The WHO estimates that there are more than 422 million people with diabetes in the world, of whom 90% are diagnosed as type 2. Hyperglycemia plays an important role in renal damage, thus diabetic nephropathy is the most common complication of this pathology. Claudins are components of paracellular transport which are determinants to the ion balance in the kidney. Any alteration in the tight junctions carry a pathophysiological renal consequences that have not yet described in diabetic type 2 model. PPARs are nuclear receptors ligand‐dependent and their alpha isoform is activated by fibrates. Pharmacological therapy with fibrates in diabetes had showed to prevent cardiovascular risk, if they have renal protective effects in diabetes and if they are involved in paracellular ion transport, is not well understood. Those actions, could be useful as a target to identify, prevent and treat diabetic nephropathy may contribute to a better understanding of this disease. Type 2 diabetes model that we used was induced to neonatal rats by the intraperitoneal administration of streptozotocin, a chemical that selectively destroys the β cells of the pancreas, diabetics rats showed moderate hyperglycemia since 4th week and at 14‐week, had a decrease in body weight gain, glucose intolerance, lower insulin secretion and an increase in renal mass. We evaluated renal function in this model and we observed that proteinuria was associated with a decrease in claudin‐5 expression in the glomerulus and the increased fractional excretion of Na+ and K+ was related with a decrease of claudin‐2 and occludin in the proximal tubule. In addition, we observed a loss of renal expression of peroxisome proliferator‐activated receptor alpha (PPAR‐α) in both segments of the nephron. The present work provides evidence that type 2 diabetes alters the renal expression of tight junctions proteins such as claudin‐5, claudin‐2 and occludin, as well as PPAR‐α. This is related to the loss of renal function, suggesting that the loss of these proteins is a fundamental part of the early stages of type 2 diabetic nephropathy.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.