberty is leptin and its interaction with the kisspeptin system, which is an important regulator of puberty. However, peripheral action of adipose tissue could also be involved in changes in the onset of puberty. In addition, nutritional factors, epigenetics, and endocrine-disrupting chemicals are potential mediators linking pubertal onset to obesity. In this review, we focused on interactions of obesity with linear growth and pubertal processes, based on basic research and clinical data in humans. Children with obesity are subject to accelerated linear growth with risk of impaired adult height and early puberty, with its psychological consequences. The data highlight another important objective in combatting childhood obesity, for the prevention of abnormal growth and pubertal patterns.

Sections du résumé

BACKGROUND BACKGROUND
The prevalence of obesity in childhood has increased dramatically in recent decades with increased risk of developing cardiometabolic and other comorbidities. Childhood adiposity may also influence processes of growth and puberty.
SUMMARY CONCLUSIONS
Growth patterns of obesity during childhood have been shown to be associated with increased linear growth in early childhood, leading to accelerated epiphyseal growth plate (EGP) maturation. Several hormones secreted by the adipose tissue may affect linear growth in the context of obesity, both via the growth hormone IGF-1 axis and via a direct effect on the EGP. The observation that children with obesity tend to mature earlier than lean children has led to the assumption that the degree of body fatness may trigger the neuroendocrine events that lead to pubertal onset. The most probable link between obesity and puberty is leptin and its interaction with the kisspeptin system, which is an important regulator of puberty. However, peripheral action of adipose tissue could also be involved in changes in the onset of puberty. In addition, nutritional factors, epigenetics, and endocrine-disrupting chemicals are potential mediators linking pubertal onset to obesity. In this review, we focused on interactions of obesity with linear growth and pubertal processes, based on basic research and clinical data in humans.
KEY MESSAGE CONCLUSIONS
Children with obesity are subject to accelerated linear growth with risk of impaired adult height and early puberty, with its psychological consequences. The data highlight another important objective in combatting childhood obesity, for the prevention of abnormal growth and pubertal patterns.

Identifiants

pubmed: 34130293
pii: 000516171
doi: 10.1159/000516171
doi:

Substances chimiques

Human Growth Hormone 12629-01-5

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

120-136

Informations de copyright

© 2021 S. Karger AG, Basel.

Auteurs

Shlomit Shalitin (S)

National Center for Childhood Diabetes, Schneider Children's Medical Center of Israel, The Jesse Z and Sara Lea Shafer Institute for Endocrinology and Diabetes, Petach Tikva, Israel.
Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.

Galia Gat-Yablonski (G)

Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Felsenstein Medical Research Center, Petach Tikva, Israel.

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Classifications MeSH