Mounting evidence substantiates the central role of the endocannabinoid system (ECS) in the modulation of both homeostatic and hedonic elements of appetite and food intake. Conversely, feeding status and dietary patterns directly influence activity of the ECS. Following a general introduction on the functioning of the ECS, the present review specifically addresses its role in the modulation of hedonic eating. Humans possess strong motivational systems triggered by rewarding aspects of food. Food reward is comprised of two components: one appetitive (orienting towards food); the other consummatory (hedonic evaluation), also referred to as ‘wanting’ and ‘liking’, respectively. Endocannabinoid tone seems to influence both the motivation to feed and the hedonic value of foods, probably by modifying palatability. Human physiology underlying hedonic eating is still not fully understood. A better understanding of the role of the ECS in the rewarding value of specific foods or diets could offer new possibilities to optimise the balance between energy and nutrient intake for different target groups. These groups include the obese and overweight, and potentially individuals suffering from malnutrition. Examples for the latter group are patients with disease-related anorexia, as well as the growing population of frail elderly suffering from persistent loss of food enjoyment and appetite resulting in malnutrition and involuntary weight loss. It has become clear that the psychobiology of food hedonics is extremely complex and the clinical failure of CB1 inverse agonists including rimonabant (Accomplia®) has shown that ‘quick wins’ in this field are unlikely.

As obesity continues to be a global epidemic, research into the mechanisms of hunger and satiety and how those signals act to regulate energy homeostasis persists. Peptide YY (PYY) is an acute satiety signal released upon nutrient ingestion and has been shown to decrease food intake when administered exogenously. More recently, investigators have studied how different factors influence PYY release and circulating levels in humans. Some of these factors include exercise, macronutrient composition of the diet, body-weight status, adiposity levels, sex, race and ageing. The present article provides a succinct and comprehensive review of the recent literature published on the different factors that influence PYY release and circulating levels in humans. Where human data are insufficient, evidence in animal or cell models is summarised. Additionally, the present review explores the recent findings on PYY responses to different dietary fatty acids and how this new line of research will make an impact on future studies on PYY. Human demographics, such as sex and age, do not appear to influence PYY levels. Conversely, adiposity or BMI, race and acute exercise all influence circulating PYY levels. Both dietary fat and protein strongly stimulate PYY release. Furthermore, MUFA appear to result in a smaller PYY response compared with SFA and PUFA. PYY levels appear to be affected by acute exercise, macronutrient composition, adiposity, race and the composition of fatty acids from dietary fat.