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Related Experiment Videos

Unopposed orexic pathways in the developing fetus.

Michael G Ross1, Mostafa El-Haddad, Mina DeSai

  • 1University of California, Los Angeles, Harbor-UCLA Medical Center, 1000 West, Carson Street, Box 3, Torrance, CA 90509, USA. mikeross@ucla.edu

Physiology & Behavior
|June 24, 2003
PubMed
Summary
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Fetal appetite and satiety mechanisms develop in utero, potentially influencing lifelong eating habits. Maternal environment during gestation may impact these developing systems, possibly leading to later appetite dysfunction or obesity.

Area of Science:

  • Developmental biology
  • Neuroscience
  • Gastroenterology

Background:

  • Fetal swallowing is crucial for gastrointestinal development and growth.
  • Ingestive behaviors must develop prenatally for neonatal feeding.
  • Mammalian fetuses possess mechanisms for food acquisition at birth.

Purpose of the Study:

  • To investigate the development of fetal appetite (orexic) and satiety mechanisms.
  • To determine if neurotransmitters involved in appetite regulation are functional in late gestation.
  • To explore the hypothesis that in utero imprinting of appetite mechanisms influences postnatal eating behaviors.

Main Methods:

  • Preliminary studies in ovine and human fetuses near term gestation.
  • Investigation of ingestive behavioral responses.

Related Experiment Videos

  • Assessment of orexic-mediated responses.
  • Main Results:

    • Preliminary data suggest the presence of orexic-mediated ingestive responses in late-gestation sheep and human fetuses.
    • Hypothesized development of both appetite and satiety mechanisms during the last third of gestation.
    • Neurotransmitters involved in appetite regulation are suggested to be functional.

    Conclusions:

    • Appetite and satiety systems likely develop in utero, with potential for early imprinting.
    • Maternal environmental factors during critical developmental stages may influence fetal appetite regulation.
    • Dysfunctional appetite and obesity may originate from prenatal influences on appetite set-points.