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Chinese olive ( Canarium album L.) fruit regulates glucose utilization by activating AMP‐activated protein kinase
Author(s) -
Yeh YuTe,
Lu TingJang,
Lian GuanTing,
Lung MengChuan,
Lee YuLin,
Chiang AnNa,
Hsieh ShuChen
Publication year - 2020
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/fj.201902494rr
Subject(s) - ampk , amp activated protein kinase , chemistry , insulin resistance , glucose transporter , glucose uptake , medicine , protein kinase a , endocrinology , glycogen , pharmacology , insulin , biochemistry , kinase , biology
A growing body of evidence demonstrates obesity‐induced insulin resistance is associated with the development of metabolic diseases. This study was designed to investigate ethyl acetate fraction of Chinese olive fruit extract (CO‐EtOAc)‐mediated attenuation of obesity and hyperglycemia in a mouse model. About 60% HFD‐fed mice were treated intragastrically with CO‐EtOAc for last 6 weeks, and body weight, blood biochemical parameters as well as hepatic inflammation response were investigated. Our results showed that CO‐EtOAc treatment significantly reduced the formation of hepatic lipid droplets, body weight gain, blood glucose, and improved serum biochemical parameters in HFD‐induced obese and insulin resistant mice. We further explored the molecular mechanism underlying the blood glucose modulating effect of CO‐EtOAc using L6 myotubes model. We conclude that CO‐EtOAc effectively increases the glycogen content and glucose uptake by stimulating the membrane translocation of glucose transporter 4. In addition, CO‐EtOAc depolarizes the mitochondrial membrane and decreases the mitochondrial oxygen consumption, which may result in AMPK activation and the consequent mitochondrial fission. This study shows that CO‐EtOAc prevents the development of obesity in mice fed with HFD and is also capable of stimulating glucose uptake. The possible mechanism might be due to the effects of CO‐EtOAc on activation of AMPK and promotion of mitochondrial fission.