Maternal obesity alters adipogenic potential and mitochondrial maximal respiration in infant mesenchymal stem cells.

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

Abstract (original English)

To assess the adipogenic potential and mitochondrial bioenergetics of umbilical cord mesenchymal stem cells (UC-MSCs) derived from infants born to mothers with divergent body mass index and to evaluate the associations between maternal BMI and adipogenic gene expression. UC-MSCs were isolated and cultured from infants born to mothers with normal weight (22.2 ± 0.3 kg/m 2 ; NW-MSCs) or with overweight or obesity (29.3 ± 0.6 kg/m 2 ; OW/OB-MSCs). Cells were collected at baseline (day 0) and after 7 and 14 days of differentiation to assess gene expression, protein levels, and mitochondrial respiration. OW/OB-MSCs exhibited an impaired adipogenic phenotype, characterized by reduced protein levels of Cebpa and Pparg during differentiation, along with diminished mitochondrial flexibility, as evidenced by a trend toward lower maximal respiration and spare respiratory capacity compared to NW-MSCs. In addition, relationships between body mass index and expressions of Cebpa and Pparg in OW/OB-MSCs differed from NW-MSCs, particularly by day 14. Prenatal exposure to maternal obesity may disrupt programming of adipose precursors in offspring, impairing their adipogenic capacity and mitochondrial function, and potentially predisposing them to metabolically compromised adipose tissue later in life.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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