Aim: Measurement of inflammatory markers for risk stratification of vascular disorders has been the focus of numerous investigations worldwide, and usually reveals augmented levels of circulating cytokines/chemokines among carriers of classic risk factors for atherosclerosis. Nonetheless, this low-grade inflammatory milieu detected in aged individuals tends to be influenced by body composition. Moreover, cardiovascular risk factors have a complex genetic etiology, and disregarding the genetic heritage may produce spurious results owing to interethnic differences. In this complex scenario, our study was designed to verify the existence and strength of the association between selected mediators of systemic inflammation and classic risk factors of cardiovascular diseases (CVD).
Methods: In a sample of post-menopausal older women, correlation analyses explored the association of circulating levels of IL1α, IL1β, IL8, IL10 and IL12 with atherosclerosis-related clinical/metabolic parameters, using age, body mass index (BMI), genetic ancestry estimates as standard correction factors. Further adjustment for use of therapeutic agents was applied when appropriate.
Results: Our analyses revealed association of log10-transformed IL-12 titers with VLDL-c levels (r=.192; p=.002) and with SBP (r-.185; p=.003), and of log10-transformed IL-8 titers with GLY (r=.235; p<.001).
Conclusion: Interpretation to the results account to a possible dysregulation of the PPAR signaling pathway to explain the association of IL12 and VLDL-c, and to IL8-driven mechanisms to promote dysglycemia. No previous report sought to investigate the relationship between this set of inflammatory markers and classic risk factors for atherosclerosis correcting for the heterogeneity in genetic admixture and body composition of Brazilian post-menopausal women.
Keywords: Admixture; Atherosclerosis; Genetic ancestry; Inflammation; Interleukin.
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