| First Author | van Vlies N | Year | 2007 |
| Journal | Biochim Biophys Acta | Volume | 1767 |
| Issue | 9 | Pages | 1134-42 |
| PubMed ID | 17692817 | Mgi Jnum | J:127048 |
| Mgi Id | MGI:3762710 | Doi | 10.1016/j.bbabio.2007.07.001 |
| Citation | van Vlies N, et al. (2007) PPAR alpha-activation results in enhanced carnitine biosynthesis and OCTN2-mediated hepatic carnitine accumulation. Biochim Biophys Acta 1767(9):1134-42 |
| abstractText | In fasted rodents hepatic carnitine concentration increases considerably which is not observed in PPAR alpha-/- mice, indicating that PPAR alpha is involved in carnitine homeostasis. To investigate the mechanisms underlying the PPAR alpha-dependent hepatic carnitine accumulation we measured carnitine biosynthesis enzyme activities, levels of carnitine biosynthesis intermediates, acyl-carnitines and OCTN2 mRNA levels in tissues of untreated, fasted or Wy-14643-treated wild type and PPAR alpha-/- mice. Here we show that both enhancement of carnitine biosynthesis (due to increased gamma-butyrobetaine dioxygenase activity), extra-hepatic gamma-butyrobetaine synthesis and increased hepatic carnitine import (OCTN2 expression) contributes to the increased hepatic carnitine levels after fasting and that these processes are PPAR alpha-dependent. |
