MEASUREMENT OF SERUM GLUTAMIC ACID DECARBOXYLASE-65 ANTIBODY (GADA65) LEVEL AND GLUTAMATE DECARBOXYLASE 2 (GAD2) GENE POLYMORPHISM IN OBESE, NON-OBESE TYPE II DIABETIC PATIENTS AND HEALTHY CONTROL GROUPS


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Al-Hayali F. E., Atak Yücel A., Ashoor Z. F.

17th International Middle Eastern Simulation and Modelling Conference, MESM 2022, Baghdad, Irak, 27 - 29 Haziran 2022, ss.27-34 identifier

  • Yayın Türü: Bildiri / Tam Metin Bildiri
  • Basıldığı Şehir: Baghdad
  • Basıldığı Ülke: Irak
  • Sayfa Sayıları: ss.27-34
  • Anahtar Kelimeler: GAD2 gene polymorphism, GADA-65 IgM, obesity, Type 2 Diabetes Mellitus
  • Gazi Üniversitesi Adresli: Evet

Özet

Background: Type 2 Diabetes Mellitus (DM2) is a metabolic disorder caused by hereditary and environmental factors that produce insulin failure in peripheral tissues and pancreatic cells. The key causes of the development of T2DM include underlying diseases like overweight and obesity. The neuronal enzyme glutamic acid decarboxylase (GAD) is involved in the creation of the neurotransmitter gamma-aminobutyric acid (GABA). Antibodies to GAD65 have been associated with a higher risk of T2DM. Obese and non-obese diabetic patients have both been connected to the GAD2 gene. Methods: In this study, 58 patients between the ages of 40 and 60 years old who visited the National Center for Diabetes Research and Treatment in Baghdad were used. The patient groups consisted of 29 obese T2DM patients and 29 non-obese T2DM patients, who were compared to 29 healthy control subjects. The serum GADA65 level was determined using an ELISA technique, and the GAD-65 (GAD-2) rs 2236418 SNP genotype was determined using RT-PCR. Results: The serum level of GADA-65 IgM was significantly higher in obese T2DM patients (mean±SD, 4.5522.265 pg\ml; p 0.0001) compared to non-obese T2DM patients (mean±SD, 3, 4121,299 pg\ml; p 0.0001) and the healthy control group (mean±SD, 0.9010141 pg\ml). The percentage of GAD-65 (GAD-2) rs 2236418 SNP mutant genotypes in obese T2DM patient groups (79.3%) was higher than the percentage of non-obese T2DM patient groups (13.8%), whereas mutant genotypes were not seen at all in healthy control groups, and there was a significant difference between them (p<0.0001). Conclusions: Obese T2DM patients had greater GADA-65 IgM serum levels compared to non-obese T2DM patients and healthy control groups. In our immunogenetic research, we discovered that obese T2DM patients had a lower percentage of GAD-2 gene polymorphism (GAD-2 rs 2236418 SNP) than non-obese T2DM patients. However, studies investigating the link between this polymorphism and obesity and T2DM have produced inconsistent results.