Abstract
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.
Highlights
Type I diabetes mellitus (T1DM) is a severe disease characterized by a loss of insulin secretion from pancreatic β-cells [1]
We first investigated the effects of green tea on the hyperglycemia and glucose intolerance of STZ-induced T1DM rats (Figure 1A)
We demonstrated that green tea ameliorated hyperglycemia in STZ-induced T1DM rats, KK-Ay mice, and high-fat diet (HFD)-fed C57BL/6 obese and diabetic mice (Figures 2, 5 and 8)
Summary
Type I diabetes mellitus (T1DM) is a severe disease characterized by a loss of insulin secretion from pancreatic β-cells [1]. Insulin stimulates glucose uptake into skeletal muscle and adipose tissue, facilitates glycogen synthesis, and suppresses gluconeogenesis. It stimulates lipogenesis and inhibits the hepatic hydrolysis of triglycerides to liberate glycerol and fatty acids. A reduction in insulin secretion causes body weight loss, hyperglycemia, and dyslipidemia. Hyperglycemia is the hallmark of diabetes mellitus (DM), and chronic oversupply of glucose causes protein glycation and oxidative stress, which plays a major role in the development of diabetic complications [3]. Blood glucose control using exogenous insulin or insulin-mimetic agents is very important for T1DM patients
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