scholarly journals C-Peptide Replacement Therapy and Sensory Nerve Function in Type 1 Diabetic Neuropathy

Diabetes Care ◽  
2006 ◽  
Vol 30 (1) ◽  
pp. 71-76 ◽  
Author(s):  
K. Ekberg ◽  
T. Brismar ◽  
B.-L. Johansson ◽  
P. Lindstrom ◽  
L. Juntti-Berggren ◽  
...  
Keyword(s):  
Diabetic Neuropathy ◽  
Replacement Therapy ◽  
Sensory Nerve ◽  
Nerve Function ◽  
C Peptide

scholarly journals Effect of C-Peptide on Diabetic Neuropathy in Patients with Type 1 Diabetes

2008 ◽  
Vol 2008 ◽  
pp. 1-5 ◽  
Author(s):  
Karin Ekberg ◽  
Bo-Lennart Johansson
Keyword(s):  
Type 1 Diabetes ◽  
Animal Models ◽  
Peripheral Nerve ◽  
Early Stage ◽  
Sensory Nerve ◽  
Autonomic Nerve ◽  
Nerve Function ◽  
C Peptide ◽  
Peripheral Nerve Function

Recent results indicate that proinsulin C-peptide, contrary to previous views, exerts important physiological effects and shows the characteristics of a bioactive peptide. Studies in type 1 diabetes, involving animal models as well as patients, demonstrate that C-peptide in replacement doses has the ability to improve peripheral nerve function and prevent or reverse the development of nerve structural abnormalities. Peripheral nerve function, as evaluated by determination of sensory nerve conduction velocity and quantitative sensory testing, is improved by C-peptide replacement in diabetes type 1 patients with early stage neuropathy. Similarly, autonomic nerve dysfunction is ameliorated following administration of C peptide for up to 3 months. As evaluated in animal models of type 1 diabetes, the improved nerve function is accompanied by reversal or prevention of nerve structural changes, and the mechanisms of action are related to the ability of C-peptide to correct diabetes-induced reductions in endoneurial blood flow and in -ATPase activity and modulation of neurotrophic factors. Combining the results demonstrates that C-peptide may be a possible new treatment of neuropathy in type 1 diabetes.

scholarly journals C-Peptide replacement therapy in type 1 diabetes: are we in the trough of disillusionment?

2017 ◽  
Vol 13 (8) ◽  
pp. 1432-1437 ◽  
Author(s):  
C. W. Pinger ◽  
K. E. Entwistle ◽  
T. M. Bell ◽  
Y. Liu ◽  
D. M. Spence
Keyword(s):  
Type 1 Diabetes ◽  
Replacement Therapy ◽  
C Peptide

C-Peptide has been discussed as a missing component in therapy for people with Type 1 diabetes. Is momentum fading, or do technology models suggest that it is right on schedule?

scholarly journals Molecular Alterations Underlie Nodal and Paranodal Degeneration in Type 1 Diabetic Neuropathy and Are Prevented by C-Peptide

Diabetes ◽  
2004 ◽  
Vol 53 (6) ◽  
pp. 1556-1563 ◽  
Author(s):  
A. A.F. Sima ◽  
W. Zhang ◽  
Z.-G. Li ◽  
Y. Murakawa ◽  
C. R. Pierson
Keyword(s):  
Diabetic Neuropathy ◽  
C Peptide ◽  
Molecular Alterations

Amelioration of Sensory Nerve Dysfunction by C-Peptide in Patients With Type 1 Diabetes

Diabetes ◽  
2003 ◽  
Vol 52 (2) ◽  
pp. 536-541 ◽  
Author(s):  
K. Ekberg ◽  
T. Brismar ◽  
B.-L. Johansson ◽  
B. Jonsson ◽  
P. Lindstrom ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Sensory Nerve ◽  
C Peptide ◽  
Nerve Dysfunction

scholarly journals Human C-peptide Dose Dependently Prevents Early Neuropathy in the BB/Wor-rat

2001 ◽  
Vol 2 (3) ◽  
pp. 187-193 ◽  
Author(s):  
W. Zhang ◽  
M. Yorek ◽  
C. R. Pierson ◽  
Y. Murakawa ◽  
A. Breidenbach ◽  
...  
Keyword(s):  
Diabetic Neuropathy ◽  
Axonal Degeneration ◽  
Diabetic Rats ◽  
Nerve Fibers ◽  
C Peptide ◽  
Conserved Sequence ◽  
Structural Abnormalities ◽  
Onset Of Diabetes ◽  
Dose Dependent

In order to explore the neuroprotective and crossspecies activities of.C-peptide on type 1 diabetic neuropathy, spontaneously diabetic BB/W-rats were given increasing doses of human recombinant Cpeptide (hrC-peptide). Diabetic rats received 10, 100, 500, or 1000 μg of hrC-peptide/kg body weight/ day from onset of diabetes. After 2 months of hrC-peptide administration, 100 μg and greater doses completely prevented the nerve conduction defect, which was associated with a significant but incomplete prevention of neuralNa+/K+-ATPase activity in diabetic rats with 500 μg or greater C-peptide replacement. Increasing doses of hrC-peptide showed increasing prevention of early structural abnormalities such as paranodal swelling and axonal degeneration and an increasing frequency of regenerating sural nerve fibers. We conclude that hrC-peptide exerts a dose dependent protection on type 1 diabetic neuropathy in rats and that this effect is probably mediated by the partially conserved sequence of the active C-terminal pentapeptide

196-LB: Stem Cell–Derived Islet Replacement Therapy (VC-02) Demonstrates Production of C-Peptide in Patients with Type 1 Diabetes (T1D) and Hypoglycemia Unawareness

Diabetes ◽  
2021 ◽  
Vol 70 (Supplement 1) ◽  
pp. 196-LB
Author(s):  
BART KEYMEULEN ◽  
DANIEL JACOBS-TULLENEERS-THEVISSEN ◽  
EVERT J. KROON ◽  
MANASI S. JAIMAN ◽  
MARK DANIELS ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Stem Cell ◽  
Replacement Therapy ◽  
Hypoglycemia Unawareness ◽  
C Peptide

scholarly journals C-peptide corrects endoneurial blood flow but not oxidative stress in type 1 BB/Wor rats

2004 ◽  
Vol 287 (3) ◽  
pp. E497-E505 ◽  
Author(s):  
Martin J. Stevens ◽  
Weixian Zhang ◽  
Fei Li ◽  
Anders A. F. Sima
Keyword(s):  
Oxidative Stress ◽  
Blood Flow ◽  
Sensory Nerve ◽  
Thermal Hyperalgesia ◽  
Nerve Blood Flow ◽  
C Peptide ◽  
Endoneurial Blood Flow ◽  
Neurovascular Dysfunction

Oxidative stress and neurovascular dysfunction have emerged as contributing factors to the development of experimental diabetic neuropathy (EDN) in streptozotocin-diabetic rodents. Additionally, depletion of C-peptide has been implicated in the pathogenesis of EDN, but the mechanisms of these effects have not been fully characterized. The aims of this study were therefore to explore the effects of diabetes on neurovascular dysfunction and indexes of nerve oxidative stress in type 1 bio-breeding Worcester (BB/Wor) rats and type 2 BB Zucker-derived (ZDR)/Wor rats and to determine the effects of C-peptide replacement in the former. Motor and sensory nerve conduction velocities (NCVs), hindlimb thermal thresholds, endoneurial blood flow, and indicators of oxidative stress were evaluated in nondiabetic control rats, BB/Wor rats, BB/Wor rats with rat II C-peptide replacement (75 nmol C-peptide·kg body wt−1·day−1) for 2 mo, and diabetes duration-matched BBZDR/Wor rats. Endoneurial perfusion was decreased and oxidative stress increased in type 1 BB/Wor rats. C-peptide prevented NCV and neurovascular deficits and attenuated thermal hyperalgesia. Inhibition of nitric oxide (NO) synthase, but not cyclooxygenase, reversed the C-peptide-mediated effects on NCV and nerve blood flow. Indexes of oxidative stress were unaffected by C-peptide. In type 2 BBZDR/Wor rats, neurovascular deficits and increased oxidative stress were unaccompanied by sensory NCV slowing or hyperalgesia. Therefore, nerve oxidative stress is increased and endoneurial perfusion decreased in type 1 BB/Wor and type 2 BBZDR/Wor rats. NO and neurovascular mechanisms, but not oxidative stress, appear to contribute to the effects of C-peptide in type 1 EDN. Sensory nerve deficits are not an inevitable consequence of increased oxidative stress and decreased nerve perfusion in a type 2 diabetic rodent model.

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