Abstract
This chapter focuses on glucagonlike peptide 1 (GLP-l) and its role in the regulation of feeding behavior. GLP-1 is a posttranslational product of the proglucagon gene. GLP-1 is released in response to meals and acts as a satiety signal. High GLP-1 concentrations as well as the widespread distribution of its receptor in the central nervous system have suggested a central role for GLP-1 in appetite suppression. GLP-1 meets the major criteria required for a neuropeptide. It is synthesized from preproglucagon by noncatecholaminergic and leptin receptor positive neurons of nucleus of the solitary tract (NTS) and the dorsal and ventral part of the reticular nucleus. GLP-1 concentrations within the physiological range reduced food intake by 21% in lean subjects. In humans, GLP-1 infusion decreased postprandial feelings of hunger, suggesting a decreased rate of entry of nutrients into the circulation by reducing the gastric emptying rate. GLP-1 infusion rate was found to be the only independent predictor of the reduction in energy intake in both lean and obese subjects.
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