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Emodin Regulates Glucose Utilization by Activating AMP-activated Protein Kinase

Author(s)
Song, ParkyongKim, Jong HyunGhim, JaewangYoon, Jong HyukLee, AreumKwon, YonghoonHyun, HyunjungMoon, Hyo-YoulChoi, Hueng-SikBerggren, Per-OlofSuh, Pann-GhillRyu, Sung Ho
Issued Date
2013-02
DOI
10.1074/jbc.M112.441477
URI
https://scholarworks.unist.ac.kr/handle/201301/3395
Fulltext
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84874314479
Citation
JOURNAL OF BIOLOGICAL CHEMISTRY, v.288, no.8, pp.5732 - 5742
Abstract
AMP-activated protein kinase has been described as a key signaling protein that can regulate energy homeostasis. Here, we aimed to characterize novel AMP-activated kinase (AMPK)-activating compounds that have a much lower effective concentration than metformin. As a result, emodin, a natural anthraquinone derivative, was shown to stimulate AMPK activity in skeletal muscle and liver cells. Emodin enhanced GLUT4 translocation and [C-14]glucose uptake into the myotube in an AMPK-dependent manner. Also, emodin inhibited glucose production by suppressing the expression of key gluconeogenic genes, such as phosphoenolpyruvate carboxykinase and glucose-6-phosphatase, in hepatocytes. Furthermore, we found that emodin can activate AMPK by inhibiting mitochondrial respiratory complex I activity, leading to increased reactive oxygen species and Ca2+/calmodulin-dependent protein kinase kinase activity. Finally, we confirmed that a single dose administration of emodin significantly decreased the fasting plasma glucose levels and improved glucose tolerance in C57Bl/6J mice. Increased insulin sensitivity was also confirmed after daily injection of emodin for 8 days using an insulin tolerance test and insulin-stimulated PI3K phosphorylation in wild type and high fat diet-induced diabetic mouse models. Our study suggests that emodin regulates glucose homeostasis in vivo by AMPK activation and that this may represent a novel therapeutic principle in the treatment of type 2 diabetic models.
Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
ISSN
0021-9258
Keyword
11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-1DEPENDENT DIABETES-MELLITUSRAT SKELETAL-MUSCLECOMPLEX-ISIGNALING PATHWAYADIPOSE-TISSUEINSULINMETFORMINCELLSTRANSPORT

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