Overeating makes the gut grow fonder; new insights in gastrointestinal satiety signaling in obesityMaljaars, JeroenCurrent Opinion in Gastroenterology: March 2013 - Volume 29 - Issue 2 - p 177–183 doi: 10.1097/MOG.0b013e32835d9fe0 NUTRITION: Edited by David H. Alpers and William F. Stenson Abstract Author Information Purpose of review: As the prevalence of overweight and obesity increases, there is a growing need to develop effective treatment strategies in addition to bariatric surgery. Research has focused on understanding the pathophysiologic mechanisms that contribute to the occurrence and maintenance of obesity and overweight, and on how bariatric surgery is able to overcome these obstacles. In this review, new insights in the gastrointestinal regulatory mechanisms in obesity and bariatric surgery will be discussed. Recent findings: Diet-induced obesity (DIO) leads to changes in gut peptide secretion and other gastrointestinal responses to nutrients. These changes reduce satiety signaling and therefore complicate loss of body weight. Weight loss by dietary restriction does not restore gastrointestinal responses to nutrients to normal, but alters these responses to further complicate weight loss. Only bariatric surgery is able to overcome these changes by mechanisms that are hitherto unclear but may involve altered gut peptide secretion or changes in bile acid metabolism. Summary: DIO alters nutrient-induced gastrointestinal signaling in a way that facilitates further weight gain and complicates weight loss. A better understanding of these mechanisms and the way bariatric surgery can overcome these changes is crucial in developing effective treatment strategies. Department of Gastroenterology-Hepatology, Leiden University Medical Centre, Leiden, the Netherlands Correspondence to Jeroen Maljaars, MD, PhD, Department of Gastroenterology-Hepatology, Leiden University Medical Centre, C4P, PO-Box 9600, 2300 RC Leiden, the Netherlands. Tel: +31 715263507; fax: +31 715248115; e-mail: P.W.J.Maljaars@LUMC.nl © 2013 Lippincott Williams & Wilkins, Inc.