Gut Hormones as Mediators of Appetite and Weight Loss After Roux-en-Y Gastric Bypass

Roux, Carel W. le; Welbourn, Richard; Werling, Malin; Osborne, Alan; Kokkinos, Alexander; Laurenius, Anna; Lönroth, Hans; Fändriks, Lars; Ghatei, Mohammad A.; Bloom, Stephen R.; Olbers, Torsten

doi:10.1097/sla.0b013e3180caa3e3

Cited by 647 publications

(564 citation statements)

References 30 publications

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“…There is a body of evidence to support the gut hormones hypothesis (57,60,61) . GLP-1, peptide YY and oxyntomodulin are anorexic hormones and have been shown to reduce hunger, promote satiety and reduce food intake when given peripherally in human subjects or centrally in rodents (62)(63)(64)(65)(66) .…”

Section: Physiological Domain Of Taste and Post-ingestive Effects Of mentioning

confidence: 99%

Food preferences and underlying mechanisms after bariatric surgery

Behary

Miras

2015

Proc. Nutr. Soc.

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Bariatric surgery leads to significant long-term weight loss, particularly Roux-en-Y gastric bypass (RYGB). The mechanisms underlying weight loss have not been fully uncovered. The aim of this review is to explore the changes in food preferences, as a novel mechanism contributing to weight loss, and also focus on the underlying processes modulating eating behaviour after bariatric surgery. Patients after gastric bypass are less hungry and prefer healthier food options. They develop an increased acuity to sweet taste, which is perceived as more intense. The appeal of sweet fatty food decreases, with functional MRI studies showing a corresponding reduction in activation of the brain reward centres to high-energy food cues. Patients experiencing post-ingestive symptoms with sweet and fatty food develop conditioned aversive behaviours towards the triggers. Gut hormones are elevated in RYGB and have the potential to influence the taste system and food hedonics. Current evidence supports a beneficial switch in food preferences after RYGB. Changes within the sensory and reward domain of taste and the development of post-ingestive symptoms appear to be implicated. Gut hormones may be the mediators of these alterations and therefore exploiting this property might prove beneficial for designing future obesity treatment.

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Section: Physiological Domain Of Taste and Post-ingestive Effects Of mentioning

confidence: 99%

Food preferences and underlying mechanisms after bariatric surgery

Behary

Miras

2015

Proc. Nutr. Soc.

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“…Anti-obesity surgery ameliorates diabetes and several other serious comorbidities [1]. One mechanism postulated to improve diabetes after gastric bypass is an augmented incretin response; postprandial plasma concentrations of the potent incretin glucagon-like peptide-1 rise after gastric bypass [2]. Recently hyperinsulinaemia and hypoglycaemia have been recognised as new complications of gastric bypass [3,4].…”

Section: Introductionmentioning

confidence: 99%

Nationwide cohort study of post-gastric bypass hypoglycaemia including 5,040 patients undergoing surgery for obesity in 1986–2006 in Sweden

et al. 2010

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Aims/hypothesis Symptomatic hypoglycaemia with related confusion, syncope, epilepsy or seizures is a newly recognised complication of gastric bypass surgery for obesity. The incidence of these conditions is not known. We therefore studied the incidence of post-gastric bypass hypoglycaemia and related symptoms in patients who have undergone gastric bypass and a reference cohort from the general population of Sweden. Methods This is a nationwide cohort study based on national registries with 5,040 persons who underwent gastric bypass, vertical banded gastroplasty or gastric banding for obesity in Sweden between 1 January 1986 and 31 December 2006 and a cohort of ten referents per patient matched for sex and age randomly sampled from the general population. The incidence rates of hospitalisation for hypoglycaemia, confusion, syncope, epilepsy or seizures before and after dates of surgery or inclusion in the reference cohort were studied. Results Preoperative incidences of hospitalisation for hypoglycaemia were similar in the surgical and referent cohorts. After gastric bypass surgery, the adjusted hazard ratios were significantly elevated for hypoglycaemia (2.7 [95% CI 1. participants affected by hypoglycaemia were very low (0.2% and 0.04%, respectively). There was no increased risk of hypoglycaemia after vertical banded gastroplasty or gastric banding compared with the referent population. Conclusions/interpretation Obese persons who have undergone gastric bypass have an increased risk of hospitalisation for diagnoses associated with post-gastric bypass hypoglycaemia, although few patients are affected.

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“…4 The first mechanisms have been shown to be at least partly physiologically induced by alterations in gastrointestinal and central neuroendocrine signalling. [5][6][7][8] The postprandial responses of the gut hormones glucagonlike peptide-1 (GLP-1) and peptide YY3-36 (PYY), which are produced from the L cells in the gut, are increased after gastric bypass. [6][7][8] We and others have demonstrated in a rodent model that these anorexigenic gut hormones reduce hunger and induce satiety in a dose-dependent manner.…”

Section: Introductionmentioning

confidence: 99%

“…[5][6][7][8] The postprandial responses of the gut hormones glucagonlike peptide-1 (GLP-1) and peptide YY3-36 (PYY), which are produced from the L cells in the gut, are increased after gastric bypass. [6][7][8] We and others have demonstrated in a rodent model that these anorexigenic gut hormones reduce hunger and induce satiety in a dose-dependent manner. 9,10 We have also found that patients with suboptimal body weight (BW) loss after gastric bypass had attenuated postprandial PYY and GLP-1 responses.…”

Section: Introductionmentioning

confidence: 99%

“…9,10 We have also found that patients with suboptimal body weight (BW) loss after gastric bypass had attenuated postprandial PYY and GLP-1 responses. 6 Inhibition of the satiety gastrointestinal hormone response with the somatostatin analogue octreotide increased appetite and food intake in gastric bypass patients, 6 whereas specific antagonism of PYY increased food intake in gastric bypass rats. 8 A single peptide is unlikely to be responsible for all of the reported gastric bypass effects, as several satiety gut hormones are released in concert.…”

Section: Introductionmentioning

confidence: 99%

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Exogenous peptide YY3-36 and Exendin-4 further decrease food intake, whereas octreotide increases food intake in rats after Roux-en-Y gastric bypass

et al. 2011

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Background: Patients show an elevated postprandial satiety gut hormone release after Roux-en-Y Gastric bypass (gastric bypass). The altered gut hormone response appears to have a prominent role in the reduction of appetite and body weight (BW) after gastric bypass. Patients with insufficient BW loss after gastric bypass have an attenuated postprandial gut hormone response in comparison with patients who lost an adequate amount of BW. The effects of additional gut hormone administration after gastric bypass are unknown. Methods: The effects of peripheral administration of peptide YY3-36 (PYY3-36; 300 nmol kg À1 ), glucagon-like peptide-1 (GLP-1) analogue Exendin-4 (20 nmol kg À1 ) and somatostatin analogue octreotide (10 mg kg À1 ) on feeding and BW were evaluated in rats after gastric bypass. Results: Gastric bypass rats weighed (Po0.01) and ate less on postoperative day 5 (Po0.001) and thereafter, whereas postprandial plasma PYY and GLP-1 levels were higher compared with sham-operated controls (Po0.001). Administration of both PYY3-36 and Exendin-4 led to a further decrease in food intake in bypass rats compared with saline treatment (P ¼ 0.02 and Po0.0001, respectively). Similar reduction in food intake was observed in sham rats (P ¼ 0.02 and Po0.001, respectively). Exendin-4 treatment resulted in a significant BW loss in bypass (P ¼ 0.03) and sham rats (P ¼ 0.04). Subsequent treatment with octreotide led to an increase in food intake in bypass (P ¼ 0.007), but not in sham rats (P ¼ 0.87). Conclusion: Peripheral administration of PYY3-36 and Exendin-4 reduces short-term food intake, whereas octreotide increases short-term food intake in rats after gastric bypass. The endogenous gut hormone response after gastric bypass can thus potentially be further enhanced by additional exogenous therapy with pharmacological doses of gut hormones in patients with insufficient weight loss or weight regain after surgery.

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Gut Hormones as Mediators of Appetite and Weight Loss After Roux-en-Y Gastric Bypass

Cited by 647 publications

References 30 publications

Food preferences and underlying mechanisms after bariatric surgery

Food preferences and underlying mechanisms after bariatric surgery

Nationwide cohort study of post-gastric bypass hypoglycaemia including 5,040 patients undergoing surgery for obesity in 1986–2006 in Sweden

Exogenous peptide YY3-36 and Exendin-4 further decrease food intake, whereas octreotide increases food intake in rats after Roux-en-Y gastric bypass

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