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Cardiac PPARalpha Protein Expression is Constant as Alternate Nuclear Receptors and PGC-1 Coordinately Increase

Norman E Buroker1, Xue-Han Ning, Michael Portman

  • 1Department of Cardiology, Children's Hospital and Regional Medical Center, 4800 Sand Point Way N.E., Seattle, WA 98105, USA.

PPAR Research
|February 22, 2008
PubMed

Insights

The study found that peroxisomal proliferator activated receptor gamma coactivator-1 (PGC-1), not PPARalpha, drives the newborn heart

Area of Science:

  • Biochemistry
  • Developmental Biology
  • Metabolic Regulation

Background:

  • The transition from carbohydrate to fatty acid oxidation in the newborn heart is crucial for postnatal survival.
  • Peroxisomal proliferator activated receptor alpha (PPARalpha) was hypothesized to regulate this metabolic switch.
  • Limited proteomic data exist to confirm PPARalpha's role in vivo.

Purpose of the Study:

  • To investigate the role of nuclear receptors in triggering the newborn metabolic switch in sheep heart.
  • To examine protein expression of metabolic enzymes and nuclear receptors during postnatal development.

Main Methods:

  • Heart tissues from fetal, newborn, and 30-day-old lambs were analyzed.
  • Protein expression levels of key metabolic enzymes, nuclear receptors, and coactivators were quantified.

Main Results:

  • Hexokinase II protein dropped transiently, while pyruvate dehydrogenase kinase increased, indicating metabolic shifts.
  • Peroxisomal proliferator activated receptor gamma coactivator-1 (PGC-1) showed a 20-fold transient increase in newborns.
  • PPARalpha levels did not increase during the transition; thyroid hormone receptor alpha1 and retinoid-activated receptor alpha increased.

Conclusions:

  • The study challenges the paradigm that PPARalpha initiates the postnatal metabolic switch in the heart.
  • Increased PGC-1, thyroid hormone receptor alpha1, and retinoid-activated receptor alpha suggest alternative nuclear receptor involvement.
  • Perinatal thyroid hormone surges likely contribute to the metabolic transition by modulating PGC-1 expression.

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