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C-peptide
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===Cellular effects of C-peptide=== C-peptide has been shown to bind to the surface of a number of cell types such as neuronal, endothelial, fibroblast and renal tubular, at nanomolar concentrations to a receptor that is likely G-protein-coupled. The signal activates Ca<sup>2+</sup>-dependent intracellular signaling pathways such as MAPK, PLCγ, and PKC, leading to upregulation of a range of transcription factors as well as eNOS and Na+K+ATPase activities.<ref>{{cite journal | vauthors = Hills CE, Brunskill NJ | title = Intracellular signalling by C-peptide | journal = Experimental Diabetes Research | volume = 2008 | pages = 635158 | year = 2008 | pmid = 18382618 | pmc = 2276616 | doi = 10.1155/2008/635158 | doi-access = free }}</ref> The latter two enzymes are known to have reduced activities in patients with type I diabetes and have been implicated in the development of long-term complications of type I diabetes such as peripheral and autonomic neuropathy. In vivo studies in animal models of type 1 diabetes have established that C-peptide administration results in significant improvements in nerve and kidney function. Thus, in animals with early signs of diabetes-induced neuropathy, C peptide treatment in replacement dosage results in improved peripheral nerve function, as evidenced by increased nerve conduction velocity, increased nerve Na+,K+ ATPase activity, and significant amelioration of nerve structural changes.<ref>{{cite journal | vauthors = Sima AA, Zhang W, Sugimoto K, Henry D, Li Z, Wahren J, Grunberger G | title = C-peptide prevents and improves chronic Type I diabetic polyneuropathy in the BB/Wor rat | journal = Diabetologia | volume = 44 | issue = 7 | pages = 889–97 | date = July 2001 | pmid = 11508275 | doi = 10.1007/s001250100570 | doi-access = free }}</ref> Likewise, C-peptide administration in animals that had C-peptide deficiency (type 1 model) with nephropathy improves renal function and structure; it decreases [[urinary albumin excretion]] and prevents or decreases diabetes-induced glomerular changes secondary to mesangial matrix expansion.<ref>{{cite journal | vauthors = Samnegård B, Jacobson SH, Jaremko G, Johansson BL, Sjöquist M | title = Effects of C-peptide on glomerular and renal size and renal function in diabetic rats | journal = Kidney International | volume = 60 | issue = 4 | pages = 1258–65 | date = October 2001 | pmid = 11576340 | doi = 10.1046/j.1523-1755.2001.00964.x | doi-access = free }}</ref><ref>{{cite journal | vauthors = Samnegård B, Jacobson SH, Jaremko G, Johansson BL, Ekberg K, Isaksson B, Eriksson L, Wahren J, Sjöquist M | display-authors = 6 | title = C-peptide prevents glomerular hypertrophy and mesangial matrix expansion in diabetic rats | journal = Nephrology, Dialysis, Transplantation | volume = 20 | issue = 3 | pages = 532–8 | date = March 2005 | pmid = 15665028 | doi = 10.1093/ndt/gfh683 | doi-access = }}</ref><ref>{{cite journal | vauthors = Nordquist L, Brown R, Fasching A, Persson P, Palm F | title = Proinsulin C-peptide reduces diabetes-induced glomerular hyperfiltration via efferent arteriole dilation and inhibition of tubular sodium reabsorption | journal = American Journal of Physiology. Renal Physiology | volume = 297 | issue = 5 | pages = F1265-72 | date = November 2009 | pmid = 19741019 | pmc = 2781335 | doi = 10.1152/ajprenal.00228.2009 }}</ref><ref>{{cite journal | vauthors = Nordquist L, Wahren J | title = C-Peptide: the missing link in diabetic nephropathy? | journal = The Review of Diabetic Studies | volume = 6 | issue = 3 | pages = 203–10 | year = 2009 | pmid = 20039009 | pmc = 2827272 | doi = 10.1900/RDS.2009.6.203 | doi-broken-date = November 1, 2024 }}</ref> C-peptide also has been reported to have anti-inflammatory effects as well as aid repair of smooth muscle cells.<ref>{{cite journal | vauthors = Luppi P, Cifarelli V, Tse H, Piganelli J, Trucco M | title = Human C-peptide antagonises high glucose-induced endothelial dysfunction through the nuclear factor-kappaB pathway | journal = Diabetologia | volume = 51 | issue = 8 | pages = 1534–43 | date = August 2008 | pmid = 18493738 | doi = 10.1007/s00125-008-1032-x | doi-access = free }}</ref><ref>{{cite journal | vauthors = Mughal RS, Scragg JL, Lister P, Warburton P, Riches K, O'Regan DJ, Ball SG, Turner NA, Porter KE | display-authors = 6 | title = Cellular mechanisms by which proinsulin C-peptide prevents insulin-induced neointima formation in human saphenous vein | journal = Diabetologia | volume = 53 | issue = 8 | pages = 1761–71 | date = August 2010 | pmid = 20461358 | pmc = 2892072 | doi = 10.1007/s00125-010-1736-6 }}</ref> A recent epidemiologic study suggests a U-shaped relationship between C-peptide levels and risk of cardiovascular disease.<ref>{{cite journal | vauthors = Koska J, Nuyujukian DS, Bahn G, Zhou JJ, Reaven PD | title = Association of low fasting C-peptide levels with cardiovascular risk, visit-to-visit glucose variation and severe hypoglycemia in the Veterans Affairs Diabetes Trial (VADT) | journal = Cardiovascular Diabetology | volume = 20 | date = 2021 | issue = 1 | page = 232 | doi = 10.1186/s12933-021-01418-z| pmid=34879878| pmc = 8656002 | doi-access = free }}</ref>
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