scholarly journals Effect of Momordica charantia on Adenosine Monophosphate-activated Protein Kinase in Genetically Type 2 Diabetic Mice Muscle

2009 ◽  
Vol 55 (5) ◽  
pp. 805-808 ◽  
Author(s):  
Toshihiro Miura ◽  
Takanori Kawata ◽  
Satoshi Takagi ◽  
Mai Nanpei ◽  
Haruka Nakao ◽  
...  
2004 ◽  
Vol 27 (2) ◽  
pp. 248-250 ◽  
Author(s):  
Toshihiro Miura ◽  
Yasushi Itoh ◽  
Naoki Iwamoto ◽  
Motoshi Kato ◽  
Torao Ishida

2014 ◽  
Vol 69 ◽  
pp. 347-356 ◽  
Author(s):  
Hsien-Yi Wang ◽  
Wei-Chih Kan ◽  
Tain-Junn Cheng ◽  
Sung-Hsun Yu ◽  
Liang-Hao Chang ◽  
...  

2012 ◽  
Vol 302 (3) ◽  
pp. E325-E333 ◽  
Author(s):  
Ying Zhang ◽  
Zhongqiu Wang ◽  
Yue Zhao ◽  
Ming Zhao ◽  
Shiming Wang ◽  
...  

Increased plasma free fatty acid (FFA) level is a hallmark of type 2 diabetes. However, the underlying molecular basis for FFA-caused hyperglycemia remains unclear. Here we identified plasma 5′-adenosine monophosphate (pAMP) markedly elevated in the plasma of type 2 diabetic mice. High levels of FFAs induced damage in vein endothelial cells and contributed to an increase in pAMP. Administration of synthetic 5′-AMP caused hyperglycemia and impaired insulin action in lean wild-type mice. 5′-AMP elevated blood glucose in mice deficient in adenosine receptors with equal efficiency as wild-type mice. The function of pAMP was initiated by the elevation of cellular adenosine levels, directly stimulating G-6-Pase enzyme activity, attenuating insulin-dependent GLUT4 translocation in skeletal muscle, and displaying a rapid and steep increase in blood glucose and a decrease in hepatic glycogen level. It was followed by an increase in the gene expression of hepatic Foxo1 and its targeting gene Pepck and G6Pase, which was similar to diabetic phenotype in db/db mice. Our results suggest that pAMP is a potential upstream regulator of hyperglycemia in type 2 diabetes.


2021 ◽  
Vol 43 (3) ◽  
pp. 1293-1306
Author(s):  
Shinji Kondo ◽  
Shin-ichi Adachi ◽  
Fumiaki Yoshizawa ◽  
Kazumi Yagasaki

Muscle is the largest tissue in our body and plays an important role in glucose homeostasis and hence diabetes. In the present study, we examined the effects of taxifolin (TXF) on glucose metabolism in cultured L6 muscle cells (myotubes) and in type 2 diabetic (T2D) model KK-Ay/Ta mice. TXF dose-dependently increased glucose uptake (GU) in L6 myotubes under the condition of insulin absence. This increase in GU was partially, but significantly canceled by TXF treatment in combination with either LY294002, an inhibitor of phosphatidylinositol 3-kinase (PI3K), which phosphorylates protein kinase B (Akt) or Compound C, an inhibitor of 5’-adenosine monophosphate-activated protein kinase (AMPK). Furthermore, TXF was demonstrated to activate (=phosphorylate) both Akt and AMPK, and promote glucose transporter 4 (GLUT4) translocation to the plasma membrane from cytosol of L6 myotubes via both PI3K/Akt and AMPK signaling pathways. Based on these in vitro findings, we conducted an in vivo experiment in KK-Ay/Ta mice with hyperglycemia and hyperuricemia. Fasting plasma glucose, insulin, uric acid levels and an index of insulin resistance (HOMA-IR) increased significantly in the T2D model mice compared with normal ones. Such rises in the T2D state were significantly suppressed by oral administration of TXF for four weeks. These results suggest that TXF is a potent antihyperglycemic and antihyperuricemic phytochemical in the T2D state.


PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e83397 ◽  
Author(s):  
Jing Dong ◽  
Huan Xu ◽  
Huan Xu ◽  
Peng-fei Wang ◽  
Gui-ju Cai ◽  
...  

2001 ◽  
Vol 47 (5) ◽  
pp. 340-344 ◽  
Author(s):  
Toshihiro MIURA ◽  
Chisa ITOH ◽  
Naoki IWAMOTO ◽  
Motoshi KATO ◽  
Masaomi KAWAI ◽  
...  

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