Gut Hypertrophy After Gastric Bypass Is Associated With Increased Glucagon-Like Peptide 2 and Intestinal Crypt Cell Proliferation

Roux, Carel W. le; Borg, Cynthia-Michelle; Wallis, Katharina; Vincent, Royce P.; Bueter, Marco; Goodlad, R A; Ghatei, Mohammed A.; Patel, Ameet G.; Bloom, Stephen R.; Aylwin, Simon

doi:10.1097/sla.0b013e3181d3d21f

Cited by 155 publications

(141 citation statements)

References 39 publications

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“…35 The gut is metabolically very active and gut hypertrophy may hence explain a higher energy requirement that contributes to body weight loss. 9,37,38 These findings are in line with previous reports demonstrating a reduced body weight without decreased food intake or malabsorption, but increased energy expenditure after GBP in rats. 39,40 Furthermore, Stylopoulos et al 41 described a 19% increase in total and a 31% increase in resting energy expenditure in rats after GBP operation.…”

Section: Experimental Datasupporting

confidence: 83%

Gastrointestinal hormones, energy balance and bariatric surgery

Bueter

Roux

2011

Int J Obes

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Despite increasing understanding of the changes in gastrointestinal and central neuroendocrine signaling following gastric bypass surgery (GBP) in morbidly obese patients, the mechanisms underlying weight loss and weight loss maintenance are not completely understood. Changes in energy expenditure are increasingly recognized as an important factor contributing to weight loss and metabolic effects in patients following GBP surgery. Experimental data regarding changes in energy balance following metabolic surgery in animal models suggest increased energy expenditure postoperatively as an important factor in the process of weight loss. However, the underlying neuroendocrine mechanisms are not well understood, and data regarding changes in energy expenditure in humans after GBP are inconsistent because of heterogenic patient populations and variable techniques. Nevertheless, a growing body of knowledge and understanding of the complex entero-neurohumoral interaction with its consequences in appetite, satiety and energy expenditure will help reveal the mechanisms of weight loss and weight loss maintenance following GBP surgery. Here we review how gastrointestinal hormones potentially regulate energy balance, and summarize current available experimental and clinical data on energy expenditure following obesity surgery.

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Section: Experimental Datasupporting

confidence: 83%

Gastrointestinal hormones, energy balance and bariatric surgery

Bueter

Roux

2011

Int J Obes

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“…Glucagon is counter-regulatory to insulin action, increasing glucose output and inhibiting glucose uptake in the liver, and it has been linked to insulin resistance in obese subjects with normal or impaired glucose tolerance (Ahrén 2006, Weiss et al 2011. However, this appears unlikely because bariatric surgery, particularly Roux-en-Y gastric bypass (RYGB) (Saeidi et al 2013), which is the most effective therapy for obesity and T2D (Carlsson et al 2012, Cummings 2012, increases blood GLP2 (by 200%) at postprandial status (le Roux et al 2010). Bariatric surgery normalizes blood glucose concentrations in the majority of T2D humans independent of weight loss (Mingrone et al 2012, Schauer et al 2012) and can induce diabetes remission up to 6 years (Cohen et al 2012).…”

Section: Glp2 and Glycaemic Controlmentioning

confidence: 99%

GLP2: an underestimated signal for improving glycaemic control and insulin sensitivity

Amato¹,

Baldassano²,

Mulè³

2016

Journal of Endocrinology

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Glucagon-like peptide 2 (GLP2) is a proglucagon-derived peptide produced by intestinal enteroendocrine L-cells and by a discrete population of neurons in the brainstem, which projects mainly to the hypothalamus. The main biological actions of GLP2 are related to the regulation of energy absorption and maintenance of mucosal morphology, function and integrity of the intestine; however, recent experimental data suggest that GLP2 exerts beneficial effects on glucose metabolism, especially in conditions related to increased uptake of energy, such as obesity, at least in the animal model. Indeed, mice lacking GLP2 receptor selectively in hypothalamic neurons that express proopiomelanocortin show impaired postprandial glucose tolerance and hepatic insulin resistance (by increased gluconeogenesis). Moreover, GLP2 acts as a beneficial factor for glucose metabolism in mice with high-fat diet-induced obesity. Thus, the aim of this review is to update and summarize current knowledge about the role of GLP2 in the control of glucose homeostasis and to discuss how this molecule could exert protective effects against the onset of related obesity type 2 diabetes.

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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%

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 Hypertrophy After Gastric Bypass Is Associated With Increased Glucagon-Like Peptide 2 and Intestinal Crypt Cell Proliferation

Cited by 155 publications

References 39 publications

Gastrointestinal hormones, energy balance and bariatric surgery

Gastrointestinal hormones, energy balance and bariatric surgery

GLP2: an underestimated signal for improving glycaemic control and insulin sensitivity

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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