Cardiac biogenic amine profile and its relationship with parameters of cardiovascular disease in obesity

Aims

To identify the cardiac biogenic amine profile of obese rats and associate these compounds with parameters of cardiovascular disease.

Main methods

Wistar rats (n = 20) were randomly distributed into two groups: control and obese. Obesity was induced by a high-sugar fat diet. Biochemical parameters were evaluated. Doppler Echocardiography and systolic blood pressure; interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α), protein carbonylation, ferric reducing antioxidant power (FRAP), and catalase activity were measured in cardiac tissue. HPLC evaluated the cardiac biogenic profile. Data were compared using the Student's T or Mann-Whitney tests and Spearman's correlation at 5% significance. The principal component analysis (PCA) was performed.

Key findings

Obesity generated hypertension, cardiac remodeling and dysfunction, and imbalanced all biochemical, inflammatory, and oxidative markers (p < 0.001). Eight biogenic amines were found in cardiac tissue. Obesity increased serotonin and decreased agmatine, putrescine, cadaverine, and spermidine. Serotonin (r = 0.534 to 0.808) was strong and positively correlated with obesity, biochemical parameters, cardiac inflammation, oxidative stress, hypertension, cardiac remodeling, and dysfunction (p < 0.001). Spermidine (r = −0.560 to −0.680), putrescine (r = −0.532 to −0.805), cadaverine (r = −0.534 to −0.860), and agmatine (r = −0.579 to −0.884) were inversely correlated with the same parameters (p < 0.001). PCA allowed for distinguishing the control and obese groups.

Significance

There are strong correlations between cardiac biogenic amine levels, cardiac remodeling, and dysfunction resulting from obesity.

Conclusion

There is an association between cardiac biogenic amines and cardiovascular disease in obesity. In addition, agmatine, putrescine, cadaverine, and, mainly, serotonin may be new biomarkers for cardiovascular health in obesity and help to improve the diagnosis and treatment of CVD resulting or not from obesity. However, more research is needed to support this conclusion.