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Chinese scientists found new mechanisms underlying green tea’s antidiabetes effect

Updated: 2012-07-09

 

Diabetes has become the third most hazardous disease, after cancer and cardio/cerebrovascular diseases, which do serious harm to human health. Resistance to insulin is one of the major causes of diabetes. According to recent findings, adipose oxidative stress may have a central role in causing insulin resistance. Oxidative stress in adipocytes impaired insulin signals and decreased insulin-stimulating glucose uptake.

Studies found that drinking green tea has an antidiabetes effect. Green tea catechins (GTCs) could protect pancreas from oxidative damage. GTCs could increase insulin sensitivity in diabetic animals, enhance GLUT-4 expression, increase glucose tolerance, promote glucose uptake in adipocytes and muscles, and decrease oxidative stress in diabetic rats. It was well established that GTCs administration improved metabolic syndrome and type 2 diabetes. But how GTCs improved the impaired insulin resistance is still not fully understood.

In a recently study, Professor ZHAO Baolu from the Institute of Biophysics, Chinese Academy of Science and his colleagues discovered new mechanisms for green tea's anti-insulin resistance effect. In their study, effects of GTC on type 2 diabetes were studied and the mechanism of GTCs on the insulin sensitive effect was investigated by feeding of GTCs to obese KK-ay mice, DIO obese rats, and 3T3-L1 adipocytes, all ameliorated insulin resistance to varying degrees. They found that GTCs ameliorate diabetic phenotype of KK-ay, attenuate oxidative stress in KK-ay mice, suppressed oxidative-related signal and increased GLUT-4 expression in KK-ay mice, and improved diet-induced obese (DIO) rat glucose metabolism. They also studied the effects of epigallocatechin gallate (EGCG) on insulin signals. They discovered that EGCG recovered the impaired insulin-stimulated glucose uptake of 3T3-L1 adipocytes, reduced DEX or TNF-α-induced ultra ROS generation, reduced JNK phosphorylation in adipocytes, enhanced translocation of GLUT-4 to plasma membrane and altered synthesis of adipokines. Their results suggest that EGCG and GTCs could improve adipose insulin resistance, and exact this effect on their ROS scavenging functions.

This work was a fruit of successful collaboration among scientists from the Institute of Biophysics, Chinese Academy of Sciences, Harbin Institute of Technology at Weihai, and the Institute of Chemistry, Chinese Academy of Sciences. It was supported the National Natural Science Foundation of China and published on the latest issue ofFree Radical Biology and Medicine.

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