Cellular and Molecular Effects of Obesity on the Heart

Abstract

Obesity is a serious chronic disease that is responsible for a large number of deaths worldwide. The Body Mass Index (BMI) is widely used to provide definitions of overweight and obesity. A BMI of 20–24 is considered normal, a BMI of 25–29 is considered overweight and a BMI of 30 and over is considered obese. Overweight and obesity are attributed to a variety of risk factors including smoking, genetics, alcohol consumption, high level of stress, physical inactivity, unhealthy diet containing excessive amounts of fat and sugar, food snacking and binging, low calorie expenditure, socio-economic and psychological issues and some medications. Overweight and obesity are also associated with various illnesses including hormonal imbalance, hypothyroidism, insulin resistance (IR), polycystic ovary syndrome and Cushing’s syndrome. Obesity is a risk factor for diabetes (diabesity) resulting in hyperglycemia which enhances the generation of reactive carbonyl species (RCS) and reactive oxygen species (ROS) in the myocardium. Both ROS and RCS elicit insults to cardiac muscle which may result in apoptosis, fibrosis, hypertrophy, mitochondrial dysfunction, derangement in cellular calcium homeostasis and electrical signaling. In response to these insults the heart goes through a process of remodeling in order to maintain the demands of the body. Over time there may be development of cardiomyopathy, reduced ejection fraction and perhaps arrhythmias and sudden cardiac death (SCD). In general obesity is a preventable illness. This review describes the cellular and molecular effects of obesity on the heart leading to SCD.