Generation of Maternal Obesity Models in Studies of Developmental Programming in Rodents

Paul D Taylor1, Phillippa A Matthews2, Imran Y Khan2

  • 1Division of Women's Health, Women's Health Academic Centre, King's College London and King's Health Partners, London, UK. Paul.taylor@kcl.ac.uk.

Insights

Maternal obesity during pregnancy, indicated by pre-pregnancy body mass index (BMI) and gestational weight gain (GWG), is linked to offspring cardio-metabolic risks. Rodent models show early life exposure to maternal obesity can lead to hypertension and metabolic syndrome in offspring.

Area of Science:

  • Reproductive biology and developmental origins of health and disease (DOHaD).
  • Metabolic and cardiovascular health research.

Background:

  • Human cohort studies link pre-pregnancy body mass index (BMI) and gestational weight gain (GWG) to offspring cardio-metabolic risk factors, including blood pressure.
  • Rodent models demonstrate that maternal obesity during pregnancy can induce metabolic syndrome and hypertension in offspring, persisting from early development.
  • These findings suggest that the in-utero environment of maternal obesity may predispose humans to early-onset metabolic syndrome and essential hypertension.

Purpose of the Study:

  • To review the development and utility of rodent models for studying maternal overnutrition and obesity.
  • To explore how these models generate hypotheses for clinical translation regarding offspring metabolic health.
  • To inform the development of interventions targeting obesity-related comorbidities in future generations.

Main Methods:

  • Development and characterization of rodent models simulating maternal overnutrition and obesity during gestation.
  • Assessment of offspring cardio-metabolic parameters, including blood pressure and metabolic syndrome markers.
  • Analysis of developmental programming related to the maternal nutritional environment.

Main Results:

  • Rodent models successfully replicate key aspects of metabolic syndrome and hypertension observed in offspring of obese mothers.
  • Early life exposure to maternal obesity in these models leads to persistent sympathetic hyperresponsiveness and elevated blood pressure.
  • These models provide a platform for investigating the mechanisms linking maternal obesity to offspring metabolic dysfunction.

Conclusions:

  • Rodent models of maternal obesity are crucial for understanding the developmental origins of metabolic syndrome and hypertension.
  • Insights from animal studies support the hypothesis that maternal nutritional status during pregnancy impacts offspring long-term health.
  • Further research using these models can guide interventions to mitigate the intergenerational effects of obesity and its comorbidities.

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