THE EFFECT OF AN EXPERIMENTAL MODEL OF HIGH GLUCOSE PLUS INSULIN ON PTEN
Noemi Rivera, Rody San Marti.
1Universidad Metropolitana, Trujillo Alto, PR, 2University Austral of Chile, Valdivia, CL.
Diabetes mellitus is one of the 10 most common causes of deaths worldwide. This chronic disease afflicts more than 437 million people around the world. The World Health Organization has estimated that this situation will continue to increase. Diabetes is characterized by chronically high levels of glucose in the blood. Over time, this disease brings severe conditions such as retinopathy, neuropathy, diabetic foot, and diabetic nephropathy (DN). DN is the principal cause of renal disease. Renal complications are present in 30-40% of diabetic individuals. The final stage of DN produces an advanced renal fibrosis. Proximal tubule epithelial cells (PTEC) have a mesenchymal origin, and are able to revert to a profibrotic phenotype through epithelial-mesenchymal transdifferentiation (EMT). EMT causes an accumulation of secretion into factors attached to the extracellular matrix, which results in renal fibrosis. PTEN is a tumor suppressor that dephosphorylates proteins to modulate the cell cycle progression. In this study, we evaluated the influence of an experimental model of high glucose plus insulin on PTEN in proximal tubule epithelial cells from humans. The results show that high glucose decreases the expression of PTEN. The results also show that the presence of insulin in HK-2 cells makes PTEN decrease, while with high glucose plus insulin PTEN expression is not altered.