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lüll C-Peptide effects on renal physiology and diabetes Rebsomen L; Khammar A; Raccah D; Tsimaratos MExp Diabetes Res 2008[]; 2008 (ä): 281536The C-peptide of proinsulin is important for the biosynthesis of insulin and has for a long time been considered to be biologically inert. Animal studies have shown that some of the renal effects of the C-peptide may in part be explained by its ability to stimulate the Na,K-ATPase activity. Precisely, the C-peptide reduces diabetes-induced glomerular hyperfiltration both in animals and humans, therefore, resulting in regression of fibrosis. The tubular function is also concerned as diabetic animals supplemented with C-peptide exhibit better renal function resulting in reduced urinary sodium waste and protein excretion together with the reduction of the diabetes-induced glomerular hyperfiltration. The tubular effectors of C-peptide were considered to be tubule transporters, but recent studies have shown that biochemical pathways involving cellular kinases and inflammatory pathways may also be important. The matter theory concerning the C-peptide effects is a metabolic one involving the effects of the C-peptide on lipidic metabolic status. This review concentrates on the most convincing data which indicate that the C-peptide is a biologically active hormone for renal physiology.|Animals[MESH]|C-Peptide/*metabolism[MESH]|Diabetes Mellitus, Experimental/metabolism/physiopathology[MESH]|Diabetes Mellitus, Type 1/metabolism/*physiopathology[MESH]|Diabetic Nephropathies/metabolism/*physiopathology[MESH]|Glomerular Filtration Rate[MESH]|Humans[MESH]|Inflammation/metabolism/physiopathology[MESH]|Kidney Glomerulus/metabolism/*physiopathology[MESH]|Kidney Tubules/metabolism/*physiopathology[MESH]|Lipid Metabolism[MESH]|Signal Transduction[MESH]|Sodium-Potassium-Exchanging ATPase/metabolism[MESH] |