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Supplementation of astaxanthin, a xanthophyll carotenoid, improved metabolic and inflammatory abnormalities associated with obesity in diet‐induced obese mice (645.8)
Author(s) -
Kim Bohkyung,
Ku Chai Siah,
Pham Tho,
Yang Yue,
Wegner Casey,
Park YoungKi,
Lee JiYoung
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.645.8
Subject(s) - endocrinology , medicine , lipopolysaccharide , lipogenesis , inflammation , astaxanthin , in vivo , xanthophyll , splenocyte , biology , carotenoid , chemistry , adipose tissue , biochemistry , spleen , microbiology and biotechnology
We previously reported that astaxanthin (ASTX), a xanthophyll carotenoid, exerted hypolipidemic and antioxidant properties in vivo. The objective of this study was to determine protective effects of ASTX against obesity‐associated metabolic and inflammatory abnormalities. Male C57BL/6J mice were fed a high fat/high sucrose control (35% fat, 35% sucrose by wt), or ASTX diet (0.03% ASTX by wt) for 30 wk. ASTX‐fed mice showed lower plasma total cholesterol, triglycerides, and alanine aminotransferase than control. ASTX tended to decrease mRNA of lipogenic and fibrogenic genes in the liver, and significantly increased genes for fatty acid ‐oxidation and mitochondria biogenesis in muscle. Epididymal fat pad weights were not significantly different between groups. However, the expression of F4/80, a macrophage marker, was significantly lower in the epididymal fat pad of ASTX mice, and markedly less macrophage infiltration in ASTX group was confirmed by histological analysis. Ex vivo analysis of splenocytes isolated from mice on a study diet showed that tumor necrosis factor α mRNA was significantly reduced upon lipopolysaccharide stimulation in ASTX mouse splenocytes. In conclusion, our results suggest that ASTX supplementation prevents obesity‐associated metabolic dysfunctions and inflammation possibly by improving capacity of muscle in handling excess energy. (Funded by USDA AFRI 2012‐67018‐19290)