108
Views
31
CrossRef citations to date
0
Altmetric
Review

C-peptide and diabetic neuropathy

Pages 1471-1488 | Published online: 02 Mar 2005

Bibliography

  • GREENE DA, SIMA AAF, FELDMAN EL, STEVENS MJ: Diabetic neuropathy. In: Ellenberg and Rifkin Diabetes Mellitus H Rifkin, D Porte, R Sherwin (Eds), Appleton and Lange, Stanford, CT, USA (1997):1009–1076.
  • SUGIMOTO K, MURAKAWA Y, SIMA AAF: Diabetic neuropathy - a continuing enigma. Diab. Metab. Res. Rev (2000) 16(6):408–433.
  • SIMA AAF, THOMAS PK, ISHII D, VINIK A: Diabetic neuropathies. Diabetologia (1997) 40\(Suppl. 3):B74–B77.
  • THOMAS PK: Classification, differential diagnosis, and staging of diabetic peripheral neuropathy. Diabetes (1997) 46\(Suppl. 2):554–557.
  • PIRART J: Diabetes mellitus and its degenerative complications: a prospective study of 4,400 patients observed between 1947 and 1973. Diabetes Metab. (1977) 3:97–107.
  • VINIK Al, LIUZZE FJ, HOLLAND MT, STANSBERRY KB, LEBEAN JM, COLEN LB: Diabetic neuropathies. Diabetes Care (1992) 15:1926–1975.
  • SIMA AAF: Pathological definition and evaluation of diabetic neuropathy and clinical correlations. Can. J. Neural. Sci. (1994) 21\(Suppl. 4):513–517.
  • TESFAYE S, STEVENS LK, STEPHANSON JM et al: Prevalence of diabetic peripheral neuropathy and its relation to glycaemic control and potential risk factors: the EURODIAB IDDM Complication Study. Diabetologia (1996) 39:1377–1384.
  • •Recent epidemiological data from the UK.
  • DYCK PJ, DAVIES JL, WILSON DM, SERVICE FJ, MELTON LJ 3rd, O'BRIEN PC: Risk factors for severity of diabetic polyneuropathy: intensive longitudinal assessment of the Rochester Diabetic Neuropathy Study Cohort. Diab. Care (1999) 22:1479–1486.
  • •Risk factors for DPN severity of which Type 1 diabetes is the strongest.
  • GREENE DA, SIMA AAF, STEVENS MJ, FELDMAN EL, LATTIMER SA: Complications: neuropathy, pathogenetic considerations. Diabetes Care (1992) 15:1902–1925.
  • LOW PA, NICKANDER KK, SCIONTI L: Role of hypwda, oxidative stress, and excitatory neurotwdns in diabetic neuropathy. In Diabetic Neuropathy. PJ Dyck, PK Thomas (Eds), W. B. Saunders, Philadelphia, PA, USA (1999):317–329.
  • SIMA AAF: Metabolic alterations of peripheral nerve in diabetes. Semin. Neurol (1996) 16:129–137.
  • FORST T, KUNT T, PFUTZNER A, BEYER J, WAHREN J: New aspects on biological activity of C-peptide in IDDM patients. Exp. Clin. Endocrinol Diabetes (1998) 106:270–276.
  • SIMA AAF, SUGIMOTO K: Experimental diabetic neuropathy: an update. Diabetologia (1999) 42:773–788.
  • SIMA AAF: Diabetic neuropathy; pathogenetic backgrounds, current and future therapies. Expert Rev Neurothempeutics (2001) 1:225–238.
  • OATES PJ, MYLARI BL: Aldose reductase inhibitors: therapeutic implications for diabetic complications. Expert Opin. Investig. Drugs (1999) 8:2095–2119.
  • •Nice review of the genetics of the ALR2 gene.
  • BRISMAR T, SIMA AAF: Changes in nodal function in nerve fibres of the spontaneously diabetic BB-Wistar rat. Potential clamp analysis. Acta Physiol Scand. (1981) 113:499–506.
  • SIMA AAF, BRISMART: Reversible diabetic nerve dysfunction. Structural correlates to electrophysiological abnormalities. Ann. Neurol (1985) 18:21–29.
  • BREWSTER WJ, FERNYHOUGH P, DIEMEL LT, MOHIUDDIN L, TOMLINSON DR: Diabetic neuropathy, nerve growth factor and other neurotrophic factors. Trends Neurosci. (1994) 17:321–325.
  • TOMLINSON DR, FERNYHOUGH P: Neurotrophism in diabetic neuropathy. In: Chronic Complications M Diabetes. Animal Models and Chronic Complications, AAF Sima (Ed.), Harwood, Amsterdam (1999):167–182.
  • BRISMAR T, SIMA AAF, GREENE DA: Reversible and irreversible nodal dysfunction in diabetic neuropathy. Ann. Neurol (1987) 21:504–507.
  • SIMA AAF, LATTIMER SA, YAGIHASHI S, GREENE DA: Axo-glial dysjunction': A novel structural lesion that accounts for poorly reversible slowing of nerve conduction in the spontaneously diabetic BB-rat. Clin. Invest. (1986) 77:474–484.
  • •The first description of axoglial dysfunction in Type 1 DPN.
  • SIMA AAF, NATHANIEL V, BRIL V, MCEWEN TAJ, GREENE DA: Histopathological heterogeneity of neuropathy in insulin-dependent and non-insulin-dependent diabetes, and demonstration of axo-glial dysjunction in human diabetic neuropathy. Clin. Invest. (1988) 81:349–364.
  • SIMA AAF, ZHANG W, XU G, SUGIMOTO K, GUBERSKI DL, YOREK MA: A comparison of diabetic polyneuropathy in type-2 diabetic BBZDR/ Wor-rat and in Type 1 diabetic BB/Wor-rat. Diabetologia (2000) 43:786–793.
  • ••Detailed depiction of the basic differencesbetween mtirine Type 1 and Type 2 DPN.
  • CHERIAN PV, KAMIJO M, ANGELIDES KJ, SIMA AAF: Nodal
  • •• Na+-channel displacement is associated with nerve conduction slowing in the chronically diabetic BB/W-rat. Prevention by an aldose reductase inhibitor. Blab. Compi (1996) 10:192–200.
  • SIMA AAF, ZHANG W-X, SUGIMOTO K et al.: C-peptide prevents and improves chronic Type 1 diabetic neuropathy in the BB/Wor-rat. Diabetologia (2001) 44:889–897.
  • SIMA AAF, PIERSON CR, ZHANG W: C-peptide prevents the molecular abnormalities of the paranode in Type 1 diabetic polyneuropathy (DPN). 18th International Diabetes Federation Congress, Paris (2003) (Abstract).
  • ••Axoglial dysfunction and its relationship to insulin action.
  • LAUDADIO C, SIMA AAF, THE PONALRESTAT STUDY GROUP: Progression rates of diabetic neuropathy in placebo patients in an 18-month clinical trial. J. Blab. Comp]. (1998) 12:121–127.
  • LAUDADIO C, SIMA AAF: Design of controlled clinical trials for diabetic polyneuropathy. Semin. Neurol (1996) 16:187–192.
  • SIMA AAF, CHERIAN PV: Neuropathology of diabetic neuropathy and its correlations with neurophysiology. Clin. Neurosci. (1997) 4:359–364.
  • SIMA AAF, BRIL V, NATHANIEL Vet al.: Regeneration and repair of myelinated fibers in sural nerve biopsies from patients with diabetic neuropathy treated with an aldose reductase inhibitor. N Engl. Med (1988) 319:548–555.
  • CHAKRABARTI S, SIMA AAF, NAKAJIMA T, YAGIHASHI S, GREENE DA: Aldose reductase in the BB rat: isolation, immunological identification and localization in the retina and peripheral nerve. Diabetologia (1987) 30:244–251.
  • STEVENS MJ, LATTIMER SA, KAMIJO M, VAN HUYSEN C, SIMA AAF, GREENE DA: Osmotically-induced nerve taurine depletion and the compatible osmolyte hypothesis in experimental diabetic neuropathy in the rat. Diabetologia (1993) 36:608–614.
  • ZHU X, EICHBERG J: A myoinositol pool utilized for phosphatidylinositol synthesis is depleted in sciatic nerve from rats with streptozotocin-induced diabetes. Proc. Nati Acad. Sci. USA (1990) 87:9818–9822.
  • ZHU X, EICHBERG J: 1,2-diacylglycerol content and its arachidonyl-containing molecular species are reduced in sciatic nerve from streptozotocin-induced diabetic rats. J. Neurocliem. (1990) 55:1087–1090.
  • GREENE DA, LATTIMER SA, SIMA AAF: Sorbitol, phosphoinositides and sodium-potassium ATPase in the pathogenesis of diabetic complications. N Engl. Med. (1987) 316:599–606.
  • ROWE-RENDLEMAN CL, EICHBERG J: PO phosphorylation in nerves from normal and diabetic rats: role of protein kinase C and turnover of phosphate groups. Neurocliem. Res. (1994) 19:1023–1031.
  • ARUOMA OI, HALLIWELL B, HOEY BM, BUTLER J: The antioxidant action of taurine, hypotaurine and their metabolic precursors. Biocliem. (1988) 256:251–255.
  • EL IDRISSI A, TRENKNER E: Growthfactors and taurine protect against excitotoxicity by stabilizing calcium homeostasis and energy metabolism. .1 Neurosci (1999) 19:9459–9468.
  • DE MATTIA G, LAURENTI 0, BRAVI C, GHISELLI A, IULIANO L, BALSANO F: Effect of aldose reductase inhibition on glutathione redox status in erythrocytes of diabetic patients. Metabolism (1994) 43:965–968.
  • ZHOU X, LI C, DLUGOSZ J, KAPOR-DREZGIC J, MUNK S, WHITESIDE C: Mesangial cell actin disassembly in high glucose mediated by protein kinase C and the polyol pathway. Kidney Int. (1997) 6:1797–1808.
  • CAMERON NE, COTTER MA: Effects of protein kinase C beta inhibition on neurovascular dysfunction in diabetic rats: interaction with oxidative stress and essential fatty acid dysmetabolism. Blab. Metab. Res. Rev (2002) 18:315–323.
  • KIM J, RUSHOVICH EH, THOMAS TP, UEDA T, AGRANOFF BW, GREENE DA: Diminished specific activity of cytosolic protein kinase C in sciatic nerve of streptozocin-induced diabetic rats and its correction by dietary myoinositol. Diabetes (1991) 40:1545–1554.
  • ROBERTS RE, MCLEAN WG: Protein kinase C isozyme expression in sciatic nerves and spinal cords of experimentally diabetic rats. Brain Res (1997) 754:147–156.
  • ISHII H, KOYA D, KING GL: Protein kinase C activation and its role in the development of vascular complications in diabetes mellitus. Ma Med (1998) 76:21–31.
  • CAMERON NE, COTTER MA, JACK AM, BASSO MD, HOHMAN TC: Protein kinase C effects on nerve function, perfusion, Na(+), K(+)- ATPase activity and glutathione content in diabetic rats. Diabetologia (1999) 42:1120–1130.
  • NAKAMURA J, KATO K, HAMADA Y et al.: A protein kinase C-beta-selective inhibitor ameliorates neural dysfunction in streptozotocin-induced diabetic rats. Diabetes (1999) 48:2090–2095.
  • AHLGREN SC, LEVINE JD: Protein kinase C inhibitors decrease hyperalgesia and C-fiber hyperexcitability in the streptozotocin-diabetic rat. Neuroplosiol. (1994) 72:684–692.
  • KISHI Y, SCHMELZER JD, YAO JK et al.: Alpha-lipoic acid: effect on glucose uptake, sorbitol pathway, and energy metabolism in experimental diabetic neuropathy. Diabetes (1999) 48:2045–2051.
  • HOTTA N, KAKUTA H, FUKASAWAH N et al.: Effect of niceritrol on streptozocin-induced diabetic neuropathy in rats. Diabetes (1992) 41:587–891.
  • ZHANG W, YOREK M, PIERSON CR, MURAKAWA Y, BREIDENBACH A, SIMA AAF: Human C-peptide dose dependently prevents early neuropathy in the BB/Wor-rat. Internatl. I Exp. Blab. Res. (2001) 2(3):187–194.
  • SIMA AAF, LI Z, ZHANGW, STEVENS M: Impaired endoneurial blood flow but not oxidative stress is prevented by C-peptide in Type 1 BB/Wor-rats. Xl/tb International Congress of Neuropathy Turin, Italy (2003) (Abstract).
  • WAHREN J, JORNVALL H: C-peptide - the comeback peptide. Blab. Metab. Res. Rev (2003) (Editorial) (In press).
  • SIMA AAF, RISTIC H, MERRY A et al.: Primary preventive and secondary interventionary effects of acetyl-L- carnitine on diabetic neuropathy in the bio-breeding Worcester rat. J. Clin. Invest. (1996) 97:1900–1907.
  • STEVENS MJ, LATTIMER SA, FELDMAN EL et al.: Acetyl-L-carnitine deficiency as a cause of altered nerve myoinositol content, Na, K-ATPase activity, and motor conduction velocity in the streptozotocin-diabetic rat. Metabolism (1996) 45:865–872.
  • HOTTA N, KOH N, SAKAKIBARA F et al.: Effect of propionyl-L-carnitine on motor nerve conduction, autonomic cardiac function, and nerve blood flow in rats with streptozotocin- induced diabetes: comparison with an aldose reductase inhibitor." Pharmacol. Exp. Ther. (1996) 276:49–55.
  • IDO Y, MCHOWAT J, CHANG KC et al.:Neural dysfunction and metabolic imbalances in diabetic rats. Prevention by acetyl-L-carnitine. Diabetes (1994) 43:1469–1477.
  • SONOBE M, YASUDA H, HISANAGA T et al.: Amelioration of nerve Na(+)-K(F)-ATPase activity independently of myo-inositol level by P GE I analogue OP-1206.alpha-CD in streptozocin- induced diabetic rats. Diabetes (1991) 40:726–730.
  • HEESOM AE, MILLWARD A, DEMAINE AG: Susceptibility to diabetic neuropathy in patients with insulin dependent diabetes mellitus is associated with a polymorphism at the 5' end of the aldose reductase gene. J. Neurol. Neurosurg. Psychiatry(1998) 64:213–216.
  • HEESOM AE, HIBBERD ML, MILLWARD BA, DEMAINE AG: A polymorphism in the 5' end of the aldose reductase gene is strongly associated with the development of diabetic nephropathy in Type 1 diabetes. Diabetes (1997) 46:287–291.
  • KO BC-B, LAM KS-L, WAT NS, CHUNG SM: An (A-C)n dinucleotide repeat polymorphic marker at the 5' end of the aldose reductase gene is associated with early onset diabetic retinopathy in NIDDM patients. Diabetes (1995) 44:727–732.
  • ARAKI N, UENO N, CHAKRABARTI B, MORINO Y, HORIUCHI S: Immunochemical evidence for the presence of advanced glycation end products in human lens proteins and its positive correlation with aging." Biol. Chem. (1992) 267:10211–10214.
  • HAMMES HP, ALT A, NIWA T et al.: Differential accumulation of advanced glycation end products in the course of diabetic retinopathy. Diabetologia (1999) 42:728–736.
  • MIYATA T, UEDA Y, HORIE K et al.: Renal catabolism of advanced glycation end products: the fate of pentosidine. Kidney Int (1998) 53:416–422.
  • VOGT BW, SCHLEICHER ED, WIELAND OH: E-Amino-lysine-bound glucose in human tissues obtained at autopsy. Increase in diabetes mellitus. Diabetes (1982) 31:1123–1127.
  • SCHMIDT AM, VIANNA M, GERLACH M et al: Isolation and characterization of two binding proteins for advanced glycosylation end products from bovine lung which are present on the endothelial cell surface. J. Biol. Chem. (1992) 267:14987–14997.
  • NEEPER M, SCHMIDT AM, BRETT J et al.: Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins. I Biol. Chem. (1992) 267:14998–15004.
  • BRETT J, SCHMIDT AM, YAN SD et al.: Survey of the distribution of a newly characterized receptor for advanced glycation end products in tissues. Am. J. Pathol (1993) 143:1699–1712.
  • SOULIS T, THALLAS V, YOUSSEF S et al.: Advanced glycation end products and their receptors co-localise in rat organs susceptible to diabetic microvascular injury. Diabetologia (1997) 40:619–628.
  • VITEK MP, BHATTACHARY AK, GLENDENING JM et al: Advanced glycation end products contribute to amyloidosis in Alzheimer's disease. Proc. Natl. Acad. Sci. USA (1994) 91:4766–4770.
  • YAN SD, CHEN X, FU J et al.: RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease. Nature (1996) 382:685–691.
  • VLASSARA H, BROWNLEE M, CERAMI A: Nonenzymatic glycosylation of peripheral nerve protein in diabetes mellitus. Proc. Natl. Acad. Sci. USA (1981) 78:5190–5192.
  • RYLE C, LEOW CK, DONAGHY M: Nonenzymatic glycation of peripheral and central nervous system proteins in experimental diabetes mellitus. Muscle Nerve (1997) 20:577–584.
  • CULLUM NA, MAHON J, STRINGER K, MCLEAN WG: Glycation of rat sciatic nerve tubulin in experimental diabetic mellitus. Diabetologia (1991) 34:387–389.
  • PEKINER C, CULLUM NA, HUGHES N et al.: Glycation of brain actin in experimental diabetes. " Neurochem. (1993) 61:436–442.
  • FEDEROFF HJ, LAWRENCE D, BROWNLEE M: Nonenzymatic glycosylation of laminin and laminin peptide CIKVAVS inhibits neurite outgrowth. Diabetes (1993) 42:509–513.
  • VLASSARA H, BLOWNLEE M, CERAMI A: Excessive nonenzymatic glycosylation of peripheral and central nervous system myelin components in diabetic rats. Diabetes (1983) 32:670–674.
  • WEIMBS T, STOFFEL W: Topology of CNS myelin proteolipid protein: Evidence for the nonenzymatic glycosylation of extracytoplamic domains in normal and diabetic animals. Biochemistry (1994) 33:10408–10415.
  • VLASSARA H, BROWNLEE M, CERAMI A: Accumulation of diabetic rat peripheral nerve myelin by macrophages increases with the presence of advanced glycosylation endproducts. Exp. Med (1984) 160:197–207.
  • VLASSARA H, BROWNLEE M, CERAMI A: Recognition and uptake of human diabetic peripheral nerve myelin by macrophages. Diabetes (1985) 34:553–557.
  • TAKAGI Y, KASHIWAGI A, TANAKA Y, ASAHINA T, KIKKAWA R, SHIGETA Y: Significance of fructose-induced protein oxidation and formation of advanced glycation end product. I Diab. Comp]. (1995) 9:87–91.
  • MCPHERSON JD, SHILTON BH, WALTON DJ: Role of fructose in glycation and cross-linking of proteins. Biochemistry (1988) 27:1901–1907.
  • LAL S, SZWERGOLD BS, TAYLOR AH et al.: Metabolism of fructose-3-phosphate in the diabetic rat lens. Arch. Biochem. Biophys. (1995) 318:191–199.
  • PHILLIPS SA, THORNALLEY PJ: The formation of methylglyoxal from triose phosphates. Investigation using a specific assay for methylglyoxal. Ear. Biochem. (1993) 212:101–105.
  • HAMADA Y, ARAKI N, HORIUCHI S, HOTTA N: Role of polyol pathway in nonenzymatic glycation. Nephrol. Dial. Transplant (1996) 11:95–98.
  • SOULIS-LIPAROTA T, COOPER ME, DUNLOP M, JERUMS G: The relative roles of advanced glycation, oxidation and aldose reductase inhibition in the development of experimental diabetic nephropathy in the Sprague-Dawley rat. Diabetologia (1995) 38:387–394.
  • BAYNES JW: Role of oxidative stress in development of complications in diabetes. Diabetes (1991) 40:405–412.
  • WILLIAMSON JR, CHANG K, FRANGOS M et al.: Hyperglycemic pseudohypoxia and diabetic complications. Diabetes (1993) 42:801–813.
  • YOSHIDA K, HIROKAWA J, TAGAMI S, KAWAKAMI Y, URATA Y, KONDO T: Weakened cellular scavenging activity against oxidative stress in diabetes mellitus: regulation of glutathione synthesis and efflux. Diabetologia (1995) 38:201–210.
  • MCCORD JM: Oxygen-derived free radicals in postischemic tissue injury. N Engl. J. Med. (1985) 312:159–163.
  • HUNT IV, WOLFF SP: Oxidative glycation and free radical production: A causal mechanism of diabetic complications. Free Rad. Res. Comms. (1991) 12–13:115–123.
  • HUNT IV, DEAN RT, WOLFF SP: Hydroxyl radical production and autoxidative glycation. Glucose autoxidation as the cause of protein damage in the experimental glycation model of diabetes mellitus and aging. Biochem. (1988) 256:205–212.
  • CAMERON NE, COTTER MA: Neurovascular dysfunction in diabetic rats. Potential contribution of autoxidation and free radicals examined using transition metal chelating agents. Clin. Invest. (1995) 96:1159–1163.
  • BIERHAUS A, CHEVION S, CHEVION M et al: Advanced glycation end product-induced activation of NF-kB is suppressed by a-lipoic acid in cultured endothelial cells. Diabetes (1997) 46:1481–1490.
  • WAUTIER IL, ZOUKOURIAN C, CHAPPEY 0 et al.: Receptor-mediated endothelial cell dysfunction in diabetic vasculopathy. Soluble receptor for advanced glycation end products blocks hyperpermeability in diabetic rats. Invest. (1996) 97:238–243.
  • SELL DR, LAPOLLA A, ODETTI P, FOGARTY J, MONNIER VM: Pentosidine formation in skin correlates with severity of complications in individuals with long-standing IDDM. Diabetes (1992) 41:1286–1292.
  • MCCANCE DR, DYER DG, DUNN JA, BAILIE KE, THORPE SR, BAYNES JW: Maillard reaction products and their relation to complications in insulin-dependent diabetes mellitus. I. Gin. Invert. (1993) 91:2470–2478.
  • BEISSWENGER PJ, MOORE LL, BRINCK-JOHNSEN T, CURPHEY TI: Increased collagen-linked pentosidine levels and advanced glycosylation end products in early diabetic nephropathy. j Clin. Invest. (1993) 92:2212–2217.
  • LIPINSKI B: Pathophysiology of oxidativestress in diabetes mellitus. J. Diab. Cowl. (2001) 15:203-219. loo. ZIEGLER D, RELJANOVIC M, MEKNERT H, GRIES FA: Alpha lipoic acid in the treatment of diabetic polyneuropathy in Germany: current evidence from clinical trials. Exp. Gin. Endocrin. Diab. (1999) 107:421–430.
  • CAMERON NE, COTTER MA: Metabolic and vascular factors in the pathogenesis of diabetic neuropathy. Diabetes (1997) 46\(Suppl. 2):531–537.
  • CAMERON NE, COTTER MA: Oxidative stress and abnormal lipid metabolism in diabetic complications. In: Chronic Complications M Diabetes. AAF Sima (Ed.), Harwood Academic Publ., Amsterdam (1999):97–130.
  • COPPEY LJ, GELLET IS, DAVIDSON EP, DUNLAP JA, YOREK MA: Changes in endoneurial blood flow, motor nerve conduction velocity and vascular relaxation of epineurial arterioles of the sciatic nerve in ZDF-obese diabetic rats. Diab. Metab. Res. Rev (2002) 18:49–56.
  • VAN DAM PS: Oxidative stress and diabetic neuropathy: pathophysiological mechanisms and treatment perspectives. Diab. Metab. Res. Rev (2002) 18:176–184.
  • EBENDAL T: Function and evolution in the NGF family and its receptors. Neurosci. Res. (1992) 32:461–470.
  • JAKOBSEN J, BRIMIJOIN S, SKAU K, SIDENIUS P, WELLS D: Retrograde axonal transport of transmitter enzymes, fucose-labeled protein, and nerve growth factor in streptozotocin-diabetic rats. Diabetes (1981) 30:797–803.
  • HELLWEG R, HARTUNG HD: Endogenous levels of nerve growth factor (NGF) are altered in experimental diabetes mellitus: a possible role for NGF in the pathogenesis of diabetic neuropathy. Neurosci. Res. (1990) 26:258–267.
  • APFEL SC, AREZZO IC, BROWNLEE M, FEDEROFF H, KESSLER JA: Nerve growth factor administration protects against experimental diabetic sensory neuropathy. Brain Res (1994) 634:7–12.
  • DIEMEL LT, BREWSTER WI, FERNYHOUGH P, TOMLINSON DR: Expression of neuropeptides in experimental diabetes; effects of treatment with nerve growth factor or brain-derived neurotrophic factor. Brain Res. Ma Brain. Res. (1994) 21:171–175.
  • NEW HV, MUD GE AW: Distribution and ontogeny of SP, CGRP, SOM, and VIP in chick sensory and sympathetic ganglia. Dev. Biol. (1986) 116:337–346.
  • HORY-LEE F, RUSSELL M, LINDSAY RM, FRANK E: Neurotrophin 3 supports the survival of developing muscle sensory neurons in culture. Proc. Nati Acad. Sci. USA (1993) 90:2613–2617.
  • ERNFORS P, LEE KF, KUCERA J, JAENISCH R: Lack of neurotrophin-3 leads to deficiencies in the peripheral nervous system and loss of limb proprioceptive afferents. Cell (1994) 77:503–512.
  • TOMLINSON DR, FERNYHOUGH P, DIEMEL LT: Role of neurotrophins in diabetic neuropathy and treatment with nerve growth factors. Diabetes (1997) 46\(Suppl. 2):S43–S49.
  • FERNYHOUGH P, DIEMEL LT, TOMLINSON DR: Target tissue production and axonal transport of neurotrophin-3 are reduced in streptozotocin-diabetic rats. Diabetologia (1998) 41:300–306.
  • APFEL SC: Neurotrophic factors in the therapy of diabetic neuropathy. Am." Med. (1999) 107:34S–42S.
  • ISHII DN: Implication of insulin-like growth factors in the pathogenesis of diabetic neuropathy. Brain Res. Rev (1995) 20:47–67.
  • CROSBY SR, TSIGOS C, ANDERTON CD, GORDON C, YOUNG RI, WHITE A: Elevated plasma insulin-like growth factor binding protein-1 levels in Type 1 (insulin-dependent) diabetic patients with peripheral neuropathy. Diabetologia (1995) 35:868–872.
  • ISHII DN, GUERTIN DM, WHALEN LR: Reduced insulin-like growth factor-I mRNA content in liver, adrenal glands and spinal cord of diabetic rats. Diabetologia (1994) 37:1073–1081.
  • WUARIN L, GUERTIN DM, ISHII DN: Early reduction in insulin-like growth factor gene expression in diabetic nerve. Exp. Neural. (1994) 130:106–114.
  • XU G, MURAKAWA Y, PIERSON CR, SIMA AAF: Altered 13-tubulin and neurofilament expression and impaired axonal growth in diabetic nerve regeneration. J. Neuropath. Exp. Neurol. (2002) 61:164–175.
  • PIERSON CR, ZHANG W, MURAKAWA Y, SIMA AAF: Early gene responses of trophic factors differ in nerve regeneration in Type 1 and Type 2 diabetic neuropathy. I Neuropath. Exp. Neurol (2002) 61:857–871.
  • •Detailed description of the differences in early gene responses in nerve regeneration in Type 1 and Type 2 diabetes.
  • PIERSON CR, ZHANG W, MURAKAWA Y, SIMA AAF: Insulin deficiency rather than hyperglycemia accounts for impaired neurotrophic responses and nerve fiber regeneration in Type 1 diabetic neuropathy. I Neuropath. Exp. Neurology(2003) 63:260–271.
  • •Description of differences between Type 1 and Type 2 diabetes with respect to neurotrophic factors and cytoskeletal protein expression.
  • LI Z, ZHANG W, GRUNBERGER G, SIMA AAF: Hippocampal neuronal apoptosis in Type 1 diabetes. Brain Res. (2002) 946:212–231.
  • ••The first experimental evidence forspontaneous cerebral apoptosis as a cause of cognitive dysfunction in Type 1 diabetes.
  • ZHUANG HX, SNYDER CK, PU SF, ISHII DN: Insulin-like growth factors reverse or arrest diabetic neuropathy: effects on hyperalgesia and impaired nerve regeneration in rats. Exp. Neurol (1996) 140:198–205.
  • ISHII DN, LUPIEN SB: Insulin-like growth factors protect against diabetic neuropathy: effects on sensory nerve regeneration in rats. J. Neurosci. Res. (1995) 40:138–144.
  • ZHUANG HX, WUARIN L, FEI ZJ, ISHII DN: Insulin-like growth factor (IGF) gene expression is reduced in neural tissues and liver from rats with non-insulin-dependent diabetes mellitus, and IGF treatment ameliorates diabetic neuropathy. Phartnacol Exp. Ther. (1997) 283:366–374.
  • PIERSON CR, ZHANG W, SIMA AAF: Proinsulin C-peptide replacement in Type 1 BB/Wor-rats prevents deficits in nerve fiber regeneration. J. Neuropath. Exp. Neurol (2003) 62(7):765–779.
  • ••Experimental evidence for the preventativeeffect of C-peptide on nerve fibre degeneration.
  • LI Z-G, ZHANG W, SIMA AAF: C-peptide prevents hippocampal apoptosis in Type 1 diabetes. Int. I Exp. Diab. Res. (2002) 3:241–246.
  • ••Evidence for the involvement of impairedinsuling/C-peptide in hippocarnpal apoptosis and its prevention by C-peptide treatment.
  • LI Z, ZHANG W, SIMA AAF: C-peptide enhances insulin-mediated cell growth and protects against high glucose induced apoptosis in SH-SY5Y cells. Diab. Metab. Res. Rey (2003) 19:375–385.
  • •Detailed in vitro study delineating the molecular basis for the anti-apoptotic effects of C-peptide.
  • RUSSELL JVV, FELDMAN EL: Insulin-like growth factor-I prevents apoptosis in sympathetic neurons exposed to high glucose. Holm. Metab. Res. (1999) 31:90–96.
  • RUSSELL JVV, SULLIVAN KA, WINDEBANK AJ, HERRMANN DN, FELDMAN EL: Neurons undergo apoptosis in animal and cell culture models of diabetes. Neurobiol. Dis. (1999) 6:347–363.
  • SCHMEICHEL AM, SCHMELZER JD, LOW PA: Oxidative injury and apoptosis of dorsal root ganglion neurons in chronic experimental diabetic neuropathy. Diabetes (2003) 52:162–171.
  • CHENG C, ZOCHODNE DW: Sensory neurons with activated caspase-3 survive long term experimental diabetes. Diabetes (2003) (In press).
  • WAHREN J, EKBERG K, JOHANSSON J, HENRIKSSON M, PRAMANIK A, JOHANSSON B-L et al.: Role of C-peptide in human physiology. Am. J. Physic] Endocrinol Metab. (2000) 278:E759–E768.
  • ••Excellent review of the physiological effectsof C-peptide.
  • SIMA AAF, GRUNBERGER G, JORNVALL H, WAHREN J, THE C-PEPTIDE STUDY GROUP: Proinsulin C-peptide - A consensus statement. Internatl. I Exp. Diab. Res. (2001) 2:145–151.
  • FORST T, DE LA TOUR DD, KUNT T et al.: Effects of proinsulin C-peptide on nitric oxide, microvascular blood flow and erythrocyte Na±,K+ ATPase activity in diabetes mellitus Type 1. Clic. Sci. (2000) 98:283–290.
  • GREENE DA, WINEGRAD Al: In vitro studies of the substrates for energy production and the effects of insulin on glucose utilization on the neural components of peripheral nerve. Diabetes (1979) 28:878–887.
  • PATEL NJ, LLEWELYN JG, WRIGHT DW, THOMAS PK: Glucose and leucine uptake by dorsal root ganglia is not insulin sensitive. J. Neurol. Sci. (1994) 121:159–162.
  • RECIO-PINTO E, RECHLER MM, ISHII DN: Effects of insulin, insulin-like growth factor-II, and nerve growth factor on neurite formation and survival in cultured sympathetic and sensory neurons. Neurosci. (1986) 6:1211–1219.
  • ZACKENFELS K, OPPENHEIM RW, ROHRER H: Evidence for an important role of IGF-I and IGF-II for the early development of chick sympathetic neurons. Neuron (1995) 14:731–741.
  • WANG C, LI Y, WIBLE B, ANGELIDES KJ, ISHII DN: Effects of insulin and insulin-like growth factors on neurofilament mRNA and tubulin mRNA content in human neuroblastoma SH-SY5Y cells. Ma Brain Res. (1992) 13:289–300.
  • FERNYHOUGH P, MILL JF, ROBERTS JL, ISHII DN: Stabilization of tubulin mRNAs by insulin and insulin-like growth Factor I during neurite formation. Ma Brain Res. (1989) 6:109–120.
  • SINGHAL A, CHENG C, SUN H, ZOCHODNE DW: Near nerve local insulin prevents conduction slowing in experimental diabetes. Brain Res. (1997) 763:209–214.
  • RECIO-PINTO E, LANG FE ISHII DN: Insulin and insulin-like growth Factor II permit nerve growth factor binding and the neurite formation response in cultured human neuroblastoma cells. Proc. Natl. Acad. Sci. USA (1984) 81:2562–2566.
  • COMBETTES-SOUVERAIN M, ISSAD T: Molecular basis of insulin action. Diabetes Metab. (1998) 24:477–489.
  • SUGIMOTO K, MURAKAWA Y, ZHANG W-X, XU G, SIMA AAF: Insulin receptor in rat peripheral nerve: its localization and alternatively spliced isoforms. Diab. Metab. Res. Rev (2000) 16(5):354–363.
  • SUGIMOTO K, MURAKAWA Y, SIMA AAF: Expression and localization of insulin receptor in rat dorsal root ganglion and spinal cord. J. Periph. Nerv. Sys] (2002) 7:44–53.
  • RITCHIE JM, BLACK JA, WAXMAN SG, ANGELIDES KJ: Sodium channels in the cytoplasm of Schwann cells. Proc. Natl. Acad. Sci. USA (1990) 87:9290–9294.
  • ARIYASU RG, NICHOL JA, ELLISMAN MH: Localization of sodium/ potassium adenosine triphosphatase in multiple cell types of the murine nervous system with antibodies raised against the enzyme from kidney. J. Neurosci (1985) 5:2581–2596.
  • MAGNANI P, CHERIAN PV, GOULD GW, GREENE DA, SIMA AAF, BROSIUS FC 3rd: Glucose transporters in rat peripheral nerve: paranodal expression of GLUT1 and GLUT3. Metabolism (1996) 45:1466–1473.
  • KORDELI E, LAMBERT S, BENNETT V: Ankyrinc. A new ankyrin gene with neural-specific isoforms localized at the axonal initial segment and node of Ranvier. I Biol. Chem. (1995) 270:352–2359.
  • MENEGOZ M, GASPAR P, LE BERT M et al.: Paranodin, a glycoprotein of neuronal paranodal membranes. Neuron (1997) 19:319–331.
  • POLIAK S, GOLLAN L, MARTINEZ R et al: Caspr2, a new member of the neurexin superfamily, is localized at the juxtaparanodes of myelinated axons and associates with K+ channels. Neuron (1999) 24:1037–1047.
  • JENSEN ME, MESSINA EJ: C-peptide induces a concentration-dependent dilation of skeletal muscle arterioles only in presence of insulin. Am. Physiol. (1999) 276:H1223–H1228.
  • ••A nice paper demonstrating theconcentration-dependent effects of C-peptide and insulin on endothelial NO.
  • JOHANSSON BL, KERNELL A, SJOBERG S, WAHREN J: Influence of combined C-peptide and insulin administration on renal function and metabolic control in diabetes Type 1. Clin. Endocrinol. Metab. (1993) 77:976–981.
  • GRUNBERGER G, XIAOLING Q, LI Z-G et al.: Molecular basis for the insulinomimetic effects of C-peptide. Diabetologia (2001) 44:1247–1257.
  • ••Detailed investigation of the signallingpathway of C-peptide and its interactions with insulin effects.
  • LI Z-G, QIANG X, SIMA AAF, GRUNBERGER G: C-peptide attenuates protein tyrosine phosphatase activity and enhances glycogen synthesis in L6 myoblasts. Biochem. Biophys. Res. Com. (2001) 26;280(3):615–619.
  • RIGLER R, PRAMANIK A, JONASSON P et al.: Specific binding of proinsulin C-peptide to human cell membranes. Proc. Natl. Acad. Sci. USA (1999) 96:13318–13323.
  • ••The demonstration of C-peptide's specificbinding to cell surfaces and the affmity thereof.
  • SCHERER SS: Molecular specialization at nodes and paranodes in peripheral nerve. Microscopy Res. Techn. (1996) 34:452–461.
  • LAMBERT S, DAVIS JQ, BENNETT V: Morphogenesis of the node of Ranvier: co-clusters of ankyrin and ankyrin-binding integral proteins define early developmental intermediaries. Neurosci (1997) 15:7025–7036.
  • ISOM LL: The role of sodium channels in cell adhesion. Front Biosci (2002) 7:12–23.
  • MALHOTRA JD, KAZEU-GILLESPIE K, HORTSCH M, ISOM LL: Sodium channel 13 subunits mediate homophilic cell adhesion and recruit ankyrin to points of cell-cell contact. J. Biol. Chem. (2000) 275:11383–11388.
  • MULLER-HUSMAN G, GLOOR S, SCHACHNER M: Functional characterization of beta iso-forms of murine Na/K-ATPase. The adhesion molecule on glia (AMOG/, beta 2) but not beta 1, promotes neurite outgrowth. j. Biol. Chem. (1993) 268:26260–26267.
  • RATCLIFF CE QU Y, MCCORMICK KA et al.: A sodium channel signaling complex: modulation by associated receptor protein tyrosine phosphatase 3. Nat. Neurosci (2000) 3:437–444.
  • PELES E, NATIV M, CAMPBELL PL et al.: The carbonic anhydrase domain of receptor tyrosine phosphatase beta is a functional ligand for the axonal cell recognition molecule contactin. Cell (1995) 82:251–260.
  • PELES E, NATIV M, LUSTIG M et al.: Identification of a novel contactin-associated transmembrane receptor with multiple domains implicated in protein-protein interactions. EMBO J. (1997) 16:978–988.
  • EINHEBER S, ZANAZZI G, CHING W et al.: The axonal membrane Caspr, a homologue of neurexin IV, is a component of the septate-like paranodal junctions that assemble during myelination. J. Cell Biol. (1997) 139:1495–1506.
  • MENEGOZ M, GASPAR P, LE BART M et al.: Paranodin, a glycoprotein of neuronal paranodal membranes. Neuron (1997) 19:319–331.
  • THOMAS PK, ELIASSON SG: Diabetic neuropathy. In: Peripheral Neuropathy PJ Dyck, PK Thomas, EH Lambert, R Bunger (Eds), W.B. Saunders, Philadelphia, PA, USA (1984):1773–1810.
  • XU G, SIMA AAF: Altered immediate early gene expression is impaired in diabetic nerve: Implications in regeneration. Neuropath. Exp. Neurology (2001) 60(10):972–983.
  • HENGERER B, LINDHOLM D, HENMANN R, RUTHER V, WAGNER EF, THOENEN H: Lesion-induced increase in nerve growth factor mRNA is mediated by c-fos. Proc. Natl. Acad. Sci. USA (1990) 87:3899–3903.
  • IDE C: Peripheral nerve regeneration. Neurosci. Res. (1996) 25:101–121.
  • KAMIJO M, MERRY AC, CHERIAN PV, AKDAS G, SIMA AAF: Nerve fiber regeneration following axotomy in the diabetic BB/VV-rat. The effect of API-treatment. J. Blab. Compl. (1996) 10:183–191.
  • SIMA AAF: Diabetic neuropathy - the utility of nerve biopsy (Chapter 64). In: Clinical Neurophysiology: from Receptors to Perception. G Comi, CH Lucking, J Kimura, PM Rossini (Eds), Elsevier Science, Amsterdam (1999):525–533.
  • YAGIHASHI S, KAMIJO M, WATANABE K: Reduced myelinated fiber size correlates with loss of axonal neurofilaments in peripheral nerve of chronically streptozotocin diabetic rats. Am. J. Pathol (1990) 136:1365–1373.
  • MACIOCE P, FILLIATREAU G, FIGLIOMENI B, HASSIG R, THIERY J, DIGIAMBERARDINO L: Slow axonal transport impairment of cytoskeletal proteins in streptozotocin-induced diabetic neuropathy. I Neurochem. (1989) 53:1261–1267.
  • HOFFMAN PN, CLEVELAND DW, GRIFFIN JW, LANDES PW, COWAN NJ, PRICE DL: Neurofilament gene expression: A major determinant of axonal caliber. Proc. Natl. Acad. Sci. USA (1987) 84:3472–2476.
  • OHARA 0, GAHARA T, MIYAKE H, TERAOKA H, KITAMURA T: Neurofilament deficiency in quail caused by nonsense mutation in neurofilament-L gene. J. Cell Biol. (1993) 121:387–395.
  • DENOULET P, EDDE B, GROS F: Differential expression of several neurospecific beta-tubulin mRNA's in the mouse brain during development. Gene (1986) 50:289–297.
  • MOURA NETO V, MALLAT M, JEANTET C, PROCHIANTZ A: Microheterogeneity of tubulin proteins in neuronal and glial cells from the mouse brain in culture. EMBO J. (1983) 2:1243–1248.
  • MITCHISON T, KIRSCHNER M: Cytoskeletal dynamics and nerve growth. Neuron (1988) 1:761–772.
  • SIMA AAF, MERRY AC, LIGHTLE R: Impaired macrophage recruitment in axotomized diabetic nerve. Exp. Clin. Endocrin. Blab. (1997) 105:62–63.
  • JOHANSSON BL, BORG K, FERNQVIST-FORBES E, ODERGREN T, REMAHL S, WAHREN J: C-peptide improves autonomic nerve function in IDDM patients. Diabetologia (1996) 39:687–695.
  • JOHANSSON B-L, BORG K, FERNQUIST-FORBES E, KERNELL A, ODERGREN T, WAHREN J: Beneficial effects of C-peptide on incipient nephropathy and neuropathy in patients with Type 1 diabetes mellitus. Blab. Merl (2000) 17:181–189.
  • ••Clinical study of the beneficial effects ofC-peptide on kidney function in Type 1 diabetic patients.
  • KUNT T, WALLERATH T, FORST T et al.: Stimulation of endothelial nitric oxide synthase by proinsulin C-peptide. Jim. Physiol (2003) (In Press).
  • JOHANSSON B-L, LINDE B, WAHREN J: Effects of C-peptide on blood flow, capillary diffusion capacity and glucose utilization in the exercising forearm of Type 1 (insulin-dependent) diabetic patients. Diabetologia (1992) 35:1151–1158.
  • FORST T, KUNT T, POHLMANN T et al.: Biological activity of C-peptide on skin microcirculation in patients with insulin-dependent diabetes mellitus. j Clin. Invest. (1998) 101:2036–2041.
  • ••Very good paper demonstrating the NOdependent effect of C-peptide on dermal circulation in Type 1 patients.
  • EKBERG K, BRISMAR T, JOHANSSON B-L, JONSSON B, LINDSTROM P, WAHREN J: Amelioration of sensory nerve dysfunction by C-peptide in patients with Type 1 diabetes. Diabetes (2003) 52:536–541.
  • ••Recent paper demonstrating the beneficialeffects of C-peptide on sensory NCV in Type 1 diabetic patients. Small but very well-performed study.
  • KRAMER L, FASCHING P, MADL C et al.: Previous episodes of hypoglycemic coma are not associated with permanent cognitive brain dysfunction in IDDM patients on intensive insulin treatment. Diabetes (1998) 47:1909–1914.
  • SCHOENLE EJ, SCHOENLE D, MOLINARI L, LARGO RH: Impaired intellectual development in children with Type 1 diabetes: association with HbAlc, age at diagnosis and age. Diabetologia (2002) 45:108–114.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.