Thiazolidinediones : Their role in the blood glucose and lipid control in prediabetes and diabetes

Manaf, Asman (2014) Thiazolidinediones : Their role in the blood glucose and lipid control in prediabetes and diabetes. In: Kongkres , Malang.

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Abstract

The phenomenon of adverse effects of hyperglycemia on insulin target tissue and on pancreatic β cells has been termed “glucotoxicity”. The DCCT ( Diabetes Control and Complication Trial ) and the UKPDS ( United Kingdom Prospective Diabetes Study ) established that hyperglycemia is the initiating cause of the diabetic tissue damage. It has been well characterized four major molecular signaling mechanisms activated by hyperglycemia in endothelial cells and other cell types vulnerable to hyperglycemic injury. These include activation of protein kinase C ( PKC ) via diacylglycerol, increased hexosamine pathway flux, increased advanced glycation end products ( AGEs ) formation, and increased polyol pathway flux. It has been recently suggested that excessive mitochondrial production of reactive oxygen species ( ROS ), specifically superoxide, will be a common unifying mechanism that integrates the above pathways. So, hyperglycemia is believed as the main accelerating factor in this process although genetic determinants and many independent factors, such as lipotoxicity, may be involved. The new paradigm of a unifying mechanism for the progress and pathogenesis of diabetic complication, may be useful in getting novel approaches for the prevention and treatment of diabetes. Thiazolidinedione is one of potent oral antihyperglycemic agents used in diabetes and prediabetes treatment. Keywords: hyperglycemia, glucotoxicity, diabetic progress, thiazolidinediones.

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