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Developmental programming in response to intrauterine growth restriction impairs myoblast function and skeletal

D T Yates1, A R Macko, M Nearing

  • 1Department of Animal Sciences, University of Arizona, Tucson, AZ 85721-0038, USA.

Journal of Pregnancy
|August 18, 2012
PubMed

Insights

Fetal growth restriction alters skeletal muscle development, impacting postnatal metabolism. Changes in adrenergic receptors in intrauterine growth restriction (IUGR) fetuses persist, affecting nutrient utilization and potentially leading to metabolic disorders.

Area of Science:

  • Developmental biology
  • Metabolic homeostasis
  • Endocrinology

Background:

  • Placental insufficiency causes fetal adaptations impacting skeletal muscle, reducing glucose oxidation, impairing insulin action, and lowering oxidative fibers.
  • Intrauterine growth restriction (IUGR) leads to fewer myonuclei in skeletal muscle fibers due to compromised myoblasts.
  • Fetal hypoxemia from placental insufficiency elevates catecholamines, hindering fetal muscle growth.

Purpose of the Study:

  • To investigate adaptations in adrenergic receptor expression in skeletal muscle and myoblasts of IUGR sheep fetuses.
  • To understand how altered adrenergic receptor profiles contribute to metabolic dysfunction in IUGR offspring.

Main Methods:

  • Analysis of adrenergic receptor expression profiles in skeletal muscle and myoblasts from IUGR sheep fetuses.
  • Comparison of receptor expression between IUGR and control fetuses/lambs.

Main Results:

  • IUGR fetuses exhibit altered β-adrenergic receptor expression: decreased Adrβ2 and increased Adrβ1 in myoblasts.
  • This altered receptor profile persists postnatally in IUGR lambs, reducing fatty acid mobilization.
  • The changes suppress insulin signaling, myoblast incorporation, and glucose oxidation in skeletal muscle.

Conclusions:

  • Developmental programming of skeletal muscle adrenergic receptors in IUGR influences postnatal metabolic homeostasis.
  • Altered β-adrenergic signaling contributes to differential nutrient utilization and metabolic differences in IUGR offspring.
  • These findings highlight a mechanism linking fetal programming to long-term metabolic health.

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