Endocrine Abstracts

JOINT1423

Background: Arterial hypertension (AH) and type 2 diabetes mellitus (T2DM) are potent risk factors for cardiovascular diseases. Cardiovascular and metabolic effects of catestatin (CST) and relaxin-2 (RLN-2) indicate their involvement in AH and T2DM pathogenesis and suggest their diagnostic potential.

Objective: To determine plasma CST and RLN-2 levels, evaluate their associations with parameters of glucose metabolism and investigate the prognostic potential of CST and RLN-2.

Materials and methods: The present study was an observational prospective cohort single-center by design with a 12-month follow-up. This study was performed in accordance with all ethical principles of the Declaration of Helsinki. All participants signed a written informed consent form prior to any protocol procedures. 106 patients with AH and 30 healthy volunteers were enrolled in the study. 55 hypertensive patients had comorbid T2DM. Plasma CST levels were measured by ELISA (E4996Hu, BT Lab, China), RLN-2 (E-EL-H1582, Elabscience, USA). The data are presented as a mean±S.D. or a median and interquartile range. Statistical significance was defined as P<0.05. Statistical data were analyzed using SPSS statistical software (SPSS 25.0 for Windows, IBM, Armonk, NY, USA).

Results: Patients with AH and T2DM had decreased CST (4.47±1.16 vs. 5.61±0.61 ng/ml; P<0.001) and RLN-2 levels (5.11 [4.97; 5.38] vs. 6.71 [6.00; 7.14] pg/ml; P<0.001) compared with hypertensive patients without T2DM. Both CST and RLN-2 had negative correlations with parameters of glucose metabolism, particularly HbA1c (r=−0.535; P<0.001 and r=−0.673, P<0.001), glucose (r=−0.450; P<0.001 and r=−0.543; P<0.001), HOMA-IR (r=−0.481; P<0.001 and r=−0.392; P<0.001). CST (0.175 [0.099 − 0.312; P<0.001) and RLN-2 levels (0.196 [0.095 − 0.405]; P<0.001) were established as significant predictors of impaired glucose metabolism by univariate binary logistic regression. Kaplan–Meier curve analysis revealed a significantly higher incidence of MACE in patients with CST levels <5.44 ng/ml (P=0.01). Cox proportional hazard model indicated CST levels (0.486 [0.285 – 0.830]; P=0.01) as an independent predictor of MACE in the study population as well as presence of T2DM (3.578 [1.102 – 11.619]; P=0.03), HOMA-IR (1.157 [1.023 – 1.309]; P=0.02), insulin levels (1.049 [1.006 – 1.094]; P=0.02).

Conclusions: In the present study, we established reduced plasma CST and RLN-2 levels in hypertensive patients with T2DM and their negative relationships with parameters of glucose metabolism. CST and RLN-2 were determined as significant predictors of impaired glucose metabolism. These findings allow us to suggest CST and RLN-2 as perspective biomarkers of AH and T2DM.