Alejandro J. Yañez
Universidad Austral de Chile, Chile
Alejandro J Yanez Carcamo has completed his PhD at the age of 32 years from Universidad Austral de Chile University and doctoral studies from UMKC, U.S.A. He is the director of Austral Omics, a service organization that provide a transversal solution to the researchers. He has published more than 60 papers in reputed journals contributing to the knowledge of metabolism and applied microbiology.
Diabetic nephropathy (DN) is one of the major complications of diabetic patients and is the leading cause of end-stage renal disease. Kidneys are major sites of deregulated glucose production in diabetic patients. It is therefore crucial to investigate the mechanisms involved in their pathogenesis. We analyzed theexpression of the insulin receptor (IR) in renal cortex and proximal tubules from diabetic rats and humans. Surprisingly, in the kidney of both human type 2 diabetic patients and in a type 1 diabetic rat model, a significant reduction in the protein levels of IR and a consequent increase of PEPCK is produced.Thus, expression of IR protein in proximal tubules from type 1 and type 2 diabetic kidney indicates that this is a commonregulatory mechanism which is altered in DN, triggering enhanced gluconeogenesis. Moreover, we detected activation of the GSK3βkinase andoverexpression of muscle glycogen synthase (MGS)and glycogen deposition in the diabetic kidney from rat and human, that correlate with induced-cell death in a model of human renal tubule cells. This differential expression suggests the participation of MGS in the renal metabolic changes associated that also are induce the increased levels of inflammation markers ( MCP-1, ICAM-1) and activation of NFk-B.Hence, alteredexpression of IR in human diabetic kidney could be one of the maintriggers for enhanced inflammation and gluconeogenesis and the consequent kidneydysfunction in DN. (FONDECYT 1131033.)