Previous research has demonstrated an association between genetic variation in the CTRB1/2 gene and response to incretin therapies. We aimed to evaluate the role of CTRB1/2 rs7202877 (T>G) polymorphism in glycemic response to liraglutide among Greek people with T2D. 116 adults with T2D (51% female, mean BMI 35.4±6.4 kg/m2, mean age 68.3±10.9 years), who had been on treatment with liraglutide for at least 6 months were genotyped for the rs7202877 polymorphism, using real-time PCR. Responders met at least one of the following criteria: i) achievement of good glycemic control defined as HbA1c level of <7%, either at 3 or 6 months after treatment initiation, ii) reduction of the baseline HbA1c levels by ≥1% after 3 or 6 months of liraglutide use, and iii) maintenance of the optimal glucose control (HbA1c <7%) that a patient had before switching to liraglutide, after 3 or 6 months of treatment. Patients who failed to fulfil any of those criteria, were characterized as non-responders. 81 (70%) patients were classified as responders and 35 (30%) as non-responders. 97 (84%) patients were homozygous for the wild type T allele (TT) and 19 (16%) patients carried one polymorphic G allele (TG). Heterozygotes tended to have better response to liraglutide treatment; still, the difference was not significant (OR: 1.25, 95% CI: 0.4, 3.8, P=0.69). The probability of being a responder was 45% greater, when the baseline HbA1c was increased by 1% (adjusted for gender and baseline weight OR: 1.45, 95% CI: 1.05, 2.1, P=0.048). Additionally, an increase in baseline weight by 10 kg was associated with 26% reduced probability of being a responder (adjusted for gender and baseline HbA1c OR: 0.97, 95% CI: 0.94, 0.99, P=0.011). Our findings do not suggest a role of CTRB1/2 rs7202877 in affecting glycemic response to liraglutide. Lower baseline body weight and higher baseline glycemia might be related to better glycemic control following treatment with liraglutide.
A. Kyriakidou: None. A.V. Kyriazou: Research Support; Self; Novo Nordisk A/S. T. Koufakis: None. Y. Vasilopoulos: None. I. Avramidis: None. S. Baltagiannis: None. E. Manthou: None. D.G. Goulis: None. P. Zebekakis: None. K. Kotsa: Advisory Panel; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, Sanofi-Aventis, Takeda Pharmaceutical Company Limited. Speaker’s Bureau; Self; Menarini Group. Other Relationship; Self; Novo Nordisk Inc.
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