Maternal obesity alters adipogenic potential and mitochondrial maximal respiration in infant mesenchymal stem cells - Scorecard - MDSpire

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

  • By

  • Henry A. Paz

  • Ying Zhong

  • David K. Williams

  • Kartik Shankar

  • Aline Andres

  • Umesh D. Wankhade

  • April 2, 2026

  • 0 min

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Clinical Scorecard: Impact of Maternal Obesity on the Adipogenic Capacity and Mitochondrial Function of Infant Mesenchymal Stem Cells

At a Glance

CategoryDetail
ConditionPrenatal exposure to maternal obesity affecting infant adipose precursor programming
Key MechanismsImpaired adipogenic differentiation via reduced Cebpa and Pparg expression and diminished mitochondrial bioenergetics in UC-MSCs
Target PopulationInfants born to mothers with normal weight versus overweight/obesity
Care SettingResearch and clinical settings focused on maternal-fetal health and early obesity risk

Key Highlights

  • UC-MSCs from infants of mothers with overweight/obesity show reduced adipogenic protein markers Cebpa and Pparg during differentiation.
  • Mitochondrial flexibility and bioenergetic capacity are diminished in UC-MSCs from offspring of mothers with elevated BMI.
  • Maternal BMI correlates differently with adipogenic gene expression in UC-MSCs by day 14 of differentiation, indicating altered developmental programming.

Guideline-Based Recommendations

Diagnosis

  • Assess maternal pre-pregnancy BMI as a risk factor for altered adipogenic programming in offspring.
  • Utilize UC-MSCs to investigate early adipogenic and mitochondrial function markers in research contexts.

Management

  • Monitor offspring of mothers with overweight/obesity for early signs of adiposity and metabolic risk.
  • Consider interventions targeting maternal weight optimization before and during pregnancy to reduce offspring metabolic programming risks.

Monitoring & Follow-up

  • Track adiposity and metabolic health longitudinally in children born to mothers with elevated BMI.
  • Evaluate mitochondrial function and adipogenic capacity in relevant research or clinical trials.

Risks

  • Increased risk of metabolically compromised adipose tissue development in offspring prenatally exposed to maternal obesity.
  • Potential predisposition to childhood and adult obesity due to impaired adipogenic differentiation and mitochondrial dysfunction.

Patient & Prescribing Data

Infants born to mothers with normal weight versus overweight/obesity

No direct treatment data; findings support preventive strategies focusing on maternal weight management to mitigate offspring metabolic risk.

Clinical Best Practices

  • Incorporate maternal BMI assessment in prenatal care to identify offspring at risk for altered adipose tissue programming.
  • Promote maternal health optimization preconception and during pregnancy to improve offspring metabolic outcomes.
  • Utilize UC-MSCs as a research tool to elucidate mechanisms of early adipogenic programming and mitochondrial function related to maternal obesity.

References

Original Source(s)

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