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Increased extracellular glucose leads to nonenzymatic glycosylation of proteins and subsequent formation of advanced glycation end products (AGE) that interact with the receptor for AGE (RAGE) on the plasma membrane and promote the production of reactive oxygen species (ROS). It is still unclear whether the ER stress response can be initiated as a direct response to the increasing load on protein synthesis and maturation due to hyperglycemia or due to the hyperglycemia-associated oxidative stress.
Intermittent high glucose enhances apoptosis related to oxidative stress in human umblical vein endothelial cells: The role of protein kinase C and NAD(P) H-oxidase activation. Constant and intermittent high glucose enhances endothelial cell apoptosis through mitochondrial superoxide overproduction. Periodic high extra cellular glucose enhances production of collagens III and IV by mesangial cells. Rapid glycaemic swings induce oxidative stress, activate poly-(ADP-ribose) polymerase and impair endothelial function in a rat model of diabetes mellitus.
Activation of oxidative stress by acute glucose fluctuations compared with sustained chronic hyperglycemia in patients with type 2 diabetes. Oscillating glucose is more deleterious to endothelial function and oxidative stress than mean glucose in normal and type 2 diabetic patients.

Measuring the impact of diabetes through patient report of treatment satisfaction, productivity and symptom experience. Effects of short-term therapy with different insulin secretagogues on glucose metabolism, lipid parameters and oxidative stress in newly diagnosed type 2 diabetes mellitus. Effects of a single administration of acarbose on postprandial glucose excursion and endothelial dysfunction in type 2 diabetic patients.
High glucose levels in circulation can divert glucose into alternative biochemical pathways leading to the increase in advanced glycation end products (AGEs), glucose autooxidation, hexosamine and polyol flux, and activation of classical isoforms of protein kinase C, that are considered to be the mediators of hyperglycemia-induced cellular injury. The possibility that ER stress response also can lead to excessive ROS formation cannot be ruled out.
Excessive ROS production in the vasculature drives changes in cell phenotype that are mediated by a range of signaling pathways and transcription factors. Many different pathways involved in hyperglycemia-mediated endothelial dysfunction induced by hyperglycemia lead to considerable generation of reactive oxygen species (ROS), which is responsible for the oxidative stress. Kidney cells also undergo cell-specific and organ-specific phenotypic changes as a result of hyperglycemia-mediated ROS production.

Glucose potentiation and stronger suppression of endogenous glucose release are the main mechanisms underlying the Staub-Traugott effect. This may be related to ROS overproduction, through PKC-dependent activation of nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase.{Figure 1}Contributions of fasting plasma glucose and postprandial glucose to oxidative stress were shown in several studies.
Twenty four hour after the clamp, endothelial function was measured using flow-mediated dilation of the brachial artery. 3-nitrotyrosirone and 24-h urinary levels of 8-iso PGF2α were measured as markers of oxidative stress. Impaired endothelial function was observed with higher levels of oxidative stress in oscillating glucose than stable constant high glucose.
An important consequence of this derangement is that hepatic glucose production is no longer suppressed during times of prandial glucose intake leading to hyperglycemic excursions.

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