The prevalence of obesity is rising worldwide; therefore, the World Health Organization introduced the term 'globesity'. This rise also causes an increase of associated diseases such as cardiovascular diseases, type 2 diabetes, several malignomas as well as psychiatric disorders. In order to face this medical challenge, a better understanding of the pathophysiological alterations under conditions of obesity is necessary. Hunger and satiety are largely regulated by peptidergic hormones predominantly produced in the gastrointestinal tract and signaling to the brain via the gut-brain axis. While several hormones are known to decrease food intake such as nesfatin-1, cholecystokinin (CKK), glucagon-like peptide 1 (GLP-1), pancreatic polypeptide (PP) and peptide YY (PYY), only one peripherally produced and centrally acting hormone - ghrelin - is known so far that stimulates food intake. Several alterations of the signaling of these hormones have been described in the past years e.g. an attenuated postprandial response of CCK, GLP-1 and PYY as well as a reduced postprandial suppression of ghrelin that might contribute to the development and/or maintenance of obesity and will be discussed in the present review. Lastly, gaps in knowledge will be highlighted.
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