Maternal Obesity Programs Adipogenic Commitment in Neonatal Mesenchymal Stem Cells: A Link to Redox-Dependent FOXO1 Signaling.
Bellalta S., Pinheiro-Machado E., Borghuis T., Prins J., Plösch T., Casanello P.
Laboratory Study with a reported sample of 15, published in J Cell Physiol (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- J Cell Physiol (2026)
- Country
- United States
- Reported sample size
- 15
- Source database
- PubMed
- PMID
- 42047265
- DOI
- 10.1002/jcp.70178
Abstract (original English)
Maternal obesity increases the risk of obesity and metabolic disease in the offspring, yet the cellular mechanisms that program adipose tissue development remain poorly understood. Mesenchymal stem cells (MSCs), the precursors of adipocytes, may represent an early target of metabolic programming during fetal development. In this study, we investigated whether maternal obesity alters stemness, redox homeostasis and adipogenic signaling through FOXO1 in neonatal MSCs. MSCs were isolated from Wharton's jelly of umbilical cords from neonates born to mothers with normal weight (NW-MSCs, n = 15) or obesity (OB-MSCs, n = 15). OB-MSCs exhibited reduced stemness characteristics, including lower OCT3/4 expression and decreased clonogenic capacity. These cells also displayed increased mitochondrial superoxide levels and reduced SOD2 expression, indicating mitochondrial oxidative stress. In addition, OB-MSCs showed increased GSH levels and decreased antioxidant enzyme response, compared to NW-MSCs. Further, OB-MSCs exhibited higher FOXO1 expression levels, reduced acetyl-FOXO1 levels, and altered subcellular localization during early adipogenesis, consistent with reduced repression of the adipogenic regulator PPARγ. Finally, OB-MSC-derived adipocytes exhibited increased PPARγ expression at later stages of differentiation. These findings suggest that maternal obesity disrupts redox balance
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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