Oxyntomodulin (OXM) is released from the gut postprandially, in proportion to energy intake, and circulating levels of OXM are elevated in several conditions associated with anorexia. Central injection of OXM reduces food intake and weight gain in rodents, suggesting that OXM signals food ingestion to hypothalamic appetite-regulating circuits. We investigated the effect of iv OXM (3.0 pmol/kgmin) on appetite andfoodintakein13healthysubjects(bodymassindex,22.5 0.9 kg/m 2 ) in a randomized, double-blind, placebo-controlled, cross-over study. Infusion of OXM significantly reduced ad libitum energy intake at a buffet meal (mean decrease, 19.3 5.6%; P < 0.01) and caused a significant reduction in scores for hunger. In addition, cumulative 12-h energy intake was significantly reduced by infusion of OXM (mean decrease, 11.3 6.2%; P < 0.05). OXM did not cause nausea or affect food palatability. Preprandial levels of the appetite-stimulatory hormone, ghrelin, were significantly suppressed by OXM (mean reduction, 44 10% of postprandial decrease; P < 0.0001). Elevated levels of endogenous OXM associated with disorders of the gastrointestinal tract may contribute to anorexia. (J Clin Endocrinol Metab 88: 4696–4701, 2003)

/pdf/oxyntomodulin-suppresses-appetite-and-reduces-food-intake-in-102n53qdav.pdf

Oxyntomodulin Suppresses Appetite and Reduces Food Intake in Humans

Energy homeostasis and medical vs. surgical methods to overcome it Obesity is now a global pandemic that continues to accelerate despite the often Herculean efforts by afflicted individuals to lose weight. These efforts are thwarted by a physiological system that regulates body weight in a manner analogous to that by which a thermostat controls ambient temperature. For each individual, there is a highly genetically influenced level of adiposity that is defended by this adipostatic control system, wherein alterations in body fat stores trigger compensatory changes in appetite and energy expenditure that resist weight change (1). It is hypothesized that these processes evolved to defend against malnutrition in times of famine, and hence, the adaptive responses to weight loss appear to be more robust than are those to weight gain (as any dieter can attest). Because of this body weight regulation system, known as energy homeostasis, nonsurgical methods are notoriously ineffective at achieving major, long-term weight reduction. In general, no more than 5–10% of body weight is lost through dieting, exercise, and the few available antiobesity medications, and recidivism after di

Gastric bypass for obesity: mechanisms of weight loss and diabetes resolution.

Objective: Limited data on patients undergoing Roux-en-Y gastric by pass surgery (RY-GBP) suggest that an improvement in insulin secretion after surgery occurs rapidly thus may not be wholly accounted for by weight loss. We hypothesized that in obese patients with type 2 diabetes mellitus (T2DM) the impaired levels and effect of incretins changed as a consequence of RY-GBP. Research Design and Methods: Incretin (GIP and GLP-1) levels and their effect on insulin secretion were measured before and 1 month after RY-GBP in eight obese women with T2DM and in seven obese non-diabetic controls. The incretin effect was measured as the difference in insulin secretion (area under the curve, AUC) in response to oral glucose tolerance test (OGTT) and to an isoglycemic IV glucose test (isoG IVGT). Results: Fasting and stimulated levels of GLP-1 and GIP were not different between Controls and Patients with T2DM before the surgery. One month after RY-GBP, body weight decreased by 9.2±7.0 kg, oral glucose-stimulated GLP-1 (AUC) and GIP peak levels increased significantly by 4368±1418 pM.L -1 .min -1 (p Conclusions: These data suggest that early after RY-GBP, the greater GLP-1 and GIP release could be potential mediators of improved insulin secretion.

https://care.diabetesjournals.org/content/diacare/30/7/1709.full.pdf

Incretin Levels and Effect Are Markedly Enhanced 1 Month After Roux-en-Y Gastric Bypass Surgery in Obese Patients With Type 2 Diabetes

https://www.gastrojournal.org/article/S0016-5085(04)01993-6/pdf

Gastrointestinal hormones and food intake.

Role of neuropeptides in appetite regulation and obesity – A review

The treatment of obesity by intestinal bypass provides a unique model for the investigation of gut hormone release from the functionally deranged bowel. We have examined the postprandial response of eight circulating gut or pancreatic peptide hormones in 16 preoperative obese patients, 20 patients with jejunoileal bypass, 38 patients with biliopancreatic bypass and 13 age and sex-matched controls. Basal and post-meal hormone concentrations were determined by specific radioimmunoassay methods. Reductions of the upper small intestinal hormones, motilin and gastric inhibitory polypeptide were found in both types of surgery. Conversely, the ileal hormones neurotensin and enteroglucagon were elevated following surgery. This pattern is consistent with the known distribution of these hormones. Variations of response due to surgical differences were noted for gastrin and the enteropancreatic axis, which was more markedly disturbed after biliopancreatic bypass. The alterations of hormone release closely reflect the anatomical changes induced by each particular surgical technique.

Gut hormone changes after jejunoileal (JIB) or biliopancreatic (BPB) bypass surgery for morbid obesity.

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Gut hormone changes after jejunoileal (JIB) or biliopancreatic (BPB) bypass surgery for morbid obesity.