scholarly journals Response to Comment on: Fraser et al. The Effects of Long-Term Oral Benfotiamine Supplementation on Peripheral Nerve Function and Inflammatory Markers in Patients With Type 1 Diabetes: A 24-Month, Double-Blind, Randomized, Placebo-Controlled Trial. Diabetes Care 2012;35:1095-1097

Diabetes Care ◽  
2012 ◽  
Vol 35 (11) ◽  
pp. e80-e80
Author(s):  
D. A. Fraser ◽  
L. M. Diep ◽  
I. A. Hovden ◽  
K. B. Nilsen ◽  
K. A. Sveen ◽  
...  
Diabetes Care ◽  
2003 ◽  
Vol 26 (8) ◽  
pp. 2400-2404 ◽  
Author(s):  
J. R. Larsen ◽  
H. Sjoholm ◽  
K. F. Hanssen ◽  
L. Sandvik ◽  
T. J. Berg ◽  
...  

2018 ◽  
Vol 34 (7) ◽  
pp. e3028 ◽  
Author(s):  
Adeniyi A. Borire ◽  
Tushar Issar ◽  
Natalie C. Kwai ◽  
Leo H. Visser ◽  
Neil G. Simon ◽  
...  

2000 ◽  
Vol 85 (9) ◽  
pp. 3297-3308
Author(s):  
Robert D. Hoeldtke ◽  
Kimberly D. Bryner ◽  
Gerald R. Hobbs ◽  
Gabriella G. Horvath ◽  
Jack E. Riggs ◽  
...  

Abstract Autoimmune mechanisms have been implicated in the pathophysiology of diabetic neuropathy. We studied the association between glutamic acid decarboxylase (GAD65) and islet cell (IA-2) autoantibodies as well as autoantibodies to the autonomic nervous system and peripheral nerve function in recent onset type 1 diabetes. Thirty-seven patients (27 females and 10 males) enrolled 2–22 months after diagnosis. Humoral factors, glycemic control, and peripheral nerve function were measured annually for 3 yr. Patients with high GAD65Ab had worse glycemic control and higher insulin requirements. Patients with high GAD65Ab had slower motor nerve conduction velocities in the median, ulnar, and peroneal nerves (P < 0.025 for each nerve). The mean motor nerve conduction velocity Z scores at the time of the third evaluation was 0.341 ± 0.25 for the low GAD65Ab patients and −0.600 ± 0.25 for the high GAD65Ab patients (P < 0.01). Similar differences between the low and high GAD65Ab groups were observed for F wave latencies, thermal threshold detection, and cardiovascular autonomic function. The composite peripheral nerve function Z scores in the low GAD65Ab patients were 0.62 ± 11, 0.71 ± 0.19, and 0.21 ± 0.14 at the first, second, and third evaluations, significantly different from those in the high GAD65Ab patients in whom they were −0.35 ± 0.15, −0.46 ± 0.18, and −0.42 ± 0.16 (P < 0.001). In summary, GAD65Ab in patients with recent onset type 1 diabetes are associated with worse glycemic control and slightly worse peripheral nerve function. Although the latter remained within normal limits and none of the patients had clinical neuropathy, the GAD65Ab-related differences in composite peripheral nerve function were highly significant (P < 0.001) and could not be attributed to GAD65Ab-related differences in glycemic control.


Diabetes Care ◽  
2001 ◽  
Vol 24 (6) ◽  
pp. 1087-1092 ◽  
Author(s):  
P. H. Riihimaa ◽  
K. Suominen ◽  
U. Tolonen ◽  
V. Jantti ◽  
M. Knip ◽  
...  

2008 ◽  
Vol 2008 ◽  
pp. 1-5 ◽  
Author(s):  
Karin Ekberg ◽  
Bo-Lennart Johansson

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.


Diabetes ◽  
2002 ◽  
Vol 51 (9) ◽  
pp. 2817-2825 ◽  
Author(s):  
R. D. Hoeldtke ◽  
K. D. Bryner ◽  
D. R. McNeill ◽  
G. R. Hobbs ◽  
J. E. Riggs ◽  
...  

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