Gut Hormones and Obesity

Feeding is ultimately controlled by the central nervous system but is strongly influenced by numerous physiological signals arising from the periphery that either promote or limit energy intake. Broadly speaking, these gut hormones act via neuroendocrine mechanisms to communicate information on changing energy status from the periphery to the brain. Some of these peptides are produced by the gastrointestinal tract itself. Most of these gastrointestinal-derived signals, including cholecystokinin, glucagon-like peptide-1, and peptide YY, promote meal termination; in contrast, the hunger hormone ghrelin promotes the ingestion of food when readily available energy is low. Additionally, supporting organs like the pancreas release feeding-relevant neuroendocrine signals that regulate the internal milieu during nutrient influx. Together, these gut peptides control energy balance through a complicated interplay of physiological, behavioral, and neuroendocrine events. Individual signals are well investigated for their role in the maintenance of normal energy balance, but their roles in obesity - whether relating to the development or consequences of elevated body weight - are often understudied. This represents a critical area of ongoing research. Here, we review several of the major gastrointestinal- and pancreatic-derived gut hormones that contribute to the control of food intake. We discuss their impact on the control of energy balance in lean (i.e., nonobese) individuals and summarize some of the major findings regarding the role of each peptide in the obese state.