We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Korean Red Ginseng Activates AMPK in Skeletal Muscle and Liver.
- Authors
Lee, Hyun Joo; Park, Sang Kyu; Han, Seung Jin; Kim, So Hun; Hur, Kyu Yeon; Kang, Eun Seok; Ahn, Chul Woo; Cha, Bong Soo; Kim, Kyung Sub; Lee, Hyun Chul
- Abstract
AMP-activated protein kinase (AMPK) is activated under a variety of conditions that signify cellular stress, usually in response to a change in the intracellular ATP-to-AMP ratio. This is well known as a major drug target of diabetes. Ginseng has been shown to antidiabetic properties in many clinical and experimental studies. In previous our study, Panax ginseng (Korean red ginseng :KRG) showed improvement of insulin resistance and preventive effect on type 2 diabetes. Here, we evaluated the hypothesis that the insulin-sensitizing effect of KRG is mediated through the action of AMPK. To investigate the chronic effect of KRG on AMPK regulation in skeletal muscle and liver in vivo, OLETF rats were randomly allocated into two experimental groups: control and KRG. KRG was given orally once daily at a dose of 200 mg/kg to 10 week-old male OLETF rats for 32 weeks. To investigate the acute effect ofKRG on AMPK signaling in skeletal muscle and liver in vitro, L6 myotubles and HepG2 cells were incubated for 1hr, 6hr and 24 hr with KRG. Western blot analysis was performed to evaluate the expression of AMPK; ACC, PPARα and glucose transport (GLUT)-4. Thr 172 phosphorylation of AMPKα was significantly decreased in liver and skeletal muscle (gastrocnemius) of untreated OLETF rats. However, KRG treatment resulted in increased phosphorylation of AMPK in both tissues. Similarly, Ser79 acetyl-coA carbosylase (ACC) phosphorylation was increased in KRG-treated OLETF rats. The expression of PPARα was also increased in skeletal muscle and liver of KRG treated OLETF rats. In addition, the expression of GLUT4 was increased in skeletal muscle. In HepG2 cell line, KRG treatment during 1hr, 6hr and 24 hr was increased phosphorylation of AMPK. This effect mimicked those of metformin 2mM. ACC phosphorylation also increased in KRG treatment. Similarly, KRG treatment was increased phoshorylation of AMPK and ACC in differentiated L6 myotubules. In summary, KRG may enhance fatty acid oxidation via the activation of AMPK in skeletal muscle and liver, which contribute to the improvement of hyperglycemia, hyperlipidemia and insulin resistance. We suggest that KRG may have potential role in treatment and prevention of metabolic syndrome and type 2 diabetes.
- Subjects
KOREA; GINSENG; ADENOSINE monophosphate; PROTEIN kinases; TYPE 2 diabetes; FATTY acids; PHOSPHORYLATION; INSULIN resistance
- Publication
Diabetes, 2007, Vol 56, pA448
- ISSN
0012-1797
- Publication type
Article