Liver-specific loss of long chain acyl-CoA synthetase-1 decreases triacylglycerol synthesis and beta-oxidation and alters phospholipid fatty acid composition.

@article{Li2009LiverspecificLO,
  title={Liver-specific loss of long chain acyl-CoA synthetase-1 decreases triacylglycerol synthesis and beta-oxidation and alters phospholipid fatty acid composition.},
  author={Lei Li and Jessica M Ellis and Heather A. Paich and Shuli Wang and Nan Gong and George Altshuller and Randy J. Thresher and Timothy R. Koves and Steven M. Watkins and Deborah M. Muoio and Gary W. Cline and Gerald I Shulman and Rosalind A Coleman},
  journal={The Journal of biological chemistry},
  year={2009},
  volume={284 41},
  pages={27816-26}
}
In mammals, a family of five acyl-CoA synthetases (ACSLs), each the product of a separate gene, activates long chain fatty acids to form acyl-CoAs. Because the ACSL isoforms have overlapping preferences for fatty acid chain length and saturation and are expressed in many of the same tissues, the individual function of each isoform has remained uncertain. Thus, we constructed a mouse model with a liver-specific knock-out of ACSL1, a major ACSL isoform in liver. Eliminating ACSL1 in liver… CONTINUE READING