Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012:2012:814945.
doi: 10.1155/2012/814945. Epub 2012 Apr 19.

PPARα as a Transcriptional Regulator for Detoxification of Plant Diet-Derived Unfavorable Compounds

Bunichiro Ashibe  1 , Yu Nakajima, Yuka Fukui, Kiyoto Motojima
Affiliations

PPARα as a Transcriptional Regulator for Detoxification of Plant Diet-Derived Unfavorable Compounds

Bunichiro Ashibe et al. PPAR Res. 2012.

Abstract

Plants contain potentially toxic compounds for animals and animals have developed physiological strategies to detoxify the ingested toxins during evolution. Feeding mice with various plant seeds and grains showed unexpected result that only sesame killed PPARα-null mice but not wild-type mice at all. A detailed analysis of this observation revealed that PPARα is involved in the metabolism of toxic compounds from plants as well as endobiotic substrates by inducing phase I and phase II detoxification enzymes. PPARα plays a vital role in direct or indirect activation of the relevant genes via the complex network among other xenobiotic nuclear receptors. Thus, PPARα plays its wider and more extensive role in energy metabolism from natural food intake to fat storage than previously thought.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Survival curve of normal and PPARα-null mice on sesame diet. Male PPARα-null mice on the sesame diet were followed until all null mice (n = 12) died. None of wild-type mice (n = 4) on the sesame diet or the PPARα-null mice on normal diet died during these period. Time 0 is the day of starting the experiment using age-matched (14 weeks) mice on the sesame diet.
Figure 2
Figure 2
Proposed physiological role of FALDH. Polyunsaturated fatty acids or branched fatty acids bind to PPARα to express FALDH and FALDH variants produced by alternative splicing share a role in protecting against oxidative stress in an organelle-specific manner.
Figure 3
Figure 3
A proposed model depicting the metabolic conversion of plant compounds in animals by the mechanism involving complex network among the xenobiotic nuclear receptors and PPARα.
See this image and copyright information in PMC

Similar articles

See all similar articles

References

    1. Fowler ME. Plant poisoning in free-living wild animals: a review. Journal of Wildlife Diseases. 1983;19(1):34–43. - PubMed
    1. Owens JB. Genetic aspects of appetite and food choice in animals. The Journal of Agricultural Science. 1992;119(2):151–155.
    1. Mitchell DY, Petersen DR. Oxidation of aldehydic products of lipid peroxidation by rat liver microsomal aldehyde dehydrogenase. Archives of Biochemistry and Biophysics. 1989;269(1):11–17. - PubMed
    1. Rizzo WB, Heinz E, Simon M, Craft DA. Microsomal fatty aldehyde dehydrogenase catalyzes the oxidation of aliphatic aldehyde derived from ether glycerolipid catabolism: implications for Sjogren-Larsson syndrome. Biochimica et Biophysica Acta. 2000;1535(1):1–9. - PubMed
    1. Willemsen MA, Rotteveel JJ, de Jong JG, et al. Defective metabolism of leukotriene B4 in the Sjogren-Larsson syndrome. Journal of the Neurological Sciences. 2001;183(1):61–67. - PubMed

LinkOut - more resources