scholarly journals Insulin as a Primary Autoantigen for Type 1A Diabetes

2005 ◽  
Vol 12 (3) ◽  
pp. 181-186 ◽  
Author(s):  
J. M. Jasinski ◽  
G. S. Eisenbarth
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Genetic Manipulation ◽  
Cell Types ◽  
Acid Decarboxylase ◽  
Heat Shock Protein 60 ◽  
Carboxypeptidase H ◽  
Specific Antigens ◽  
Type 1A Diabetes

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.

Autoimmune thyroid disease in patients with anti-GAD positive type 1 diabetes mellitus

Open Medicine ◽  
2009 ◽  
Vol 4 (4) ◽  
pp. 415-422
Author(s):  
Kamile Gul ◽  
Ihsan Ustun ◽  
Yusuf Aydin ◽  
Dilek Berker ◽  
Halil Erol ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Statistical Significance ◽  
Control Group ◽  
Acid Decarboxylase ◽  
Thyroid Peroxidase ◽  
The Difference ◽  
Type 1 Dm

AbstractThe aim of the study was to determine the frequency and titers of anti-thyroid peroxidase (Anti-TPO), anti-thyroglobulin (Anti-TG), and anti-glutamic acid decarboxylase (Anti-GAD) antibodies in Turkish patients with type 1 diabetes mellitus (DM), and to compare the frequency of anti-TPO and anti-TG titers in the presence or absence of anti-GAD. A total of 104 patients including 56 males and 48 females with type 1 DM and their age-, gender-, and body mass index-matched control group, including 31 males and 27 females, 58 cases in total with an age range of 15-50 years, were recruited into this study. In patients with type 1 DM, positive anti-GAD was detected in 30.8% (n=32). In patients with positive anti-GAD, rate of positive anti-TPO was 37.5%; however, in patients with negative anti-GAD, the rate of positive anti-TPO was 9.7% and the difference was statistically significant (p=0.001). In patients with positive anti-GAD, the rate of positive anti-TG was 18.8%. In patients with negative anti-GAD, the rate of positive anti-TG was 2.8%, and the difference between them was statistically significant (p=0.005). In patients with positive and negative anti-GAD, rates of both positive anti-TPO and anti-TG were 15.6% and 1.4%, respectively, with the difference showing statistical significance (p=0.004). Thyroid autoimmunity in type 1 DM patients with positive anti-GAD was apparently higher; therefore, these patients should be followed more frequently and carefully.

scholarly journals MECHANISMS IN ENDOCRINOLOGY: Seizures and type 1 diabetes mellitus: current state of knowledge

2012 ◽  
Vol 167 (6) ◽  
pp. 749-758 ◽  
Author(s):  
Alberto Verrotti ◽  
Alessandra Scaparrotta ◽  
Cristina Olivieri ◽  
Francesco Chiarelli
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Neurological Diseases ◽  
Underlying Mechanism ◽  
Acid Decarboxylase ◽  
Diabetic Patients ◽  
Current State ◽  
Metabolic Conditions

In this review, we will try to analyze the possible coexistence between epilepsy or seizures and type 1 diabetes mellitus (T1DM), in order to establish if there is more than a casual association, and to investigate possible mechanisms underlying this link. Anti-glutamic acid decarboxylase antibodies (GAD-Abs) have been associated with T1DM and a great number of neurological diseases such as epilepsy. Epilepsy can be a feature of a large variety of autoimmune or inflammatory disorders. GAD-Abs can have a role at the basis of the possible link between epilepsy and T1DM, although their real pathogenetic mechanism in neurological diseases is still unknown. Metabolic conditions such as hypoglycemia and hyperglycemia, common problems in diabetic patients, may be also implicated, even if their underlying mechanism is minimally understood.

scholarly journals A rationally designed peptide IA-2-P2 against type 1 diabetes in streptozotocin-induced diabetic mice

2017 ◽  
Vol 14 (3) ◽  
pp. 184-190 ◽  
Author(s):  
Lili Shen ◽  
Shiping Lu ◽  
Dongcheng Huang ◽  
Guoliang Li ◽  
Kunfeng Liu ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Type 1 Diabetes Mellitus ◽  
Rabbit Model ◽  
Immunological Tolerance ◽  
Heat Shock Protein 60 ◽  
P2 Peptide

Recent studies have investigated the potential of type 1 diabetes mellitus–related autoantigens, such as heat shock protein 60, to induce immunological tolerance or to suppress the immune response. A functional 24-residue peptide derived from heat shock protein 60 (P277) has shown anti-type 1 diabetes mellitus potential in experimental animals and in clinical studies, but it also carries a potential atherogenic effect. In this study, we have modified P277 to retain an anti-type 1 diabetes mellitus effect and minimize the atherogenic potential by replacing the P277 B epitope with another diabetes-associated autoantigen, insulinoma antigen-2 (IA-2), to create the fusion peptide IA-2-P2. In streptozotocin-induced diabetic C57BL/6J mice, the IA-2-P2 peptide displayed similar anti-diabetic effects to the control P277 peptide. Also, the IA-2-P2 peptide did not show atherogenic activity in a rabbit model. Our findings indicate the potential of IA-2-P2 as a promising vaccine against type 1 diabetes mellitus.

scholarly journals Factors associated with increased irisin levels in the type 1 diabetes mellitus

2017 ◽  
Vol 51 (1) ◽  
pp. 1-7 ◽  
Author(s):  
I. Ates ◽  
M. F. Arikan ◽  
K. Erdogan ◽  
M. Kaplan ◽  
M. Yuksel ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Glycosylated Hemoglobin ◽  
Islet Cell Antibody ◽  
Acid Decarboxylase ◽  
Insulin Autoantibody ◽  
Cell Antibody ◽  
Positive Groups

Abstract Objective. The aim of the present study was to determine the irisin levels in patients with the type 1 diabetes mellitus (T1DM) and to examine the relation of irisin levels with the inflammation and autoimmunity.Methods. This study included 35 cases diagnosed with T1DM and 36 healthy volunteers. Antiglutamic acid decarboxylase (anti-GAD), islet cell antibody (ICA), and insulin autoantibody levels were measured in patients at the time when they were included into the study and recorded from the patient files. Serum irisin levels were measured by ELISA kit.Results. The median irisin levels were determined higher in T1DM group compared to the control one (6.8 ng/ml vs. 4.8 ng/ml, p=0.022; respectively). Median irisin levels were higher in anti-GAD (p=0.022) and ICA (p=0.044) positive groups compared to negative groups. In T1DM group, irisin levels displayed positive correlation with glycosylated hemoglobin (HbA1c) (r=0.377, p<0.001) and anti-GAD (r=0.392, p=0.020) and negative correlation with creatinine (r=-0390, p=0.021). In multivariate regression model, HbA1c (B±SE: 2.76±17683, p<0.001), and anti-GAD (B±SE: 2.311±0.610, p=0.001) were determined as independent predictors for predicting the irisin levels.Conclusion. In patients with T1DM, which chronic inflammation and autoimmunity take part in their etiopathogenesis, anti-GAD levels were an independent risk factor for the irisin. Th is may suggest that factors such as inflammation and autoimmunity can be effective in the synthesis of irisin.

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