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Related Experiment Video

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Instrumentation of Near-term Fetal Sheep for Multivariate Chronic Non-anesthetized Recordings
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Published on: October 25, 2015

Changed mitochondrial function by pre- and/or postpartum diet alterations in sheep.

Wenche Jørgensen1, Christiane Gam, Jesper Løvind Andersen

  • 1Department of Biomedical Sciences, Nuclear Magnetic Resonance Center, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark. wenche@sund.ku.dk

American Journal of Physiology. Endocrinology and Metabolism
|October 15, 2009
PubMed
Summary

Maternal diet restriction during pregnancy can cause lasting mitochondrial dysfunction in offspring. A high-fat diet in young sheep boosts mitochondrial function temporarily, but fetal programming effects appear later in life.

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Area of Science:

  • * Nutritional programming and metabolic health
  • * Mitochondrial physiology and function
  • * Skeletal muscle adaptation

Background:

  • * Fetal programming investigates how maternal nutrition impacts offspring development and long-term health.
  • * Skeletal muscle mitochondria are crucial for energy metabolism and are susceptible to environmental influences.
  • * Understanding diet-induced changes in mitochondria is key to addressing metabolic disorders.

Purpose of the Study:

  • * To investigate the impact of maternal gestational diet and postnatal diet on skeletal muscle mitochondrial function in sheep.
  • * To determine if fetal programming effects on mitochondria are reversible.
  • * To examine the influence of diet on mitochondrial respiration, coupling, and gene expression.

Main Methods:

  • * Sheep model with maternal dietary manipulation (normal vs. 50% restriction) during late gestation.
  • * Offspring fed normal or high-fat diets for the first 6 months.
  • * Mitochondrial function assessed in muscle fibers at 6 and 24 months of age.

Main Results:

  • * Postnatal high-fat diet increased mitochondrial VO(2max) and respiratory coupling ratio (RCR) in adolescents, but these effects were reversible.
  • * Maternal gestational undernutrition led to reduced VO(2max), state 4 respiration, and RCR in adulthood (fetal programming).
  • * Type I fiber-rich muscle was more susceptible to fetal programming effects.

Conclusions:

  • * Gestational undernutrition causes persistent fetal programming, reducing adult mitochondrial VO(2max).
  • * Postnatal high-fat diet transiently enhances mitochondrial function in adolescence but does not override fetal programming long-term.
  • * Dietary interventions can reverse some postnatal effects, but fetal programming impacts are evident in adulthood.