Rectal epithelial cell mitosis and expression of macrophage migration inhibitory factor are increased 3 years after Roux-en-Y gastric bypass (RYGB) for morbid obesity: implications for long-term neoplastic risk following RYGB

Kant, Prashant; Sainsbury, A; Reed, Karen Ruth; Pollard, S.; Scott, Nigel; Clarke, Alan R.; Coletta, P. Louise; Hull, Mark A.

doi:10.1136/gut.2010.230755

Cited by 46 publications

(36 citation statements)

References 32 publications

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“…However, no compelling evidence for such a link has emerged from clinical use of bariatric surgery in humans during the past w50 years. Kant et al (2011) 40-fold increase in protumorigenic cytokine MIF level following RYGB and raised the question of colorectal neoplastic risk. Long-term clinical studies of neoplastic risk following RYGB are needed to reconcile or resolve observations and controversies along this line.…”

Section: Discussionmentioning

confidence: 99%

Pancreatic hyperplasia after gastric bypass surgery in a GK rat model of non-obese type 2 diabetes

Zhou

Qian

et al. 2015

Journal of Endocrinology

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Gastric bypass surgery produces clear antidiabetic effects in a substantial proportion of morbidly obese patients. In view of the recent trend away from 'bariatric' surgery and toward 'metabolic' surgery, it is important to elucidate the enhancing effect of bypass surgery on pancreatic b-cell mass, which is related to diabetes remission in non-obese patients. We investigated the effects of gastric bypass surgery on glycemic control and other pancreatic changes in a spontaneous non-obese type 2 diabetes Goto-Kakizaki rat model. Significant improvements in postprandial hyperglycemia and plasma c-peptide level were observed when glucose was administered orally post-surgery. Other important events observed after surgery were enhanced first phase insulin secretion in a in site pancreatic perfusion experiment, pancreatic hyperplasia, improved islet structure (revealed by immunohistochemical analysis), striking increase in b-cell mass, slight increase in ratio of b-cell area to total pancreas area, and increased number of small islets closely related to exocrine ducts. No notable changes were observed in ratio of b-cell to non-b endocrine cell area, b-cell apoptosis, or b-cell proliferation. These findings demonstrate that gastric bypass surgery in this rat model increases endocrine cells and pancreatic hyperplasia, and reflect the important role of the gastrointestinal system in regulation of metabolism. Key Words" type 2 diabetes mellitus " gastric bypass surgery

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Section: Discussionmentioning

confidence: 99%

Pancreatic hyperplasia after gastric bypass surgery in a GK rat model of non-obese type 2 diabetes

Zhou

Qian

et al. 2015

Journal of Endocrinology

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“…The colon does not seem the most likely location for the increased calprotectin excretion, as its anatomy is not altered in RYGB. However, there are persistent pro-inflammatory changes in the rectum after RYGB [31]. It is possible that the elevation of fecal calprotectin is a sign of low-grade colonic inflammation, in line with these findings.…”

Section: Discussionmentioning

confidence: 91%

Fecal Calprotectin, Elastase, and Alpha-1-Antitrypsin Levels After Roux-en-Y Gastric Bypass; Calprotectin Is Significantly Elevated in the Majority of Patients

et al. 2016

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BackgroundRoux-en-Y gastric bypass (RYGB) causes several alterations in gastrointestinal function. We hypothesized that levels of three commonly used fecal tests change after RYGB.MethodsFecal levels of calprotectin, elastase, and alpha-1-antitrypsin were determined in 122 patients without signs of gastrointestinal disease 1 to 2 years after RYGB. Medians, distribution of values, and the percentage of patients with levels above or below reference values were determined.ResultsMedian fecal calprotectin level was 163.5 (<30–1587) μg/g; in 87 % of patients, it was above the reference value (<50 μg/g). Median fecal elastase level was 444 (<15–647) μg/g; 13 % was below the reference value (>200 μg/g). Median fecal alpha-1-antitrypsin level was 0.51 (<0.20–2.20) mg/g, comparable to the reference values.ConclusionsFecal calprotectin levels are significantly higher than the reference value in most patients after RYGB. Fecal elastase is significantly lower. This might indicate that the validity of fecal calprotectin testing is impaired after RYGB and the specificity for fecal elastase is decreased. Clinical awareness of altered fecal markers after RYGB is essential to prevent unnecessary diagnostic tests, such as colonoscopy. Fecal alpha-1-antitrypsin is not influenced by RYGB.

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“…Some authors 16 point out that it is hard to understand how cancer risk could be increased when restrictive procedures were performed since the anatomical or absorptive function of the gastrointestinal tract remained untouched. However, rectal mucosal hyperproliferation persists at least 3 years after Roux-en-Y gastric bypass, which has been associated with increased mucosal expression of the protumorigenic cytokine macrophage migration inhibitory factor, 17 and recent studies have also stated alterations in the intestinal microbiota and an increased mucosal bile salt exposure, 18 both implicated in long-term neoplastic risk. Moreover, the effect of postsurgical neurohormonal modulation may also play a role.…”

Section: Discussionmentioning

confidence: 99%

Does bariatric surgery reduce cancer risk? A review of the literature

Maestro

Rigla

Caixàs

2015

Endocrinología y Nutrición

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Rectal epithelial cell mitosis and expression of macrophage migration inhibitory factor are increased 3 years after Roux-en-Y gastric bypass (RYGB) for morbid obesity: implications for long-term neoplastic risk following RYGB

Cited by 46 publications

References 32 publications

Pancreatic hyperplasia after gastric bypass surgery in a GK rat model of non-obese type 2 diabetes

Pancreatic hyperplasia after gastric bypass surgery in a GK rat model of non-obese type 2 diabetes

Fecal Calprotectin, Elastase, and Alpha-1-Antitrypsin Levels After Roux-en-Y Gastric Bypass; Calprotectin Is Significantly Elevated in the Majority of Patients

Does bariatric surgery reduce cancer risk? A review of the literature

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