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Maternal obesity alters adiposity and monoamine function in genetically predisposed offspring.

Barry E Levin1, Ambrose A Dunn-Meynell

  • 1Neurology Service, Veterans Affairs Medical Center, East Orange, NJ 07018-1095, USA. levin@umdnj.edu

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|October 12, 2002
PubMed
Summary

Maternal obesity alters offspring brain monoamine metabolism, affecting norepinephrine and serotonin transporters. These changes vary based on genetic background and offspring obesity development, impacting brain nuclei size.

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Area of Science:

  • Neuroscience
  • Metabolic Research
  • Developmental Biology

Background:

  • Maternal obesity is a growing concern with potential long-term health implications for offspring.
  • Brain monoamine systems play crucial roles in regulating mood, appetite, and stress responses.
  • Understanding the prenatal programming of these systems is vital for addressing metabolic and neurological disorders.

Purpose of the Study:

  • To investigate the impact of maternal obesity on brain monoamine transporter function in adult offspring.
  • To examine how genetic background (diet-induced obesity vs. diet resistance) influences these effects.
  • To correlate changes in monoamine transporter binding with alterations in hypothalamic nucleus size.

Main Methods:

  • Utilized a rodent model with dams selectively bred for diet-induced obesity (DIO) or diet resistance (DR).

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  • Maternal obesity was induced during gestation and lactation.
  • Offspring brain tissue was analyzed for hypothalamic nucleus size and radioligand binding to norepinephrine transporters (NET) and serotonin transporters (SET).

    • Main Results:

    • Maternal obesity led to hypothalamic nucleus enlargement (ventromedial and dorsomedial nuclei) in both DIO and DR offspring.
    • Offspring of obese DIO dams showed significantly reduced NET binding in multiple brain regions.
    • Offspring of obese DR dams exhibited altered NET binding and increased SET binding across hypothalamic areas.

    Conclusions:

    • Maternal obesity induces significant alterations in offspring brain monoamine transporter systems.
    • The specific changes in NET and SET binding are dependent on the offspring's genetic predisposition and obesity status.
    • These findings highlight the critical role of the maternal metabolic environment in programming offspring neurodevelopment and monoamine function.