title: [C-peptide structure, functions and molecular mechanisms of action].
abstract: C-peptide, which is formed during the biosynthesis of insulin, has long been considered as a biologically inactive substance. However in the recent years there is convincing evidence that the deficit of C-peptide in type 1 diabetes mellitus (DM) or its excess in DM2 lead to the development of disorders in the cardiovascular, nervous, excretory, and other systems of organism. It is shown than C-peptide in the physiological concentrations has anti-inflammatory, immunomodulatory and neuroprotective effects, so that it and its synthetic analogs can be widely used to treat diabetic patients and to prevent DM complications diabetes. To effectively use C-peptide in medicine it is necessary to study its structural-functional organization and the molecular mechanisms of regulatory action of C-peptide on the fundamental cellular processes. It is established that C-peptide coupled with Gi/o protein-coupled receptors of the serpentine type regulates the functional activity of many intracellular signaling pathways, which include phospholipase Cbeta, different forms of protein kinase C, phosphatidylinositol 3-kinases and mitogen-activated protein kinases, endothelial NO-synthase, Na+/K+-ATPase, a wide range of transcription factors and nuclear receptors. C-peptide controls the stability of the insulin hexamer complexes, and, thus,affects on the activity of insulin and insulin-regulated signaling pathways. The present review analyse the current state of the problem of structural-functional organization of C-peptide and its mechanism of action on the intracellular signaling pathways, as well as the prospects for the use of C-peptide in the fundamental biology and clinical medicine.
authors.forename: A O
authors.initials: AO
authors.lastname: Shpakov
authors.forename: A O
authors.initials: AO
authors.lastname: Granstrem
mesh_terms: D000818:Animals; D002096:C-Peptide / Q000737:chemistry / Q000378:metabolism*; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D006801:Humans; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D054799:Phospholipase C beta / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*; D013329:Structure-Activity Relationship
chemical_list: D002096:C-Peptide; D043562:Receptors, G-Protein-Coupled; D019869:Phosphatidylinositol 3-Kinases; D048049:Extracellular Signal-Regulated MAP Kinases; D054799:Phospholipase C beta