There is considerable evidence that hyperglycemia results in the generation of reactive oxygen species (ROS), ultimately leading to increased oxidative stress in a variety of tissues.
Kuppusamy et al. assessed the oxidative stress levels in the 3 major ethnic groups in Malaysia and evaluated the association between glycemic control and oxidant-antioxidant levels in 650 Type 2 Diabetes melliters patients and 280 healthy age-matched controls. The results from the study showed that Type 2 DM patients had significantly lower levels of antioxidant enzymes and non-enzymatic antioxidant (FRAP) and increased levels of HbA( I c), fasting blood glucose (FBG), malondialdehyde (MDA) and xanthine oxidase (XO) when compared with control subjects. Correlation analysis of oxidant-antioxidant parameters as a function of HbA( I c) in each ethnic group revealed a strong association of HbA( I c) with oxidative indices pointing to the possible contribution of XO to oxidative stress and the pathophysiology of diabetes.
The effect of green tea in mitigating the effects of pro-oxidant enzymes
Rah et al. investigated the potential protective roles played by green tea polyphenol (GTP) against the injurious effects of reactive oxygen species in human microvascular endothelial cells (HUMVECs). Oxidative stress was induced either by adding 10 mM H'O' or by the action of IOU/I XO in the presence of xanthine (250 microM). Both treatments produced a significant reduction (to 68% and 71 %, respectively) in HUMVEC viability and morphological changes and necrotic detachment. The H'O'-induced alterations were completely prevented b
Green tea supplementation by inhibiting the action of pro-oxidant enzymes like xanthine oxidase (XO) and malondialdehyde (MDA) has been shown to reduce oxidative stress as in case of hyperglycemic states and assist in blood glucose control.
Other beneficial actions of green tea in diabetes
Apart from reducing the oxidative stress in hyperglycemic states, the catechins in green tea also suppress hepatic glucose production and regulate high glucose induced apoptosis, all of which help in the control of hyperglycemia and the complications of diabetes.
Suppression of hepatic glucose production
Waltner et al. showed that the regulation of hepatic glucose production is decreased by epigallocatechin gallate (EGCG). Furthermore, like insulin, EGCG increases tyrosine phosphorylation of the insulin receptor and insulin receptor substrate-I (IRS-I), and it reduces phosphoenolpyruvate carboxykinase gene expression in a phosphoinositide 3-kinasedependent manner. Epigallocatechin gallate also mimics insulin by increasing phosphoinositide 3-kinase, mitogen-activated protein kinase, and p70(s6k) activity. However, EGCG differs from insulin, in that it affects several insulin-activated kinases with slower kinetics. Furthermore, EGCG regulates genes that encode gluconeogenic enzymes and protein-tyrosine phosphorylation by modulating the redox state of the cell. These results demonstrate that changes in the redox state may have beneficial effects for the treatment of diabetes and suggest a potential role for EGCG, or derivatives, as an antidiabetic agent.
Regulation of high-glucose induced apoptosis
Compounds that scavenge ROS may confer regulatory effects on high glucose-induced apoptosis. The authors of this study investigated the effect of EGCG on high glucose-induced apoptosis in U937 cells. Upon exposure to 35 mM glucose for 2 days, there was a distinct difference between untreated cells and cells pretreated with I microM EGCG for 2 h in regard to cellular redox status and oxidative DNA damage to cells. Epigallocatechin gallate pre-treated cells showed significant suppression of apoptotic features such as DNA fragmentation, damage to mitochondrial function, and modulation of apoptotic marker proteins upon exposure to high glucose. This study indicates that EGCG may play an important role in regulating the apoptosis induced by high glucose presumably through scavenging of ROS.