Research published in Cell has shed light on the reorganization of circadian rhythm by nutrients. Mice fed a high-fat diet displayed extensive reprogramming of the hepatic clock with profound effects on key metabolic pathways. These changes involved repression of the Clock–Bmal1 network and PPARγ-regulated induction of a novel gene set.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 12 print issues and online access
$209.00 per year
only $17.42 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
References
Eckel-Mahan, K. L. et al. Reprogramming of the circadian clock by nutritional challenge. Cell 155, 1464–1478 (2013).
Panda, S. et al. Coordinated transcription of key pathways in the mouse by the circadian clock. Cell 109, 307–320 (2002).
Turek, F. W. et al. Obesity and metabolic syndrome in circadian Clock mutant mice. Science 308, 1043–1045 (2005).
Kohsaka, A. et al. High-fat diet disrupts behavioral and molecular circadian rhythms in mice. Cell Metab. 6, 414–421 (2007).
Jonker, J. W. et al. A PPARγ-FGF1 axis is required for adaptive adipose remodelling and metabolic homeostasis. Nature 485, 391–394 (2012).
Cho, H. et al. Regulation of circadian behaviour and metabolism by REV-ERB-α and REV-ERB-β. Nature 485, 123–127 (2012).
Yang, X. et al. Nuclear receptor expression links the circadian clock to metabolism. Cell 126, 801–810 (2006).
Fontaine, C. et al. The orphan nuclear receptor Rev-Erbα is a peroxisome proliferator-activated receptor (PPAR) γ target gene and promotes PPARγ-induced adipocyte differentiation. J. Biol. Chem. 278, 37672–37680 (2003).
Ji, Y. et al. Short term high fat diet challenge promotes alternative macrophage polarization in adipose tissue via natural killer T cells and interleukin-4. J. Biol. Chem. 287, 24378–24386 (2012).
Matsusue, K. et al. Liver-specific disruption of PPARγ in leptin-deficient mice improves fatty liver but aggravates diabetic phenotypes. J. Clin. Invest. 111, 737–747 (2003).
Acknowledgements
S.L. and R.M.E. are funded by a research grant from the Leona M. and Harry B. Helmsley Charitable Trust (#2012-PG-MED002) and an educational grant from Ipsen–Biomeasure.
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Competing interests
The authors declare no competing financial interests.
PowerPoint slides
Rights and permissions
About this article
Cite this article
Liu, S., Evans, R. Tick, tock, a high-fat clock. Nat Rev Endocrinol 10, 191–192 (2014). https://doi.org/10.1038/nrendo.2014.23
Published:
Issue Date:
DOI: https://doi.org/10.1038/nrendo.2014.23
