The prevalence of hypertension and cardiovascular disease has increased in recent decades in parallel with increasing obesity. This project explores the hypothesis that a person's physical activity levels influence expression of receptors for leptin, a hormone produced primarily by adipose tissue that increases blood pressure. Leptin also modifies the function of monocytes, cells that play a central role in the pathogenesis of atherosclerosis. Healthy subjects between the ages of 21 and 40 will be assessed for body fat, habitual physical activity levels, aerobic capacity, cardiovascular function, and monocyte leptin receptor expression. The goals of this project are to (a) identify and validate a biomarker (leptin receptor expression on monocytes) that may provide a novel method for determining cardiovascular disease risk and for monitoring the response to exercise intervention;and (b) to determine how leptin affects monocyte function. If physical activity is shown to reduce leptin receptor expression, thus breaking a critical link between fatness and cardiovascular disease, such information can be used as incentive in exercise-based preventive and treatment programs. Less emphasis could be placed on weight loss itself, which is so difficult to attain or maintain, and more emphasis could be placed on the health benefits of exercise, regardless of weight outcomes.
Being overweight puts an individual at greater risk of cardiovascular disease. This project will investigate how fat cells communicate with cells of the immune system to cause high blood pressure and atherosclerosis, and how physical activity disrupts this unhealthy communication.
