Decreased adiposity and enhanced glucose tolerance in shikonin treated mice

被引:18
作者
Bettaieb, Ahmed [1 ]
Hosein, Ellen [1 ]
Chahed, Samah [1 ]
Abdulaziz, Ahlam [1 ]
Kucera, Heidi R. [2 ]
Gaikwad, Nilesh W. [1 ,2 ]
Haj, Fawaz G. [1 ,3 ,4 ]
机构
[1] Univ Calif Davis, Dept Nutr, Davis, CA 95616 USA
[2] Univ Calif Davis, Dept Environm Toxicol, Davis, CA 95616 USA
[3] Univ Calif Davis, Dept Internal Med, Div Endocrinol Diabet & Metab, Davis, CA 95616 USA
[4] Univ Calif Davis, Ctr Comprehens Canc, Davis, CA 95616 USA
关键词
INSULIN-RESISTANCE; METABOLIC SYNDROME; PHOSPHATASE; INHIBITION; MEDICINE; INSIGHTS; DISEASE; OBESITY;
D O I
10.1002/oby.21263
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
ObjectiveObesity represents a major public health problem, and identifying natural compounds that modulate energy balance and glucose homeostasis is of interest for combating obesity and its associated disorders. The naphthoquinone shikonin has diverse beneficial properties including anti-inflammatory, anti-oxidant, and anti-microbial effects. The objective of this study is to investigate the effects of shikonin on adiposity and glucose homeostasis. MethodsThe metabolic effects of shikonin treatment on mice fed regular chow or challenged with a high-fat diet (HFD) were determined. ResultsShikonin treated mice fed regular chow exhibited improved glucose tolerance compared with controls. In addition, shikonin treated mice fed HFD displayed decreased weight gain and resistance to HFD-induced glucose intolerance. Further, shikonin treatment decreased HFD-induced hepatic dyslipidemia. These findings correlated with enhanced hepatic insulin signaling in shikonin treated mice as evidenced by increased tyrosyl phosphorylation of the insulin receptor and enhanced downstream signaling. ConclusionsThese studies identify shikonin as a potential regulator of systemic glucose tolerance, energy balance, and adiposity in vivo.
引用
收藏
页码:2269 / 2277
页数:9
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