| [ Summary ] |
Obesity arises from an imbalance between food intake and energy expenditure. Recently, it has been recognized that various hormones act as regulators of energy balance, and that a dysfunction of these hormones causes inadequate eating behaviors, resulting in the subsequent onset of obesity. The adipocyte hormone leptin informs the brain about the available energy storages, and in return, the brain adjusts food intake accordingly. Gut peptides such as peptide YY, glucagon‒like peptide 1, and cholecystokinin are involved in the perception of satiety and act to reduce food intake. The gastric hormone ghrelin, conversely, is secreted before food intake, and can stimulate feeding. The satiety and emptiness signals generated by these hormones are conveyed to the central nervous system through afferent fibers of the vagus nerve that expand from the gut to the nucleus of the solitary tract. In addition to these mechanisms, recent studies suggest that obesity is probably mediated, at least in part, by changes within the intestinal bacterial flora. These findings may offer the key to enable the development of more effective approaches regarding the treatment of obesity. |