Genetic pleiotropy between birth weight and adipose tissue regulation in determining the risk of childhood obesity
Although obesity primarily stems from an imbalance between energy intake and expenditure, recent research over the past years has highlighted the role of various other contributing factors, including fetal growth and birth weight. Although the link between birth weight and adult body mass index remains unclear, some genomic alterations are thought to influence both fetal growth and post-natal body mass. Specifically, potential involvement of gene variants and epigenetic modifications associated with both birth weight and adipose tissue regulation could be proposed, suggesting that a genetic pleiotropy may modify growth efficiency during the fetal stage, contributing to the development of diseases later in life and serving as a link between birth weight and obesity. Given the dual role of the insulin-like growth factor 1/insulin axis, insulin-like growth factor 2, and peroxisome proliferator-activated receptors in fetal growth and adipogenesis, the potential involvement of a pleiotropic genetic effect in the relationship between birth weight and obesity warrants further consideration. Understanding the genetic interplay between birth weight and adipose tissue regulation offers valuable insights into the developmental origins of childhood obesity. These findings highlight the critical importance of prioritizing both maternal and fetal health during pregnancy. Future research should aim to integrate genetic, epigenetic, and environmental factors to develop early, targeted interventions for high-risk populations, ultimately helping to alleviate the global obesity burden.
Authors
- Gianvincenzo Zuccotti (ORCID: https://orcid.org/0000-0002-2795-9874)
- Valeria Calcaterra (ORCID: https://orcid.org/0000-0002-2137-5974)
Publication Details
- Journal
- Gene & Protein in Disease
- Published
- 2025-05-28
- DOI
- https://doi.org/10.36922/gpd025070011
- Primary Topic
- Birth, Development, and Health
- Type
- article
- Field-Weighted Citation Impact
- 0.00