ABSTRACT
The discovery of leptin has heralded the beginning of decades of significant research contributing to our understanding of the system that governs energy homeostasis and the pathways that modulate appetite, satiety, and metabolism. The complex neuronal circuits that receive hormonal and signaling input from the gut, adipose tissue, pancreas, and other organs; and secrete neurotransmitters and peptides in order to integrate information about energy intake and expenditure with the ultimate goal of regulating body weight. Anti-obesity medications (AOMs) that are currently in use utilize these pathways to create a negative energy balance that promotes weight loss. The goal of using AOMs is to promote sustainable weight loss and thereby prevention of obesity complications. AOMs currently used in the clinical setting work via decreasing appetite and increasing satiety with a net effect of decreased food intake rather than increasing energy expenditure. The investigation and promotion of safety and tolerability of drugs which increase energy expenditure has been elusive due to the inevitable increased peripheral sympathetic tone, which generally results in intolerable side effects such as increased heart rate, blood pressure, and increased myocardial oxygen demand. Hence, this chapter will focus on the mechanisms by which current anti-obesity agents regulate energy intake.
