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Correction: Desai et al. TNFα-Induced Oxidative Stress and Mitochondrial Dysfunction Alter Hypothalamic Neurogenesis and Promote Appetite Versus Satiety Neuropeptide Expression in Mice. <i>Brain Sci.</i><b>2022</b>, <i>12</i>, 900.

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Control of Eating Behavior Using a Novel Feedback System
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Developmental programming of appetite/satiety.

Michael G Ross1, Mina Desai

  • 1Perinatal Research Laboratories, Department of Obstetrics and Gynecology, David Geffen School of Medicine, University of California, Los Angeles, Calif., USA.

Annals of Nutrition & Metabolism
|July 26, 2014
PubMed
Summary
This summary is machine-generated.

Maternal nutrition during pregnancy significantly impacts offspring obesity risk. Both small for gestational age infants and those born to mothers on high-fat diets face increased odds of developing obesity due to altered appetite regulation.

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Area of Science:

  • Developmental biology
  • Metabolic disorders
  • Neuroscience

Background:

  • Obesity is commonly linked to Western lifestyle factors like diet and activity levels.
  • However, maternal/fetal nutrition during gestation is increasingly recognized as a critical determinant of offspring obesity risk.
  • Infants small for gestational age (SGA) and those born to obese mothers on high-fat diets exhibit elevated risk for adult obesity.

Purpose of the Study:

  • To investigate how maternal/fetal under- or overnutrition influences offspring appetite regulation and obesity development.
  • To elucidate the specific molecular and cellular mechanisms underlying altered appetite pathways in response to gestational nutritional status.

Main Methods:

  • Analysis of hypothalamic tissue and ex vivo cultures from SGA and maternally high-fat-exposed newborns.
  • Measurement of key proteins involved in energy sensing (SIRT1, pAMPK) and neurogenesis (Hes1, Mash1, Ngn3).
  • Assessment of appetite (NPY) versus satiety (POMC) neuron expression.

Main Results:

  • SGA infants show impaired satiety signaling, enhanced orexigenic responses, and altered neurogenesis, favoring appetite over satiety neurons.
  • Maternal high-fat diet exposure leads to reduced pAMPK levels, indicating energy excess.
  • Both conditions result in biased neurogenesis, leading to increased appetite and reduced satiety.

Conclusions:

  • Gestational nutrition profoundly impacts fetal development of appetite regulatory pathways, predisposing offspring to obesity.
  • Specific molecular changes in the fetus, including altered SIRT1 and pAMPK signaling and biased neurogenesis, contribute to hyperphagia and reduced satiety.
  • Despite developmental programming, opportunities for therapeutic interventions targeting neuronal remodeling exist.