Can Tea Extracts Exert a Protective Effect Against Diabetes by Reducing Oxidative Stress and Decreasing Glucotoxicity in Pancreatic β-Cells?

Glucose is the main physiological stimulus of pancreatic β-cells. However, chronic exposure of β-cells to elevated glucose concentrations induces glucotoxicity. In animal models of type 2 diabetes, it has been shown that several days of hyperglycemia impairs glucose-stimulated insulin secretion and increases β-cell apoptosis. In patients with type 2 diabetes, the multiple disorders caused by chronic hyperglycemia in β-cells include elevated basal insulin secretion, increased sensitivity to glucose, diminished response to insulinotropic stimuli and substantial depletion of insulin hoarding [1,2]. These defects associated with insulin resistance lead to a progressive loss of β-cell mass and function and to the onset of diabetes. It is crucial to study the mechanisms by which glucotoxicity induces β-cell failure to develop therapeutic strategies for protecting and recovering a functional β-cell mass. Several mechanisms might explain the glucotoxicity due to prolonged hyperglycemia, such as β-cell exhaustion, oxidative stress induced by free radical oxygen species, endoplasmic reticulum (ER) stress, inflammation caused by proinflammatory cytokines and chemokines, loss of neogenesis, proliferation of β-cells, and so on [3,4,5,6,7,8,9,10]. However, the precise mechanisms of glucotoxicity and its contribution to the pathology of type 2 diabetes mellitus (T2DM) are still not fully understood.