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Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

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Emodin Regulates Glucose Utilization by Activating AMP-activated Protein Kinase

Cited 0 times inthomson ciCited 6 times inthomson ci
Title
Emodin Regulates Glucose Utilization by Activating AMP-activated Protein Kinase
Author
Song, ParkyongKim, Jong HyunGhim, JaewangYoon, Jong HyukLee, AreumKwon, YonghoonHyun, HyunjungMoon, Hyo-YoulChoi, Hueng-SikBerggren, Per-OlofSuh, Pann-GhillRyu, Sung Ho
Keywords
AMP-activated protein kinase; Blood glucose level; Glucose tolerance; Glucose uptake; In-vivo; Insulin sensitivity; Potential values; Skeletal muscle
Issue Date
201302
Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
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.
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DOI
http://dx.doi.org/10.1074/jbc.M112.441477
ISSN
0021-9258
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