After ingestion of
carbohydrate- and fat-rich meals, the
incretin hormone glucagon-like peptide 1 (GLP-1) is secreted from the L-cells in the distal put into the circulation. Its major physiological effect lies in a strongly
glucose-dependent stimulation of insulin secretion from pancreatic B-cells. Furthermore,
GLP-1 suppresses
glucagon secretion, stimulates B-cell neogenesis as well as
proinsulin biosynthesis and inhibits gastric emptying and
acid secretion. Recently,
GLP-1 could be shown to reduce caloric intake and to enhance satiety, most likely via specific receptors within the central nervous system, resulting in reduced
weight gain in experimental animals. In nondiabetic and Type 2 diabetic human subjects, exogenous
GLP-1 reduces hunger, caloric intake and
body weight. Therefore, in addition to its well-characterized antidiabetogenic effect, the
anorectic effect may offer
GLP-1 a potential in the
pharmacotherapy of
obesity. It is still unknown whether the
GLP-1 effect on caloric intake is sustained after long-term treatment. Furthermore, the exact mechanisms by which the
peptide exerts its biological effects have not yet been clarified. Due to the rapid degradation of native
GLP-1, its therapeutic application is limited by the short half-life. Therefore, suitable modes of administration are needed in order to reach stable plasma concentrations. The present review aims to describe the role of
GLP-1 in the central regulation of feeding and to discuss its possible application in the
pharmacotherapy of
obesity.