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Gastroesophageal reflux disease seems more frequent after laparoscopic sleeve gastrectomy (LSG) than Roux-en-Y gastric bypass (LRYGB). Retrospective case series have raised concerns about a high incidence of Barrett esophagus (BE) after LSG. This prospective clinical cohort study compared the incidence of BE ≥5 years after LSG and LRYGB. St. Clara Hospital, Basel, and University Hospital, Zürich, Switzerland. Patients were recruited from 2 bariatric centers where preoperative gastroscopy is standard practice and LRYGB is preferred for patients with preexisting gastroesophageal reflux disease. At follow-up ≥5 years after surgery, patients underwent gastroscopy with quadrantic biopsies from the squamocolumnar junction and metaplastic segment. Symptoms were assessed using validated questionnaires. Wireless pH measurement assessed esophageal acid exposure. A total of 169 patients were included, with a median 7.0 ± 1.5 years after surgery. In the LSG group (n = 83), 3 patients had endoscopically and histologically confirmed de novo BE; in the LRYGB group (n = 86), there were 2 patients with BE, 1 de novo and 1 preexisting (de novo BE, 3.6% versus 1.2%; P =.362). At follow-up, reflux symptoms were reported more frequently by the LSG group than by the LRYGB group (51.9% versus 10.5%). Similarly, moderate-to-severe reflux esophagitis (Los Angeles grade B–D) was more common (27.7% versus 5.8%) despite greater use of proton pump inhibitors (49.4% versus 19.7%), and pathologic acid exposure was more frequent in patients who underwent LSG than in patients who underwent LRYGB. After at least 5 years of follow-up, a higher incidence of reflux symptoms, reflux esophagitis, and pathologic esophageal acid exposure was found in patients who underwent LSG compared with patients who underwent LRYGB. However, the incidence of BE after LSG was low and not significantly different between the 2 groups. • Gastro-Esophageal Reflux Disease (GERD) is more frequent after LSG than LRYGB. • Retrospective series report a >10% incidence of Barrett Esophagus (BE) after LSG. • Aim: Prospective study to compare the incidence of BE ≥5 years after LSG and LRYGB. • Result: BE incidence after LSG and LRYGB was low (de novo 3.6% vs. 1.2%; P=0.362). • Reflux symptoms, esophagitis and PPI use were more frequent after LSG than LRYGB. • Conclusion: The prevalence of BE after bariatric surgery is low. • Severe GERD is common after LSG and may justify endoscopic surveillance. [ABSTRACT FROM AUTHOR]

Background: Glucose induces the release of gastrointestinal (GI) satiation hormones, such as glucagon-like peptide 1 (GLP-1) and peptide tyrosine tyrosine (PYY), in part via the activation of the gut sweet taste receptor (T1R2/T1R3).Objectives: The primary objective was to investigate the importance of T1R2/T1R3 for the release of cholecystokinin (CCK), GLP-1, and PYY in response to D-allulose and erythritol by assessing the effect of the T1R2/T1R3 antagonist lactisole on these responses and as secondary objectives to study the effect of the T1R2/T1R3 blockade on gastric emptying, appetite-related sensations, and GI symptoms.Methods: In this randomized, controlled, double-blind, crossover study, 18 participants (5 men) with a mean ± SD BMI (in kg/m2) of 21.9 ± 1.7 and aged 24 ± 4 y received an intragastric administration of 25 g D-allulose, 50 g erythritol, or tap water, with or without 450 parts per million (ppm) lactisole, respectively, in 6 different sessions. 13C-sodium acetate was added to all solutions to determine gastric emptying. At fixed time intervals, blood and breath samples were collected, and appetite-related sensations and GI symptoms were assessed. Data were analyzed with linear mixed-model analysis.Results: D-allulose and erythritol induced a significant release of CCK, GLP-1, and PYY compared with tap water (all PHolm < 0.0001, dz >1). Lactisole did not affect the D-allulose- and erythritol-induced release of CCK, GLP-1, and PYY (all PHolm > 0.1). Erythritol significantly delayed gastric emptying, increased fullness, and decreased prospective food consumption compared with tap water (PHolm = 0.0002, dz = -1.05; PHolm = 0.0190, dz = 0.69; and PHolm = 0.0442, dz = -0.62, respectively).Conclusions: D-allulose and erythritol stimulate the secretion of GI satiation hormones in humans. Lactisole had no effect on CCK, GLP-1, and PYY release, indicating that D-allulose- and erythritol-induced GI satiation hormone release is not mediated via T1R2/T1R3 in the gut. [ABSTRACT FROM AUTHOR]

Bariatric surgery is an effective therapeutic procedure for morbidly obese patients. The 2 most common interventions are sleeve gastrectomy (SG) and laparoscopic Roux-en-Y gastric bypass (LRYGB). The aim of this study was to compare microbiome long-term microbiome after SG and LRYGB surgery in obese patients. University Hospital, France; University Hospital, United States; and University Hospital, Switzerland. Eighty-nine and 108 patients who underwent SG and LRYGB, respectively, were recruited. Stools were collected before and 6 months after surgery. Microbial DNA was analyzed with shotgun metagenomic sequencing (SOLiD 5500 xl Wildfire). MSPminer, a novel innovative tool to characterize new in silico biological entities, was used to identify 715 Metagenomic Species Pan-genome. One hundred forty-eight functional modules were analyzed using GOmixer and KEGG database. Both interventions resulted in a similar increase of Shannon's diversity index and gene richness of gut microbiota, in parallel with weight loss, but the changes of microbial composition were different. LRYGB led to higher relative abundance of aero-tolerant bacteria, such as Escherichia coli and buccal species, such as Streptococcus and Veillonella spp. In contrast, anaerobes, such as Clostridium , were more abundant after SG, suggesting better conservation of anaerobic conditions in the gut. Enrichment of Akkermansia muciniphila was also observed after both surgeries. Function-level changes included higher potential for bacterial use of supplements, such as vitamin B12, B1, and iron upon LRYGB. Microbiota changes after bariatric surgery depend on the nature of the intervention. LRYGB induces greater taxonomic and functional changes in gut microbiota than SG. Possible long-term health consequences of these alterations remain to be established. [ABSTRACT FROM AUTHOR]

Background Despite the increasing use of bariatric surgery as the most effective treatment of morbid obesity, there is still no consensus on its preoperative diagnostic workup. The aim of this study was to identify the pathologies of the endoscopic and radiologic investigations before performing bariatric surgery and to evaluate their impact on the patient management. Methods Retrospective analysis of prospectively collected data of 1225 consecutive patients who underwent laparoscopic Roux-en-Y gastric bypass (n = 834) or sleeve gastrectomy (n = 391) at our institution. An abdominal ultrasound was performed in 1188 patients, 1190 patients underwent upper gastrointestinal (GI) endoscopy, 1178 patients underwent upper GI series, and 610 patients underwent esophageal manometry. Setting Private hospital, Switzerland. Results Gallstones were detected in 222 (21.0%) patients, and a synchronous cholecystectomy was performed in 220 (18.0%) patients. The upper GI series indicated hiatal hernias in 325 (27.6%) patients. The most common findings of the upper GI endoscopy were type-C gastritis (224 patients, 18.8%), reflux esophagitis (229 patients, 19.2%), Helicobacter pylori –positive gastritis (158, 13.3%), and hiatal hernia (55 patients, 4.6%). Additionally, we detected 1 Barrett’s high-grade dysplasia, 2 Barrett’s carcinomas, and 1 stomach cancer in asymptomatic patients, who were scheduled to have a sleeve gastrectomy. Esophageal motility disorders were detected in 104 (17.0%) individuals, who underwent esophageal manometry. Conclusions We recommend performing abdominal sonography and upper GI endoscopy before bariatric surgery as they reveal findings, which influence the therapeutic approach. Upper GI series and esophageal manometry help to define patients not suitable for sleeve gastrectomy. [ABSTRACT FROM AUTHOR]

Background: Green tea (Camellia sinensis) is a beverage consumed for thousands of years. Numerous claims about the benefits of its consumption were stated and investigated. As green tea is experiencing a surge in popularity in Western culture and as millions of people all over the world drink it every day, it is relevant to understand its effects on the human brain.Purpose: To assess the current state of knowledge in the literature regarding the effects of green tea or green tea extracts, l-theanine and epigallocatechin gallate both components of green tea-on general neuropsychology, on the sub-category cognition and on brain functions in humans.Methods: We systematically searched on PubMed database and selected studies by predefined eligibility criteria. We then assessed their quality and extracted data. We structured our effort according to the PRISMA statement.Outcome: We reviewed and assessed 21 studies, 4 of which were randomised controlled trials, 12 cross-over studies (both assessed with an adapted version of the DELPHI-list), 4 were cross-sectional studies and one was a cohort study (both assessed with an adapted version of the Newcastle-Ottawa assessment scale). The average study quality as appraised by means of the DELPHI-list was good (8.06/9); the studies evaluated with the Newcastle-Ottawa-scale were also good (6.7/9).Conclusions: The reviewed studies presented evidence that green tea influences psychopathological symptoms (e.g. reduction of anxiety), cognition (e.g. benefits in memory and attention) and brain function (e.g. activation of working memory seen in functional MRI). The effects of green tea cannot be attributed to a single constituent of the beverage. This is exemplified in the finding that beneficial green tea effects on cognition are observed under the combined influence of both caffeine and l-theanine, whereas separate administration of either substance was found to have a lesser impact. [ABSTRACT FROM AUTHOR]

Background After laparoscopic Roux-en-Y gastric bypass (LRYGB), many patients suffer from dumping syndrome. Oral glucose tolerance tests are usually carried out with 50–75 g of glucose. The aim of this study was to examine whether minimal glucose loads of 10 g and 25 g induce a reliable secretion of satiation peptides without dumping symptoms after LRYGB. In addition, lean and obese controls were examined. Objective The objective of this study was to determine the effects of low oral glucose loads on incretin release and gastric emptying. Setting All surgical procedures were performed by the same surgeon (RP) at the St. Claraspital Basel in Switzerland. Oral glucose challenges were carried out at the University Hospital of Basel (Phase 1 Research Unit). Methods Eight patients 10±.4 weeks after LRYGB (PostOP; body mass index [BMI]: 38.6 kg/m 2 ±1.7) as well as 12 lean controls (LC; BMI: 21.8 kg/m 2 ±.6) and 12 obese controls (OC; BMI 38.7 kg/m 2 ±1.3) received 10 g and 25 g of oral glucose. We examined clinical signs of dumping syndrome; plasma glucose, insulin, glucagon-like peptide 1, glucose-dependent insulinotropic peptide, and peptide tyrosine tyrosine concentrations; and gastric emptying with a 13 C-sodium acetate breath test. Results No signs of dumping were seen in PostOP. Compared with OC, LC showed lower fasting glucose, insulin, and C-peptide, and lower homeostasis model assessment (HOMA) and AUC-180 for insulin and C-peptide. In PostOP, fasting insulin, HOMA and AUC-180 for insulin was lower and no difference was found in fasting C-peptide or AUC-180 for C-peptide compared to OC. There was no significant difference in fasting glucose, insulin, C-peptide, HOMA and AUC-180 for insulin in PostOP compared to LC, but AUC-180 for C-peptide was higher in PostOP. AUC-60 for gut hormones was similar in OC and LC and higher in PostOP compared to OC or LC. gastric emptying was slower in LC and OC compared with PostOP. Conclusion After LRYGB, 25 g oral glucose is well tolerated and leads to reliable secretion of gut hormones. Fasting glucose, insulin and C-peptide are normalized, while glucagon-like peptide 1, glucose-dependent insulinotropic peptide and peptide tyrosine tyrosine are overcorrected. Pouch emptying is accelerated after LRYGB. [ABSTRACT FROM AUTHOR]

Background: Exogenous glucagon-like peptide-1 (GLP-1) inhibits eating in healthy, overweight, and diabetic subjects. Objective: The GLP-1 receptor antagonist exendin(9-39)NH2 (ex9-39) was used to further explore the role of GLP-1 as an endogenous satiation signal. Design: Two double-blind, 4-way crossover studies were performed, each of which included 10 healthy men. In study A, subjects received an intravenous infusion of ex9-39 or saline plus an oral glucose preload and an intraduodenal infusion of saline or glucose for 60 min. In study B, intravenous infusions were identical, but an oral mixed-liquid meal preload and a 60-min intraduodenal infusion of saline or oleic acid were administered. Thirty minutes after oral preloads, subjects ate and drank ad libitum, and amounts ingested and the time to meal completion were quantified. In addition, appetite and plasma GLP-1, peptide YY (PYY), insulin, glucagon, and blood glucose concentrations were measured. Results: In both studies, GLP-1, PYY, and glucagon were substantially higher with intravenous ex9-39 than with intravenous saline (P ≤ 0.001). Insulin was lower with intravenous ex9-39 during intraduodenal glucose (P ≤ 0.05). The decrease in prospective food consumption and desire to eat during ad libitum eating after glucose ingestion was slightly attenuated (P ≤ 0.05 and P ≤ 0.01, respectively) with ex9-39. However, with intravenous ex9-39, food and fluid intakes and eating duration were not changed in either study. Conclusions: GLP-1 receptor antagonism slightly modulates appetite during ad libitum eating, but food and fluid intakes and meal duration remain unchanged, suggesting that endogenous GLP-1 is a weak satiation signal. However, concomitant substantial increases in plasma PYY and glucagon may counteract a desatiating effect of ex9-39. The effect of ex9-39 on PYY secretion supports an auto-inhibitory feedback mechanism that controls L cell secretion; the effect on insulin and glucagon confirms the role of GLP-1 in glycemic control through its action on pancreatic α and β cells. This trial was registered at clinicaltrials.gov as NCT01900340. [ABSTRACT FROM AUTHOR]

Background: In patients undergoing routine upper EGD, propofol is increasingly used without pharyngeal anesthesia because of its excellent sedative properties. It is unclear whether this practice is non-inferior in regard to ease of endoscopic intubation and patient comfort. Objective: To assess the relevance of local pharyngeal anesthesia regarding the ease of EGD performance in patients sedated with propofol as monotherapy. Design: Randomized, double-blind, placebo-controlled, non-inferiority trial. Setting: One community hospital and one university hospital in Switzerland. Patients: We enrolled 300 consecutive adult patients undergoing elective EGD. Intervention: Pharyngeal anesthesia with 4 squirts of lidocaine spray versus placebo spray immediately before propofol sedation. Main Outcome Measurements: Number of gag reflexes (primary endpoint), number of intubation attempts, and degree of salivation during intubation (secondary endpoints) assessed by the endoscopists and staff. Results: In the lidocaine group, 122 patients (82%) had no gag events, and 25 patients had a total of 39 gag events, whereas in the placebo group 104 patients (71%) had no gag events, and 43 patients had a total of 111 gag events. The rate ratio of gagging with quasi-likelihood estimation of placebo compared with lidocaine was 2.85 (95% confidence interval [CI], 1.42-6.19; P = .005). In adjusted logistic regression analysis, the odds ratio for gagging for placebo pharyngeal anesthesia compared with lidocaine was 1.9 (95% CI, 1.03-3.54). The number of intubation attempts and the degree of salivation were similar in both groups. Two patients in the placebo group experienced oxygen desaturation and needed short-term mask ventilation. Limitations: The level of sedation and possible long-term side effects of pharyngeal anesthesia were not assessed. Conclusion: Topical pharyngeal anesthesia reduces the gag reflex in patients sedated with propofol even though it does not seem to have an influence on the ease of the procedure and on patient or endoscopist satisfaction in adequately sedated patients. (Clinical trial registration number: NCT01081002.) [Copyright &y& Elsevier]

Abstract: The chemical environment of the intestinal lumen and the presence of nutrients in the gut result in the secretion of regulatory peptides and in the discharge of intestinal sensory afferent fibers. Since afferent nerve terminals do not directly extend into the intestinal lumen, their activation presumably depends on intermediary steps — post-absorptive mechanisms, i.e. direct neuronal activation by absorbed substances and pre-absorptive mechanisms, i.e. neuronal activation by a secondary substance released from the mucosal epithelium. Entero-endocrine cells (EEC) are able to ‘taste’ the luminal content and to function as chemosensory transducers to provide the interface between the intestinal lumen and the afferent nerve terminals. Their secretory products – mainly peptide hormones – are released upon stimulation by nutrients into the extracellular space of the lamina propria to either act 1) locally in a paracrine fashion to activate afferent terminals or other cells or 2) in an endocrine fashion via intestinal capillaries and the lymphatic system to bind to specific receptors at more distant targets. The chemosensory mechanisms by which EEC sense the intestinal lumen remain, however, poorly understood. Recent information suggest that taste signaling mechanisms known from the oral epithelium also operate in the mucosal epithelium. Several nutrient-responsive G-protein coupled receptors (GPCRs) have been identified in EEC including the sweet-taste responsive T1R2/T1R3 heterodimer or GPR120, responsive to free fatty acids (FFAs). This review provides a brief overview on gastrointestinal chemosensory mechanisms and their functional involvement in the secretion of satiation peptides with a focus on human studies albeit most evidence at present comes from in vitro or animal studies. [Copyright &y& Elsevier]

Abstract: Background: Laparoscopic Roux-en-Y gastric bypass (LRYGB) and laparoscopic sleeve gastrectomy (LSG) lead to rapid improvement in insulin sensitivity even before weight loss occurs. Adipokines are closely linked to obesity and insulin resistance. To date, it is unclear whether the different anatomic changes of the various bariatric procedures have different effects on hormones of adipocyte origin. In the present prospective, randomized study, we compared the 1-year follow-up results of LRYGB and LSG concerning weight loss, metabolic control, and fasting adipokine levels. Methods: Of 23 nondiabetic morbidly obese patients, 12 were randomized to LRYGB and 11 to LSG. The patients were investigated before and 1 week, 3 months, and 12 months after surgery. The fasting levels of glucose, insulin, lipids, and adipokines (leptin, adiponectin, and fibroblast growth factor-21) were analyzed. Results: The body weight decreased markedly (P <.001) after either procedure (percentage of weight loss 16.4% ± 1.3%, 24.8% ± 1.7%, and 34.5% ± 2.7% after LRYGB and 13.1% ± 1.1%, 20.7% ± 1.5%, and 27.9% ± 2.6% after LSG at 2, 6, and 12 mo, respectively). The Homeostasis Model Assessment Index declined from 8.0 ± 1.5 preoperatively to 2.9 ± .2 at 12 months after LRYGB and from 7.5 ± 1.7 preoperatively to 3.3 ± .3 at 12 months after LSG. The lipid profiles were normalized. The concentrations of circulating leptin levels decreased by almost 50% as early as 1 week postoperatively and continued to decrease until 12 months postoperatively. Adiponectin increased progressively. The fibroblast growth factor-21 levels did not change over time. No difference was found between the LRYGB and LSG groups. Conclusion: Both procedures led to significant weight loss associated with the resolution of the metabolic syndrome. The serum leptin levels decreased and adiponectin increased with weight loss, paralleled by improved insulin sensitivity. [Copyright &y& Elsevier]

Background & Aims: Endoscopist-directed propofol sedation (EDP) remains controversial. We sought to update the safety experience of EDP and estimate the cost of using anesthesia specialists for endoscopic sedation. Methods: We reviewed all published work using EDP. We contacted all endoscopists performing EDP for endoscopy that we were aware of to obtain their safety experience. These complications were available in all patients: endotracheal intubations, permanent neurologic injuries, and death. Results: A total of 646,080 (223,656 published and 422,424 unpublished) EDP cases were identified. Endotracheal intubations, permanent neurologic injuries, and deaths were 11, 0, and 4, respectively. Deaths occurred in 2 patients with pancreatic cancer, a severely handicapped patient with mental retardation, and a patient with severe cardiomyopathy. The overall number of cases requiring mask ventilation was 489 (0.1%) of 569,220 cases with data available. For sites specifying mask ventilation risk by procedure type, 185 (0.1%) of 185,245 patients and 20 (0.01%) of 142,863 patients required mask ventilation during their esophagogastroduodenoscopy or colonoscopy, respectively (P < .001). The estimated cost per life-year saved to substitute anesthesia specialists in these cases, assuming they would have prevented all deaths, was $5.3 million. Conclusions: EDP thus far has a lower mortality rate than that in published data on endoscopist-delivered benzodiazepines and opioids and a comparable rate to that in published data on general anesthesia by anesthesiologists. In the cases described here, use of anesthesia specialists to deliver propofol would have had high costs relative to any potential benefit. [Copyright &y& Elsevier]

Background & Aims: We investigated Helicobacter pylori (H pylori)-infection as a cause of iron deficiency (ID) and iron-deficiency anemia (IDA) or treatment failure of iron supplementation. Methods: We randomized 200 Hp-infected children (positive urea breath test) 2–5 years of age with IDA (hemoglobin level <110 g/L; serum ferritin level <12 μg/L; and soluble transferrin receptor >8.3 mg/L) or ID (serum ferritin level <12 μg/L or soluble transferrin receptor level >8.3 mg/L) to 1 of 4 regimens: 2-week anti-Hp therapy (amoxicillin, clarithromycin, and omeprazole) plus 90-day oral ferrous sulfate (anti-Hp plus iron), 2-week anti-Hp therapy alone, 90-day oral iron alone, or placebo. Sixty noninfected children with IDA received iron treatment as negative control. Results: Hp-infected children receiving iron had significantly less frequent treatment failure compared with those with no iron in correcting IDA (11% [95% confidence interval (CI), 2%–20%] for anti-Hp plus iron, 0% for iron alone vs 33% [95% CI, 26%–46%] for anti-Hp and 45% [95% CI, 31%–59%] for placebo; χ2 = 127; P < .0001), ID (19% [95% CI, 8%–30%] for anti-Hp plus iron, 7% [95% CI, 0%–14%] for iron alone vs 65% [95% CI, 52%–78%] for anti-Hp alone, and 78% [95% CI, 66%–90%] for placebo; χ2 = 124; P < .0001), or anemia (34% [95% CI, 20%–40%] for anti-Hp plus iron, 27% [95% CI, 14%–40%] for iron alone vs 65% [95% CI, 52%–78%] for anti-Hp alone and 78% [95% CI, 66%–90%] for placebo; χ2 = 46; P < .0001). Cure rates of IDA, ID, or anemia with iron were comparable with that of the negative control group. Improvements in iron status also were significantly greater in groups with iron. Conclusions: H pylori is neither a cause of IDA/ID nor a reason for treatment failure of iron supplementation in young Bangladeshi children. [Copyright &y& Elsevier]

More than 95% of malignant tumours of the pancreas are exocrine carcinomas. The exocrine carcinomas have to be distinguished from benign serous cystadenomas and tumours, the latter including mucinous cystic neoplasms, serous cysts, and solid pseudopapillary neoplasms. Cystic lesions have to be separated from pseudocysts, which are the most common cysts. Pseudocysts are due to extensive confluent autodigestive tissue necrosis caused by alcoholic, biliary, or traumatic acute pancreatitis. This review focuses on the classification of the different types of solid and cystic lesions based on histological criteria. The various imaging procedures are also discussed, along with their strengths and limitations. [Copyright &y& Elsevier]

Abstract: The present review summarizes the appetite suppressing effects of PYY and GLP-1 in the regulation of food intake in humans. Current evidence supports a role for gastrointestinal peptides as regulators of satiety. The regulation of satiety is, however, complex and it is not surprising that multiple control systems exist. It is interesting to note that nutrients in the small intestine such as hydrolysis products of fat stimulate the release of satiety peptides such as GLP-1 or PYY that serve as satiety signals. Both peptides, released from L-cells from the gastrointestinal tract by the local action of digested food, exert various regulatory functions: stimulation of insulin secretion and inhibition of glucagon secretion as typical actions of GLP-1, inhibition of gastric emptying, and inhibition of appetite for both GLP-1 and PYY. The review focuses on the question, whether the two peptides are true endocrine factors that act as physiologic, hormonal regulators of appetite. [Copyright &y& Elsevier]

The pancreas plays a major role in nutrient digestion. Therefore, in both acute and chronic pancreatitis, exocrine and endocrine pancreatic insufficiency can develop, impairing digestive and absorptive processes. These changes can lead to malnutrition over time. In parallel to these changes, decreased caloric intake and increased metabolic activity are often present. Nutritional deficiencies negatively affect outcome if they are not treated. Nutritional assessment and the clinical severity of the disease are important for planning any nutritional intervention. In severe acute pancreatitis, enteral nutrition with a naso-jejunal feeding tube and a low molecular diet displays clear advantages compared to parenteral nutrition. Infectious complications, length of hospital stay and the need for surgery are reduced. Furthermore, enteral nutrition is less costly than parenteral nutrition. Parenteral nutrition is reserved for patients who do not tolerate enteral nutrition. Abstinence from alcohol, dietary modifications and pancreatic enzyme supplementation is sufficient in over 80% of patients with chronic pancreatitis. In addition, oral supplements are helpful. Enteral nutrition can be necessary if weight loss continues. Parenteral nutrition is very seldom used in patients with chronic pancreatitis. [Copyright &y& Elsevier]

Background & Aims: Studies in animals and humans suggest a role for peptide YY (PYY3–36) in regulating satiety. The physiologic role of PYY3–36, however, has not been investigated in detail. Methods: The present study was designed to examine PYY release in response to 2 meals differing in their calorie content and to relate the plasma levels to those obtained after exogenous infusion. In a second step, the effect of graded intravenous doses (0, 0.2, 0.4, and 0.8 pmol·kg−1 ·min−1) of synthetic human PYY3–36 on food intake was investigated in healthy male volunteers in a double-blind, placebo-controlled fashion. Results: Plasma PYY concentrations increased in response to food intake reflecting the size of the calorie load. Graded PYY3–36 infusions resulted in a dose-dependent reduction in food intake (maximal inhibition, 35%; P < .001 vs control) and a similar reduction in calorie intake (32%; P < .001). Fluid ingestion was also reduced by PYY (18% reduction; P < .01). Nausea and fullness were the most common side effects produced by PYY, especially at the highest dose. Furthermore, subjects experienced less hunger and early fullness in the premeal period during PYY3–36 infusion at the highest dose (P < .05). Conclusions: This study shows that intravenous infusions of PYY3–36 decrease spontaneous food intake; the inhibition is, however, only significant at pharmacologic plasma concentrations. Whether PYY3–36 has a physiologic role in the regulation of satiety in humans remains to be defined. [Copyright &y& Elsevier]

Abstract: The present review summarizes the appetite-suppressing effects of intestinal fat in the regulation of food intake in humans, with a special focus on the role of cholecystokinin (CCK). Current evidence supports a role for intestinal fat (especially long-chain free fatty acids) acting via the peptide CCK as a physiological satiety pathway. The regulation of satiety is, however, complex and it is not surprising that multiple control systems exist. It is interesting to note that nutrients, such as hydrolysis products of fat in the small intestine, stimulate the release of satiety peptides, such as CCK or PYY, that serve as satiety signals. CCK, released from the gastrointestinal tract by the local action of digested food, exerts various functions: stimulation of gallbladder contraction and exocrine pancreatic secretion, inhibition of gastric emptying, and inhibition of appetite. CCK functions therefore (1) as a positive feedback signal to stimulate digestive processes and (2) as negative feedback signal to limit the amount of food consumed during an individual meal. [Copyright &y& Elsevier]

Mainly because of the loss of reservoir function, loss of sphincter function, and exclusion of the duodenal route, patients who undergo gastrectomy suffer from many adverse effects postoperatively. The ileocecal interpositional graft is an attractive method to use as a gastric substitute after gastrectomy and distal esophagectomy. A pedunculated ileocecal graft is placed between the esophagus and the duodenum. The cecum acts as a reservoir while the ileocecal valve protects against enteroesophageal reflux. The duodenal passage is also preserved. Fourteen patients underwent this operation. The technique-related morbidity was low and the quality of life was good. During a mean follow-up of 6 months, no evidence of severe dumping syndrome or reflux esophagitis was observed. Further prospective randomized studies are warranted to compare this technique with the standard methods of gastric reconstruction. [ABSTRACT FROM AUTHOR]

Abstract: New revelations that have revitalized obesity-related research using a peripheral approach prompted us to organize a workshop titled “The intestinal wall – THE regulatory interface in energy homeostasis,” which was held June 20–25, 2010, in Ascona, Switzerland, at the Centro Stefano Franscini of the Swiss Federal Institute of Technology (ETH). Throughout an exciting week of seminars and discussions, the workshop brought together around 70 expert researchers and clinicians from around the world who attempted to evaluate and integrate many important aspects of the role of the digestive tract in the regulation of energy homeostasis at the molecular, cellular, and systemic levels, as well as the implications for the prevention or treatment of obesity. [Copyright &y& Elsevier]

Probiotics are suggested to improve depressive symptoms via the microbiota-gut-brain axis. We have recently shown a beneficial clinical effect of probiotic supplementation in patients with depression. Their underlying neural mechanisms remain unknown. A multimodal neuroimaging approach including diffusion tensor imaging, resting-state functional MRI, and arterial spin labeling was used to investigate the effects of a four-weeks probiotic supplementation on fronto-limbic brain structure, function, and perfusion and whether these effects were related to symptom changes. Thirty-two patients completed both imaging assessments (18 placebo and 14 probiotics group). Probiotics maintained mean diffusivity in the left uncinate fasciculus, stabilized it in the right uncinate fasciculus, and altered resting-state functional connectivity (rsFC) between limbic structures and the temporal pole to a cluster in the precuneus. Moreover, a cluster in the left superior parietal lobule showed altered rsFC to the subcallosal cortex, the left orbitofrontal cortex, and limbic structures after probiotics. In the probiotics group, structural and functional changes were partly related to decreases in depressive symptoms. This study has a rather small sample size. An additional follow-up MRI session would be interesting for seeing clearer changes in the relevant brain regions as clinical effects were strongest in the follow-up. Probiotic supplementation is suggested to prevent neuronal degeneration along the uncinate fasciculus and alter fronto-limbic rsFC, effects that are partly related to the improvement of depressive symptoms. Elucidating the neural mechanisms underlying probiotics' clinical effects on depression provide potential targets for the development of more precise probiotic treatments. • Probiotic add-on intervention improved depressive symptoms in patients. • However, underlying neural mechanisms still remain unknown. • Probiotics impact fronto-limbic structure and function. • These brain changes are partly associated with clinical improvements. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article regarding the 20-year prospective, population-based study on the increasing incidence of eosinophilic esophagitis in Olten County, Switzerland.

Backround & Aims: Topical corticosteroids are effective in inducing clinical and histologic remission in patients with eosinophilic esophagitis (EoE). However, the best long-term management strategy for this chronic inflammatory disease has not been determined. Methods: In a randomized, double-blind, placebo-controlled, 50-week trial, we evaluated in 28 patients the efficacy of twice-daily swallowed budesonide (0.25 mg each) to maintain quiescent EoE in remission. Pretreatment and posttreatment activity was assessed clinically, endoscopically, histologically, immunohistologically, and by endosonography. The primary end point was the therapy''s ability to maintain EoE in histologic remission. Secondary end points were efficacy in symptom control, prevention of tissue remodeling, and safety. Results: In patients given low-dose budesonide, the load of esophageal eosinophils increased from 0.4 to 31.8 eosinophils/high-power field (P = .017). In patients given placebo, the load increased from 0.7 to 65.0 eosinophils/high-power field (P = .0001); this increase was significantly greater than in patients given budesonide (P = .024). The symptom scores developed in a similar manner in the 2 groups. Budesonide, but not placebo, reduced noneosinophilic markers of inflammation, epithelial cell apoptosis, and remodeling events. Compared with control individuals, patients had significantly thickened esophageal walls, based on endosonography (3.05 vs 2.18 mm; P < .0001). Budesonide therapy was associated with a significant reduction in mucosal thickness (0.75–0.45 mm; P = .025), but epithelial thickness remained stable (261.22 vs 277.23 μm; P = .576). No serious adverse events occurred. Conclusions: Low-dose budesonide is more effective than placebo in maintaining EoE in histologic and clinical remission. Signs of esophageal remodeling showed a trend toward normalization. Long-term administration of topical corticosteroids was well tolerated without induction of epithelial atrophy. [Copyright &y& Elsevier]

Background & Aims: Eosinophilic esophagitis (EoE) is a chronic inflammatory disease of the esophagus characterized by dense tissue eosinophilia; it is refractory to proton pump inhibitor therapy. EoE affects all age groups but most frequently individuals between 20 and 50 years of age. Topical corticosteroids are effective in pediatric patients with EoE, but no controlled studies of corticosteroids have been reported in adult patients. Methods: We performed a randomized, double-blind, placebo-controlled trial to evaluate the effect of oral budesonide (1 mg twice daily for 15 days) in adolescent and adult patients with active EoE. Pretreatment and posttreatment disease activity was assessed clinically, endoscopically, and histologically. The primary end point was reduced mean numbers of eosinophils in the esophageal epithelium (number per high-power field [hpf] = esophageal eosinophil load). Esophageal biopsy and blood samples were analyzed using immunofluorescence and immunoassays, respectively, for biomarkers of inflammation and treatment response. Results: A 15-day course of therapy significantly decreased the number of eosinophils in the esophageal epithelium in patients given budesonide (from 68.2 to 5.5 eosinophils/hpf; P < .0001) but not in the placebo group (from 62.3 to 56.5 eosinophils/hpf; P = .48). Dysphagia scores significantly improved among patients given budesonide compared with those given placebo (5.61 vs 2.22; P < .0001). White exudates and red furrows were reversed in patients given budesonide, based on endoscopy examination. Budesonide, but not placebo, also reduced apoptosis of epithelial cells and molecular remodeling events in the esophagus; no serious adverse events were observed. Conclusions: A 15-day course of treatment with budesonide is well tolerated and highly effective in inducing a histologic and clinical remission in adolescent and adult patients with active EoE. [ABSTRACT FROM AUTHOR]