IMPE Abstracts

Background: Type 1 diabetes mellitus (T1DM) and autoimmune diseases, such as autoimmune thyroiditis (AT) or coeliac disease (CD) frequently occur together. Adiponectin is the most abundant circulating adipokine that plays a key role as an insulin-sensitizing protein in metabolic diseases. Autoimmune diseases are associated with decreased levels of adiponectin, previous studies suggesting that adiponectin may be related to disease activity and/or severity in such conditions. SNP +276G>T of AdipoQ gene was associated with the risk of developing Type 1 diabetes mellitus (T1DM). The aim of our study was to determine whether +276 G>T polymorphism of the AdipoQ gene might have any impact on the risk of developing associated autoimmune diseases (AAD) in T1DM children from Romania.

Material and Methods: This cross-sectional study enrolled seventy-two patients with Type 1 Diabetes that regularly attended the Pediatric Diabetes Department of the Emergency Clinic Hospital for Children in Cluj-Napoca, Romania. Serum levels of adiponectin were measured by enzyme-linked immunoassay. The presence of CD was screened with IgA anti-transglutaminase antibodies and the presence of autoimmune Hashimoto thyroiditis through anti-Thyroid peroxidase and anti-Thyroglobulin antibodies. Adiponectin +276G>T gene polymorphism was evaluated using the method of restriction fragment length polymorphism.

Results: The prevalence of AAD in the enrolled diabetic children was 33.3% (24 out of 72 children). The frequency of the TT genotype in the AAD group was significantly higher (64%) compared to GG or GT genotype (P<0.001). There was a significant association between the presence of TT genotype and the development of AT (P=0.001, OR 4.55 95% CI 1.41-6.71). Regarding genotype frequencies in the CD group there was a significant increase in TT genotype (P=0.003, OR 4.63, 95% CI 1.04 – 7.48) compared to non-CD group. The carriers of TT genotype in the AAD group had significantly lower adiponectin levels (11.25 μg/L ±3.92) compared with the carriers of at least one G allele (15.18 μg/L ±5.18) (P=0.04).

Conclusions: Based on our findings, carriers of AdipoQ +276 TT genotype have an increased risk for developing AAD in T1DM, resulting in lower adiponectin levels. In addition, this may suggest that the carriers of the G allele can offer a protective effect in the development of AAD in T1DM patients in our population. Further studies are needed to reinforce our conclusions.