Abstract
The Diabetes Control and Complication Trial recently reported that the strict maintenance of euglycemia by intensive insulin treatment can prevent the development and progression of diabetic nephropathy [1], suggesting the adverse effects of hyperglycemia on metabolic pathways are main cause of chronic complications in diabetes such as kidney disease. The importance of hyperglycemia in the development of diabetic nephropathy is supported by the results of Heilig et al. who have found that the overexpression of glucose transporter 1 (GLUTI) into glomerular mesangial cells enhanced the production of extracellular matrix components which can contribute mesangial expansion and finally glomerulosclerosis, even in normal glucose levels [2]. Multiple biochemical mechanisms have been proposed to explain the adverse effects of hyperglycemia. Activation of diacylglycerol (DAG) -protein kinase C (PKC) pathway [3,4], enhanced polyol pathway related with myo-inositol depletion [5], altered redox state [6], overproduction of advanced glycation products [7], and enhanced growth factor and cytokine production [8.9] have all been proposed as potential cellular mechanisms by which hyperglycemia induces the chronic diabetic complications.
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Koya, D., King, G.L. (1998). Protein Kinase C in Diabetic Renal Involvement, the Perspective of its Inhibition. In: Mogensen, C.E. (eds) The Kidney and Hypertension in Diabetes Mellitus. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-6752-0_28
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DOI: https://doi.org/10.1007/978-1-4757-6752-0_28
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