scholarly journals Green Tea Ameliorates Hyperglycemia by Promoting the Translocation of Glucose Transporter 4 in the Skeletal Muscle of Diabetic Rodents

2019 ◽  
Vol 20 (10) ◽  
pp. 2436 ◽  
Author(s):  
Manabu Ueda-Wakagi ◽  
Hironobu Nagayasu ◽  
Yoko Yamashita ◽  
Hitoshi Ashida
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Green Tea ◽  
Glucose Intolerance ◽  
Glucose Transporter ◽  
Epigallocatechin Gallate ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Glucose Transporter 4 ◽  
Obesity And Diabetes

It is known that green tea helps prevent obesity and diabetes mellitus. In this study, we aimed to determine whether green tea ameliorates hyperglycemia and the mechanism involved in diabetic rodents. Green tea consumption reduced blood glucose and ameliorated glucose intolerance, which was assessed using an oral glucose tolerance test in both streptozotocin-induced type 1 diabetic rats and type 2 diabetic KK-Ay mice. Green tea also reduced the plasma fructosamine and glycated hemoglobin concentrations in both models. Furthermore, it increased glucose uptake into the skeletal muscle of both model animals, which was accompanied by greater translocation of glucose transporter 4 (GLUT4). Moreover, epigallocatechin gallate (EGCG), the principal catechin in green tea, also ameliorated glucose intolerance in high-fat diet-induced obese and diabetic mice. These results suggest that green tea can ameliorate hyperglycemia in diabetic rodents by stimulating GLUT4-mediated glucose uptake in skeletal muscle, and that EGCG is one of the effective compounds that mediate this effect.

scholarly journals Effects of Intrabrachial Metacholine Infusion on Muscle Capillary Recruitment and Forearm Glucose Uptake during Physiological Hyperinsulinemia in Obese, Insulin-Resistant Individuals

2008 ◽  
Vol 93 (7) ◽  
pp. 2764-2773 ◽  
Author(s):  
Giuseppe Murdolo ◽  
Mikaela Sjöstrand ◽  
Lena Strindberg ◽  
Soffia Gudbjörnsdóttir ◽  
Lars Lind ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Glucose Tolerance Test ◽  
Forearm Blood Flow ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Capillary Recruitment ◽  
Insulin Resistant

Abstract Context: Impairment of insulin-mediated capillary recruitment in skeletal muscle contributes to a hampered glucose uptake in obesity. Objective: The objective of this study was to evaluate whether metacholine (MCh), a nitric oxide vasodilator, potentiates muscle capillary recruitment and forearm glucose uptake (FGU) during physiological hyperinsulinemia. Design: The double-forearm technique [i.e. infused vs. control (Ctrl) forearm] was combined with im microdialysis during an oral glucose tolerance test in 15 nondiabetic, obese subjects divided into a group of insulin-resistant (IR) (n = 7) and insulin-sensitive (n = 8) individuals. Results: After the oral glucose tolerance test, forearm blood flow in the Ctrl forearm was unchanged, whereas it increased about 3-fold (P < 0.0001 vs. baseline) in response to MCh. Capillary permeability surface area product for glucose (PSglu) (capillary recruitment), FGU, and interstitial insulin concentrations increased significantly over time (P < 0.001) in both forearms. Compared with insulin-sensitive, the IR subjects exhibited lower PSglu (P < 0.001) and FGU (P < 0.01) in the Ctrl arm, whereas this difference was insignificant in the MCh arm despite the blunted forearm blood flow increase. Moreover, in IR individuals MCh significantly (P < 0.05) ameliorated the delayed onset of insulin action, i.e. the FGU response to hyperinsulinemia. Finally, we found PSglu to be a strong and independent predictor of FGU response (adjusted R2 0.72; P < 0.0001). Conclusions: MCh-induced vasodilation may improve the microvascular and metabolic responses to physiological hyperinsulinemia in obese, IR individuals. Further studies are required to unravel whether stimulation of nitric oxide production in skeletal muscle may represent an attractive therapeutic approach to bypassing cellular resistance to glucose disposal.

scholarly journals A Novel Xanthene Derivative, DS20060511, Attenuates Glucose Intolerance by Inducing Skeletal Muscle-specific GLUT4 Translocation in Diabetic Mice

2020 ◽  
Author(s):  
Shinji Furuzono ◽  
Tetsuya Kubota ◽  
Junki Taura ◽  
Masahiro Konishi ◽  
Asuka Naito ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Surface ◽  
Glucose Uptake ◽  
Muscle Cell ◽  
Glucose Intolerance ◽  
Actin Polymerization ◽  
Glucose Transporter ◽  
Skeletal Muscle Cell ◽  
Diabetic Mice ◽  
Glut4 Translocation

Abstract Reduced glucose uptake into the skeletal muscle is an important pathophysiological abnormality in type 2 diabetes, and is caused by impaired translocation of glucose transporter 4 (GLUT4) to the skeletal muscle cell surface. We found a novel xanthene compound, DS20060511, which induces GLUT4 translocation to the skeletal muscle cell surface, thereby stimulating glucose uptake into the skeletal muscle. DS20060511 induced GLUT4 translocation and glucose uptake into differentiated L6-miytubes and into the skeletal muscles of live mice. These effects were completely abolished in GLUT4 knockout mice. Induction of GLUT4 surface translocation by DS20060511 was independent of the insulin signaling pathways including IRS1-Akt-AS160 phosphorylation and IRS1-Rac1-actin polymerization, eNOS pathway and AMPK pathway. Acute and chronic DS20060511 treatment attenuated the glucose intolerance in obese diabetic mice. Taken together, DS20060511 acts as a skeletal muscle specific-GLUT4 translocation enhancer to facilitate glucose utilization. Further studies with DS20060511 would help to develop a novel antidiabetic medicine.

Fermented Tea Improves Glucose Intolerance in Mice by Enhancing Translocation of Glucose Transporter 4 in Skeletal Muscle

2012 ◽  
Vol 60 (45) ◽  
pp. 11366-11371 ◽  
Author(s):  
Yoko Yamashita ◽  
Lihua Wang ◽  
Zhang Tinshun ◽  
Toshiyuki Nakamura ◽  
Hitoshi Ashida
Keyword(s):  
Skeletal Muscle ◽  
Glucose Intolerance ◽  
Glucose Transporter ◽  
Glucose Transporter 4
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