ABSTRACT
Interactions between the gut and the brain arewell recognized to play important roles in the control of energy intake (1). In particular, hormones released from the gut signal information to the CNS regarding the ingestion of nutrient and these signals in turn influence food intake (2). Some effects of the gut hormonesmaybemediatedbydirect actiononCNSneurons, for example, in the hypothalamus.Many effects, however, aremediated by afferent fibers in the vagal nerve (1). The same afferent neurons may also function as mechanoreceptors. Cholecystokinin (CCK) was the first of theguthormones tobe shown to influence food intake (3), and its actionviavagal neurons, which also function as gastricmechanoreceptors, is nowwell defined (4). Subsequently, a variety of other peptide hormones from the gutwere shown to inhibit nutrient ingestion, including peptide YY (PYY) and glucagon-like peptide (GLP)-1 (5). In recent years, gut peptide hormones that stimulate food intake have also been identified, for example, ghrelin. It is now clear that there are complex interactions at the level of vagal afferent neurons between anorexic and orexigenic hormones such as CCK and ghrelin (6,7). Interestingly, this signaling system has been shown to involve not just peptide hormones and their receptors but also the endocannabinoid (EC) system (8,9). Moreover, the role of the latter in controlling feeding behavior appears to be independent of EC signaling within the CNS. The present chapter provides an overview of recent progress in elucidating gut-brain signaling mechanisms with special relevance to the role of the EC system.
