title: C-peptide: new findings and therapeutic possibilities.
abstract: Much new information on C-peptide physiology has appeared during the past 20 years. It has been shown that C-peptide binds specifically to cell membranes, elicits intracellular signaling via G-protein and Ca2+ -dependent pathways, resulting in activation and increased expression of endothelial nitric oxide synthase, Na+, K+ -ATPase and several transcription factors of importance for anti-inflammatory, anti-oxidant and cell protective mechanisms. Studies in animal models of diabetes and early clinical trials in patients with type 1 diabetes demonstrate that C-peptide in replacement doses elicits beneficial effects on early stages of diabetes-induced functional and structural abnormalities of the peripheral nerves, the kidneys and the retina. Much remains to be learned about C-peptide's mechanism of action and long-term clinical trials in type 1 diabetes subjects will be required to determine C-peptide's clinical utility. Nevertheless, even a cautious evaluation of the available evidence presents the picture of a bioactive endogenous peptide with therapeutic potential.
authors: Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; Cebix AB, Stockholm, Sweden. Electronic address: john.wahren@ki.se.
authors: John
authors: J
authors: Wahren
authors: Cebix AB, Stockholm, Sweden.
authors: Charlotte
authors: C
authors: Larsson
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D002096:C-Peptide / Q000378:metabolism / Q000502:physiology* / Q000627:therapeutic use; D002462:Cell Membrane / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000628:therapy*; D003929:Diabetic Neuropathies / Q000188:drug therapy; D006801:Humans; D008297:Male; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000893:Anti-Inflammatory Agents; D002096:C-Peptide; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III
keywords: Na(+), K(+)-ATPase; Nephropathy; Neuropathy; Reactive oxygen species; Retinopathy; eNOS