Introduction
Over the past few decades obesity has become a major burden on health worldwide. The prevalence of hypertension has increased with a significant increase in the prevalence of overweight and obesity. Recent studies indicate an important role of adipose tissue hormones called adipokines in obesity-associated complications. Apelin has recently been added to the family of adipokines. One of the physiologic functions of the apelin/APJ system is regulation of the cardiovascular function. The aim of this study was to determine the relation of serum apelin to obesity-associated hypertension as well as to myocardial performance.
Patients and methods
The study included 30 obese hypertensive patients, 30 obese nonhypertensive patients, and 25 age-matched and sex-matched controls. In all studied participants we determined the lipid profile, serum insulin, fasting blood glucose level, HOMA-IR, serum apelin, and echocardiographic results of left ventricular systolic and diastolic function.
Results
Higher levels of fasting blood glucose, fasting serum insulin, HOMA-IR, triglycerides, total cholesterol, and low-density lipoprotein were detected in obese hypertensive and nonhypertensive patients. Left ventricular mass index (LVMI) was increased in both obese hypertensive and nonhypertensive patients in comparison with healthy individuals. Left ventricular ejection fraction and E/A ratio were significantly lower in hypertensive obese versus nonhypertensive obese individuals ( = 0.004 and <0.001, respectively), whereas LVMI was higher in hypertensive versus nonhypertensive patients ( < 0.001). Apelin levels were significantly equally higher in obese hypertensive and nonhypertensive patients (6.10 ± 1.88 and 6.40 ± 1.60 ng/ml) compared with controls (4.22 ± 0.86 ng/ml, < 0.001). In hypertensive obese individuals, serum apelin correlated negatively with left ventricular ejection fraction ( = 0.02) and directly with E/A ratio ( = 0.03).
Conclusion
Apelin levels are significantly higher in obese hypertensive and nonhypertensive patients. This increase might be a compensatory mechanism against myocardial dysfunction with obesity.