C-peptide replacement: a possible treatment for diabetic neuropathy

2007 ◽  
Vol 3 (4) ◽  
pp. 325-325
Keyword(s):  
Diabetic Neuropathy ◽  
C Peptide

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 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

Assessment of the Effect of C-Peptide Level on Na-K ATPase Activity In Individuals with Type II Diabetic Peripheral Neuropathy

2021 ◽  
Vol 53 (03) ◽  
pp. 213-219
Author(s):  
Eman H Al-Rikabi ◽  
Keyword(s):  
Enzyme Activity ◽  
Diabetic Neuropathy ◽  
Atpase Activity ◽  
Negative Correlation ◽  
Clinical Symptoms ◽  
The Other ◽  
C Peptide ◽  
Other Hand ◽  
Peptide Level

Background: Both Type 1 and Type 2 diabetes can cause neuropathy, which is a frequent and severe consequence. C-peptide depletion may be partly related to in the occurrence of certain diabetic complications. It has been demonstrated that even a little amount of residual C-peptide has a considerable metabolic advantage. Objective: The study’s objective was to predict the relation of plasma C-peptide levels in patients with diabetic neuropathy, and its effect on Na-K ATPase activity. Design and Methods: In this case-control study, 150 individuals have been included: 80 patients with diabetic neuropathy, 40 diabetics without neuropathy and 30 non-diabetic subjects as a control. Patients in the first group were carefully chosen based on their clinical symptoms and nerve conduction studies results. The assessment of plasma C-peptide was done by ELISA, Na-K ATPase enzyme activity by spectrophotometer, and HbA1C by HPLC. Results: Mean plasma C-peptide level and Erythrocyte Na-K ATPase activity were substantially lower in neuropathy type 2 DM patients compared to diabetes without neuropathy and control (p= 0.002, 0.000 respectively). The negative correlation between C-peptide with HbA1c, and diabetes period were all negligible (p= 0.447,0.098), Even though there was a notable negative correlation with age (p= 0.03). On the other hand, the relationship linking C-peptide and Na-K ATPase enzyme activity was shown to be insignificant (p=0.69). Conclusions: Diabetic neuropathy is related to a low C-peptide level. The association between C-peptide and Na-K ATPase enzyme activity, on the other hand, was shown to be insignificant. C-peptide HbA1c, and duration of diabetes all had minor negative associations.

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

scholarly journals Clinical and Pharmacological Basis for the Use of Drugs Inhibiting of the RAAS in Patients with Diabetic Neuropathy

2018 ◽  
Vol 3 (2) ◽  
Keyword(s):  
Diabetic Neuropathy ◽  
Theoretical Orientation ◽  
Vital Role ◽  
Type I ◽  
C Peptide ◽  
Group I ◽  
Activation Of Transcription ◽  
Mediators Of Inflammation ◽  
Transcription Factor Nfκb ◽  
Pharmacological Basis

Diabetes mellitus (DM) is the most common cause of diabetic neuropathy (DN) comprises a heterogeneous group of disorders that can cause neuronal dysfunction throughout the human body. The incidence of diabetes and its complications is increasing to staggering proportions. In 2014 the WHO estimated an overall prevalence of 422 million (8, 5%). The incidence of diabetic neuropathy approaches 50% in most diabetic populations; there is no treatment, and its consequences in the form of foot ulceration and amputation. The recent studies suggest that the renin angiotensin aldosterone system (RAAS) plays a vital role in regulating glucose metabolism and blood pressure. In the same time the metabolic abnormalities associated with diabetes lead to activation RAAS, which might promote the formation of reactive oxygen species to lead the endothelial and neuronal dysfunctions. Furthermore, TNFα is part of the response of the organism to hypertension and is originally described as one of the central mediators of inflammation trough the activation of transcription factor NFκB an important factor in the control of cell proliferation, differentiation, and apoptosis. Methodology & Theoretical Orientation: The study is going on in parallel groups. The patients (enrolled on randomized principle) with DPN will be investigated. The enrolled subjects was divided into two main groups: group I with Type I and Type II DM, complicated by DPN to take Aliskiren and group II with the same pathology, proceeding with the treatment without Aliskiren but given Telmisartan, for certainty of Aliskiren efficacy. At the start of the trial and on completion of the six week period TNFα level and C-peptide will be determined. Findings: Telmisartan has less TNFα modulatory effects then Aliskiren, Namely, the symptoms of neuropathy a well as blood TNFα level and C-peptide level are not changed significantly. Conclusion & Significance: TNFα is involved in DPN pathogenesis formation and clinical manifestation. Aliskiren ameliorates symptoms in DPN patients by modulatory impact on TNFα, so we have results for clinical and pharmacological analysis of Aliskiren application in DPN. The involvements of RAAS system in developments of DNP needs further research study.

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