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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Microbiome and Metabolism Research » Research » Publications at this Location » Publication #436210
Research Project: Early Life Factors and Microbiota Impact on Healthy Development

Location: Microbiome and Metabolism Research

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

Author
item PAZ, HENRY - Arkansas Children'S Nutrition Research Center (ACNC)
item ZHONG, YING - University Arkansas For Medical Sciences (UAMS)
item WILLIAM, DAVID - University Arkansas For Medical Sciences (UAMS)
item Shankar, Kartik
item ANDRES, ALINE - Arkansas Children'S Nutrition Research Center (ACNC)
item WANKHADE, UMESH - Arkansas Children'S Nutrition Research Center (ACNC)

Submitted to: Frontiers in Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/16/2026
Publication Date: 4/2/2026
Citation: Paz, H.A., Zhong, Y., William, D.K., Shankar, K., Andres, A., Wankhade, U. 2026. Maternal obesity alters adipogenic potential and mitochondrial maximal respiration in infant mesenchymal stem cells. Frontiers in Endocrinology. 17. https://doi.org/10.3389/fendo.2026.1786389.
DOI: https://doi.org/10.3389/fendo.2026.1786389

Interpretive Summary: Infants born to mothers with obesity are at greater risk of developing obesity themselves. This research utilized a novel non-invasive resource of stem cells derived from the umbilical cord of infants following birth to investigate if a mother's weight during pregnancy altered how stem cells develop into fat cells and manage energy. By examining umbilical cord stem cells from infants born to either normal-weight or overweight mothers, researchers tracked how well these cells matured over two weeks. The studie's findings indicate that stem cells from infants of overweight mothers did not develop into healthy fat cells and had less efficient mitochondria compared to those from normal-weight mothers. Overall, the research suggests that exposure to maternal obesity before birth can negatively program cells of the adipose tissue, potentially setting the stage for poor metabolic health later in life.

Technical Abstract: Objective: 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. Methods: UC-MSCs were isolated and cultured from infants born to mothers with normal weight (22.2 ± 0.3 kg/m2; NW-MSCs) or with overweight or obesity (29.3 ± 0.6 kg/m2; 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. Results: 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.Conclusions: 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.