Refinement of the previously mentioned hypothesis proposes that the insulin dysregulation after RYGB is a result of rapid delivery of nutrients to the distal intestine, leading to an exaggerated response of the incretins GLP-1 and gastric inhibitory peptide (GIP), which causes postprandial hyperinsulinemia/hypoglycemia without necessarily leading to islet cell hyperplasia [10]. Here, GIP is linked to hyperinsulinism.