Diabetes, glucose toxicity, and oxidative stress: A case of double jeopardy for the pancreatic islet β cell

摘要: Diabetes is commonly referred to in terms of type 1 and 2. Both forms involve pancreatic islet β-cell abnormalities, characterized by death accelerated apoptosis The resultant chronic hyperglycemia leads oxidative stress for all tissues because glucose abnormally high concentrations reactive oxygen species. It has been repeatedly emphasized that this can lead damage the classical secondary targets diabetes, such as eyes, kidneys, nerves, blood vessels. However, it much less appreciated β cell itself also a prime target, case double jeopardy. This situation more pernicious islets contain among lowest levels antioxidant enzyme activities compared other tissues. adverse effect toxicity. A major manifestation toxicity defective insulin gene expression, diminished content, secretion. molecular mechanisms development decreased two very important promoter transcription factors, PDX-1 MafA. Studies with animal models 2 diabetes have established pharmacologic protection against ameliorates severity progression. Translational research humans now under way ascertain whether be provided patients experiencing inadequate glycemic control.