Role for Taurine in Development of Oxidative Metabolism After Birth

The heart undergoes a major metabolic transition after birth, a change largely caused by alterations in substrate availability, hormone levels and transcription factor content. However, another factor that could contribute to the resulting upregulation of oxidative metabolism is the increase in taurine levels. We proposed that by increasing UUG decoding and the biosynthesis of mitochondria encoded proteins, elevations in taurine content enhance electron transport flux and increase oxidative metabolism. To test our hypothesis, the effect of reduced taurine content on oxidative metabolism of myocardial mitochondria and neonatal cardiomyocytes was examined. Taurine deficient neonatal mitochondria exhibited impaired oxidation of complex I specific- but not complex II specific-substrates, indicating that taurine deficiency regulates complex I activity. Taurine deficiency also reduced respiration of neonatal cardiomyocytes oxidizing carbohydrate (glucose, lactate and pyruvate). However, cardiomyocytes from 2-3 day-old hearts respiring either β-hydroxybutyrate, an important substrate in the neonatal heart, or palmitate, which is poorly metabolized during the early neonatal period, were resistant to the metabolic defects of taurine deficiency, These data support the hypothesis that taurine contributes to development of respiratory chain function after birth, which is required for oxidative metabolism of multiple substrates.