scholarly journals Prevention of Type 1A Diabetes Mellitus

2012 ◽  
Vol 18 (5) ◽  
pp. 745-749 ◽  
Author(s):  
George Eisenbarth
2011 ◽  
pp. P3-474-P3-474
Author(s):  
Tom Donner ◽  
Jens Sandahl Christiansen ◽  
Paul Miller ◽  
Wei Liu ◽  
Aoife M Brennan

2005 ◽  
Vol 12 (3) ◽  
pp. 181-186 ◽  
Author(s):  
J. M. Jasinski ◽  
G. S. Eisenbarth

Type 1A diabetes mellitus is caused by specific and progressive autoimmune destruction of the beta cells in the islets of Langerhans whereas the other cell types in the islet (alpha, delta, and PP) are spared. The autoantigens of Type 1A diabetes may be divided into subgroups based on their tissue distributions: Beta-cell-specific antigens like insulin, insulin derivatives, and IGRP (Islet-specific Glucose-6-phosphatase catalytic subunit Related Peptide); neurendocrine antigens such as carboxypeptidase H, insulinoma-associated antigen (IA-2), glutamic acid decarboxylase (GAD65), and carboxypeptidase E; and those expressed ubiquitously like heat shock protein 60 (a putative autoantigen for type 1 diabetes). This review will focus specifically on insulin as a primary autoantigen, an essentia l target for disease, in type 1A diabetes mellitus. In particular, immunization with insulin peptide B:9-23 can be used to induce insulin autoantibodies and diabetes in animal models or used to prevent diabetes. Genetic manipulation of the insulin 1 and 2 genes reciprocally alters development of diabetes in the NOD mouse, and insulin gene polymorphisms are important determinants of childhood diabetes. We are pursuing the hypothesis that insulin is a primary autoantigen for type 1 diabetes, and thus the pathogenesis of the disease relates to specific recognition of one or more peptides.


2001 ◽  
Vol 2 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Darrell M Wilson ◽  
Bruce Buckingham

2011 ◽  
Vol 91 (3) ◽  
pp. e61-e63 ◽  
Author(s):  
Diego Peteiro-González ◽  
Beatriz Fernández-Rodríguez ◽  
José Manuel Cabezas-Agrícola ◽  
David Araújo-Vilar

Cytokine ◽  
2013 ◽  
Vol 62 (2) ◽  
pp. 327-333 ◽  
Author(s):  
V.S. Costa ◽  
A.S. Santos ◽  
R.T. Fukui ◽  
T.C.C. Mattana ◽  
S.R. Matioli ◽  
...  

2001 ◽  
Vol 2 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Darrell M Wilson ◽  
Bruce Buckingham

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Lingwen Ying ◽  
Xiaojing Ma ◽  
Yun Shen ◽  
Jingyi Lu ◽  
Wei Lu ◽  
...  

Background. Fulminant type 1 diabetes mellitus (FT1DM) onsets abruptly and usually occurs within 1 week after the onset of hyperglycemic symptoms. Glycated albumin (GA) and 1,5-anhydroglucitol (1,5-AG) are indicators that reflect short-term glucose levels. This study was aimed at investigating whether the 1,5-AG/GA index (AGI) is a suitable indicator for early FT1DM identification. Methods. A total of 226 subjects were enrolled, all with glycated hemoglobin A1c HbA1c<8.7%. FT1DM was diagnosed based on the 2012 Japan Diabetes Society criteria. Results. The AGI level was 0.54 (0.17–1.36) in the whole group. It was lower in FT1DM patients (0.16 [0.10–0.25]). Among the participants whose HbA1c did not exceed 7.0%, the AGI of FT1DM decreased significantly compared to type 1A diabetes (T1ADM) and latent autoimmune diabetes in adults (LADA) patients (0.16 [0.12–0.26] vs. 0.46 [0.24–0.72] vs. 0.31 [0.19–0.43], both P<0.05). The receiver operating characteristic (ROC) curve showed that AGI can be used to distinguish FT1DM and T1ADM patients with HbA1c<8.7%. Diagnosing FT1DM based on AGI≤0.3 only can help narrow down suspected FT1DM by up to 26.87%. If we diagnosed FT1DM when AGI was ≤0.3 and HbA1c was ≤7.0%, the success rate further increased to 86.57%, among which 85.00% of FT1DM and 87.23% of T1ADM patients were successfully identified. Therefore, using the combination criteria of AGI and HbA1c would improve the differential diagnosis efficacy by 61.11% compared with the AGI criterion only. Conclusion. AGI can help facilitate the early differential diagnosis of FT1DM and T1ADM when HbA1c<8.7%, with an optimal cut-off point of 0.3.


1998 ◽  
Vol 39 (5) ◽  
pp. 663-668 ◽  
Author(s):  
Harry N. Bawden ◽  
Aidan Stokes ◽  
Carol S. Camfield ◽  
Peter R. Camfield ◽  
Sonia Salisbury

Author(s):  
Bruce R. Pachter

Diabetes mellitus is one of the commonest causes of neuropathy. Diabetic neuropathy is a heterogeneous group of neuropathic disorders to which patients with diabetes mellitus are susceptible; more than one kind of neuropathy can frequently occur in the same individual. Abnormalities are also known to occur in nearly every anatomic subdivision of the eye in diabetic patients. Oculomotor palsy appears to be common in diabetes mellitus for their occurrence in isolation to suggest diabetes. Nerves to the external ocular muscles are most commonly affected, particularly the oculomotor or third cranial nerve. The third nerve palsy of diabetes is characteristic, being of sudden onset, accompanied by orbital and retro-orbital pain, often associated with complete involvement of the external ocular muscles innervated by the nerve. While the human and experimental animal literature is replete with studies on the peripheral nerves in diabetes mellitus, there is but a paucity of reported studies dealing with the oculomotor nerves and their associated extraocular muscles (EOMs).


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