Association of circulating biomarkers of glycocalyx injury, sirtuin 1, and NFκB p65 in individuals with type 2 diabetes and concurrent arterial hypertension.

PURPOSE: Type 2 diabetes (T2D) and arterial hypertension are major cardiovascular risk factors, with endothelial dysfunction being a central pathological mechanism. This study investigated the concurrent T2D and arterial hypertension on plasma levels of endothelial glycocalyx components and inflammatory/vasoprotective markers.

METHODS

In this cross sectional study, we assessed 68 individuals (44 female and 24 male) aged 41-69 years. Thirty-one individuals had T2D and thirty-seven had concurrent T2D and arterial hypertension. Anthropometry parameters and biomarkers profile were evaluated. Plasma syndecan-1, syndecan-4, hyaluronic acid, NFκB p65, and sirtuin 1 were measured using ELISA assay.

RESULTS

Our findings revealed that individuals with coexisting hypertension and T2D exhibited significantly elevated hyaluronic acid (p = 0.013), syndecan-4 (p = 0.028), and NFκB p65 (p = 0.002), and markedly reduced sirtuin 1 (p = 0.007), compared to T2D-only participants. Effect size analysis showed moderate effect magnitudes for hyaluronic acid (Ƞ2p = 0.10), syndecan-4 (Ƞ2p = 0.10), NFκB p65 (Ƞ2p = 0.14), and sirtuin 1 (Ƞ2p = 0.11). In unadjusted analyses, sirtuin 1 was inversely correlated with hyaluronic acid (rho = -0.259; p = 0.033), syndecan-4 (rho = -0.307; p = 0.011), and NFκB p65 (rho = -0.276; p = 0.023), whereas hyaluronic acid was positively correlated with syndecan-4 (rho = 0.359; p = 0.003). After adjustment for diabetes duration, the associations of hyaluronic acid with syndecan-4 and of sirtuin 1 with NFκB p65 remained significant, whereas the correlations of sirtuin 1 with hyaluronic acid and syndecan-4 were no longer significant.

CONCLUSION

Our results suggest that the coexistence of T2D and arterial hypertension is associated with unfavorable vascular biomarker profile, characterized by glycocalyx injury, greater inflammatory activation, and reduced vasoprotective signaling.