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The natural carotenoid astaxanthin, a PPAR-alpha agonist and PPAR-gamma antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes

Authors
Jia, YaoyaoKim, Jin-YoungJun, Hee-JinKim, Sun-JoongLee, Ji-HaeHoang, Minh HienHwang, Kwang-YeonUm, Soo-JongChang, Hyo IhlLee, Sung-Joon
Issue Date
6월-2012
Publisher
WILEY
Keywords
Astaxanthin; Lipid metabolism; PPAR; Transcriptome; Seafood
Citation
MOLECULAR NUTRITION & FOOD RESEARCH, v.56, no.6, pp.878 - 888
Indexed
SCIE
SCOPUS
Journal Title
MOLECULAR NUTRITION & FOOD RESEARCH
Volume
56
Number
6
Start Page
878
End Page
888
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/108229
DOI
10.1002/mnfr.201100798
ISSN
1613-4125
Abstract
Scope: A natural carotenoid abundant in seafood, astaxanthin (AX), has hypolipidemic activity, but its underlying mechanisms of action and protein targets are unknown. We investigated the molecular mechanism of action of AX in hepatic hyperlipidemia by measuring peroxisome proliferator-activated receptors (PPAR) activity. Methods and results: We examined the binding of AX to PPAR subtypes and its effects on hepatic lipid metabolism. AX binding activated PPAR-alpha, but inhibited PPAR-gamma transactivation activity in reporter gene assay and time-resolved fluorescence energy transfer analyses. AX had no effect on PPAR delta/beta transactivation. AX bound directly to PPAR-alpha and PPAR-gamma with moderate affinity, as assessed by surface plasmon resonance experiments. The differential effects of AX on PPARs were confirmed by measuring the expression of unique responsive genes for each PPAR subtype. AX significantly reduced cellular lipid accumulation in lipid-loaded hepatocytes. Transcriptome analysis revealed that the net effects of stimulation with AX (100 mu M) on lipid metabolic pathways were similar to those elicited by fenofibrate and lovastatin (10 mu M each), with AX rewiring the expression of genes involved in lipid metabolic pathways. Conclusion: AX is a PPAR-alpha agonist and PPAR-gamma antagonist, reduces hepatic lipid accumulation by rewiring the transcriptome in lipid-loaded hepatocytes.
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