- Made available online as an Accepted Preprint 21 September 2009
- Accepted Preprint first posted online on 21 September 2009
PPAR control: it's SIRTainly as easy as PGC
- Centre for Diabetes, Queen Mary University of London, Blizard Institute of Cell and Molecular Science, St Bartholomew's and the Royal London School of Medicine and Dentistry, 4 Newark Street, Whitechapel, London E1 2AT, UK
- (Correspondence should be addressed to M C Sugden; Email: m.c.sugden{at}qmul.ac.uk)
Abstract
This review describes recent advances in our knowledge of the regulatory interactions influencing the expression of peroxisome proliferator-activated receptor (PPAR)-regulated genes. We address recent advances highlighting the role of PPARγ (PPARG) coactivator-1 (PGC-1) and lipin-1 in co-ordinating the expression of genes controlling nutrient handling. We evaluate the possibility that SIRT1 lies at the heart of a regulatory loop involving PPARα, PGC-1α (PPARA, PPARGC1A as given in the HUGO Database), and lipin-1 (LPIN1 as listed in the HUGO Database) that ultimately controls the metabolic response to varying nutrient and physiological signals via a common mechanism mediated by post-translation modifications (deacetylation) of both PPARα and PGC-1s. Finally, we comment on the potential of pharmaceutical manipulation of these targets as well as the possible problems associated with this strategy.
- Received in final form 16 September 2009
- Accepted 21 September 2009
- © 2010 Society for Endocrinology
