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Glucose intolerance as a consequence of hematopoietic stem cell dysfunction in offspring of obese mice

Merve Denizli1, James Ropa2, Lindsay Beasley3

  • 1Department of Pediatrics, Neonatal-Perinatal Medicine, Indiana University School of Medicine, Indianapolis, 46202, USA.

Molecular Metabolism
|August 14, 2024
PubMed

Insights

Maternal obesity affects offspring hematopoietic stem and progenitor cells (HSPCs) differently based on sex. Male offspring of obese mothers showed impaired HSPC function and glucose intolerance, highlighting sex-specific impacts on metabolic health.

Area of Science:

  • Reproductive biology
  • Developmental biology
  • Metabolic health

Background:

  • Maternal obesity is a growing concern, increasing offspring's risk for diseases related to hematopoietic and metabolic systems.
  • Offspring sex influences disease susceptibility, suggesting maternal obesity may cause sex-specific changes in hematopoietic stem and progenitor cell (HSPC) function.
  • The precise impact of maternal obesity on offspring HSPC function and their role in metabolic regulation remains unclear.

Purpose of the Study:

  • To investigate the sex-specific effects of maternal obesity on offspring HSPC function.
  • To determine if altered HSPC function in offspring of obese mothers contributes to metabolic dysfunction.
  • To test the hypothesis that maternal obesity induces sex-dependent reprogramming of offspring HSPC impacting metabolic health.

Main Methods:

  • Assessed HSPC phenotype in mice born to control and diet-induced obese dams at postnatal day 21 and 8 weeks.
  • Performed competitive primary and secondary transplants using sorted HSPCs from P21 mice.
  • Conducted transcriptomic analysis (RNA-seq) on HSPCs and metabolic assessments (glucose and insulin tolerance tests) in transplant recipients.

Main Results:

  • Male offspring from obese dams exhibited reduced HSPC numbers and impaired engraftment capacity compared to controls.
  • Female offspring from obese dams showed largely unaffected HSPC numbers and function, with RNA-seq indicating immune-stimulatory pathways.
  • Transplant recipients of HSPCs from male offspring of obese dams developed glucose intolerance, while recipients of female offspring HSPCs did not.

Conclusions:

  • Maternal obesity exposure has lasting, sex-specific effects on offspring HSPC function.
  • Offspring HSPCs play a role in mediating the metabolic consequences of maternal obesity.
  • These findings underscore the importance of considering sex in the context of maternal obesity and offspring health.
Abstract

Keywords:
Hematopoietic stem cellOffspring exposed to maternal obesityStem cell transplant

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