scholarly journals Glucose Intolerance in Spontaneously Hypertensive and Wistar-Kyoto Rats: Enhanced Gene Expression and Synthesis of Skeletal Muscle Glucose Transporter 4.

1997 ◽  
Vol 20 (4) ◽  
pp. 279-286 ◽  
Author(s):  
Shigehiro Katayama ◽  
Munemichi Inaba ◽  
Yoshiko Maruno ◽  
Toshisuke Morita ◽  
Takuya Awata ◽  
...  
2012 ◽  
Vol 60 (45) ◽  
pp. 11366-11371 ◽  
Author(s):  
Yoko Yamashita ◽  
Lihua Wang ◽  
Zhang Tinshun ◽  
Toshiyuki Nakamura ◽  
Hitoshi Ashida

2019 ◽  
Vol 20 (10) ◽  
pp. 2436 ◽  
Author(s):  
Manabu Ueda-Wakagi ◽  
Hironobu Nagayasu ◽  
Yoko Yamashita ◽  
Hitoshi Ashida

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.


2007 ◽  
Vol 21 (9) ◽  
pp. 2152-2163 ◽  
Author(s):  
Lily C. Chao ◽  
Zidong Zhang ◽  
Liming Pei ◽  
Tsugumichi Saito ◽  
Peter Tontonoz ◽  
...  

Abstract Innervation is important for normal metabolism in skeletal muscle, including insulin-sensitive glucose uptake. However, the transcription factors that transduce signals from the neuromuscular junction to the nucleus and affect changes in metabolic gene expression are not well defined. We demonstrate here that the orphan nuclear receptor Nur77 is a regulator of gene expression linked to glucose utilization in muscle. In vivo, Nur77 is preferentially expressed in glycolytic compared with oxidative muscle and is responsive to β-adrenergic stimulation. Denervation of rat muscle compromises expression of Nur77 in parallel with that of numerous genes linked to glucose metabolism, including glucose transporter 4 and genes involved in glycolysis, glycogenolysis, and the glycerophosphate shuttle. Ectopic expression of Nur77, either in rat muscle or in C2C12 muscle cells, induces expression of a highly overlapping set of genes, including glucose transporter 4, muscle phosphofructokinase, and glycogen phosphorylase. Furthermore, selective knockdown of Nur77 in rat muscle by small hairpin RNA or genetic deletion of Nur77 in mice reduces the expression of a battery of genes involved in skeletal muscle glucose utilization in vivo. Finally, we show that Nur77 binds the promoter regions of multiple genes involved in glucose metabolism in muscle. These results identify Nur77 as a potential mediator of neuromuscular signaling in the control of metabolic gene expression.


1996 ◽  
Vol 24 (2) ◽  
pp. 234S-234S
Author(s):  
SAMANTHA L. PEARSON ◽  
YONG-LING LIU ◽  
MICHELLE DAVENPORT ◽  
STEPHEN A. SMITH ◽  
SIMON J. DUNMORE

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