Abstract
Perspective: Inexorable beta cell deterioration via oxidative stress as a secondary complication of Type 2 Diabetes
Highlights
Oxidative stress consequent to chronic hyperglycemia accompanies the development of microvascular and macrovascular disease and is typically cited in textbooks of endocrinology as a basic mechanism for the development of functional and structural abnormalities in eyes, nerves, and kidneys as well as large arteries
In regard to the beta cell, in the 1990s it was demonstrated in beta cell lines that prolonged culturing in media containing high glucose concentrations caused the loss of insulin secretion, which was preceded by loss of the critical transcription factors PDX-1 and MafA [1,2,3]
Reactive oxygen species (ROS) are normally formed during metabolism of glucose and in normal concentrations participate in many physiologic processes, including regulation of gene expression, protective effects against bacterial invasion, cell growth, differentiation, apoptosis, autophagy, and senescence [6]
Summary
Oxidative stress consequent to chronic hyperglycemia accompanies the development of microvascular and macrovascular disease and is typically cited in textbooks of endocrinology as a basic mechanism for the development of functional and structural abnormalities in eyes, nerves, and kidneys as well as large arteries. In regard to the beta cell, in the 1990s it was demonstrated in beta cell lines that prolonged culturing in media containing high glucose concentrations caused the loss of insulin secretion, which was preceded by loss of the critical transcription factors PDX-1 and MafA [1,2,3]. In physiologic levels glucose is normally metabolized via oxidative phorphorylation, which generates normal concentrations of ROS.
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