Duodenal Pressure Research Articles

Multicenter study comparing EUS-guided hepaticogastrostomy and ERCP for malignant biliary obstruction in patients with accessible papillae.

One advantage of endoscopic ultrasound-guided hepaticogastrostomy (EUS-HGS) is that it is difficult for reflux cholangitis, caused by duodenal pressure increasing due to duodenal obstruction, to occur. In addition, since stent deployment is performed away from the malignant stricture site, longer stent patency than with endoscopic retrograde cholangiopancreatography (ERCP) may be obtained. However, no study has previously compared EUS-HGS and ERCP for patients without duodenal obstruction or surgically altered anatomy. The aim of the present study was to compare clinical outcomes between EUS-HGS and ERCP in normal anatomy patients without duodenal obstruction. In the ERCP group, patients who initially underwent biliary drainage were included. In the EUS-HGS group, patients who underwent EUS-HGS due to failed biliary cannulation were included. Patients with an inaccessible papilla, such as with surgically altered anatomy or duodenal obstruction, were excluded. A total of 314 patients who underwent ERCP and EUS-HGS were enrolled in this study. Of the 314 patients, 289 underwent biliary stenting under ERCP guidance, and 25 patients underwent biliary stenting under EUS-HGS. After propensity score-matching analysis, the adverse event rate tended to be lower in the EUS-HGS group than in the ERCP group. Although overall survival was not significantly different between the EUS-HGS and ERCP groups (p = .228), stent patency was significantly longer in the EUS-HGS group (median 366.0 days) than in the ERCP group (median 76.5 days). EUS-HGS had a lower adverse event rate, shorter procedure time, and longer stent patency than ERCP in cases of normal anatomy without duodenal obstruction.

The herbal preparation, STW5-II, reduces proximal gastric tone and stimulates antral pressures in healthy humans.

The herbal preparation, STW5-II, improves upper gastrointestinal symptoms, including abdominal fullness, early satiation, and epigastric pain, in patients with functional dyspepsia, and in preclinical models decreases fundic tone and increases antral contractility. The effects of STW5-II on esophago-gastric junction pressure, proximal gastric tone and antropyloroduodenal pressures, disturbances of which may contribute to symptoms associated with disorders of gut-brain interaction, including functional dyspepsia, in humans, have, hitherto, not been evaluated. STW5-II or placebo (matched for color, aroma, and alcohol content) were each administered orally, at the recommended dose (20 drops), to healthy male and female volunteers (age: 27 ± 1 years) in a double-blind, randomized fashion, on two separate occasions, separated by 3-7 days, to evaluate effects on (i) esophago-gastric junction pressures following a standardized meal using solid-state high-resolution manometry (part 1, n = 16), (ii) proximal gastric volume using a barostat (part 2, n = 16), and (iii) antropyloroduodenal pressures assessed by high-resolution manometry (part 3, n = 18), for 120 min (part 1) or 180 min (parts 2, 3). STW5-II increased maximum intrabag volume (ml; STW5-II: 340 ± 38, placebo: 251 ± 30; p = 0.007) and intrabag volume between t = 120 and 180 min (p = 0.011), and the motility index of antral pressure waves between t = 60 and 120 min (p = 0.032), but had no effect on esophago-gastric junction, pyloric, or duodenal pressures. STW5-II has marked region-specific effects on gastric motility in humans, which may contribute to its therapeutic efficacy in functional dyspepsia.

SmartPill™ Administration to Assess Gastrointestinal Function after Spinal Cord Injury in a Porcine Model-A Preliminary Study.

Gastrointestinal (GI) complications, including motility disorders, metabolic deficiencies, and changes in gut microbiota following spinal cord injury (SCI), are associated with poor outcomes. After SCI, the autonomic nervous system becomes unbalanced below the level of injury and can lead to severe GI dysfunction. The SmartPill™ is a non-invasive capsule that, when ingested, transmits pH, temperature, and pressure readings that can be used to assess effects in GI function post-injury. Our minipig model allows us to assess these post-injury changes to optimize interventions and ultimately improve GI function. The aim of this study was to compare pre-injury to post-injury transit times, pH, and pressures in sections of GI tract by utilizing the SmartPill™ in three pigs after SCI at 2 and 6 weeks. Tributyrin was administered to two pigs to assess the influences on their gut microenvironment. We observed prolonged GET (Gastric Emptying Time) and CTT (Colon Transit Time), decreases in contraction frequencies (Con freq) in the antrum of the stomach, colon, and decreases in duodenal pressures post-injury. We noted increases in Sum amp generated at 2 weeks post-injury in the colon, with corresponding decreases in Con freq. We found transient changes in pH in the colon and small intestine at 2 weeks post-injury, with minimal effect on stomach pH post-injury. Prolonged GETs and CTTs can influence the absorptive profile in the gut and contribute to pathology development. This is the first pilot study to administer the SmartPill™ in minipigs in the context of SCI. Further investigations will elucidate these trends and characterize post-SCI GI function.

Effects of intraduodenal or intragastric administration of a bitter hop extract (Humulus lupulus L.), on upper gut motility, gut hormone secretion and energy intake in healthy-weight men

Gastrointestinal functions, particularly pyloric motility and the gut hormones, cholecystokinin and peptide YY, contribute to the regulation of acute energy intake. Bitter tastants modulate these functions, but may, in higher doses, induce GI symptoms. The aim of this study was to evaluate the effects of both dose and delivery location of a bitter hop extract (BHE) on antropyloroduodenal pressures, plasma cholecystokinin and peptide YY, appetite perceptions, gastrointestinal symptoms and energy intake in healthy-weight men. The study consisted of two consecutive parts, with part A including n = 15, and part B n = 11, healthy, lean men (BMI 22.6 ± 1.1 kg/m2, aged 25 ± 3 years). In randomised, double-blind fashion, participants received in part A, BHE in doses of either 100 mg (“ID-BHE-100”) or 250 mg (“ID-BHE-250”), or vehicle (canola oil; “ID-control”) intraduodenally, or in part B, 250 mg BHE (“IG-BHE-250”) or vehicle (“IG-control”) intragastrically. Antropyloroduodenal pressures, hormones, appetite and symptoms were measured for 180 min, energy intake from a standardised buffet-meal was quantified subsequently. ID-BHE-250, but not ID-BHE-100, had modest, and transient, effects to stimulate pyloric pressures during the first 90 min (P < 0.05), and peptide YY from t = 60 min (P < 0.05), but did not affect antral or duodenal pressures, cholecystokinin, appetite, gastrointestinal symptoms or energy intake. IG-BHE-250 had no detectable effects. In conclusion, BHE, when administered intraduodenally, in the selected higher dose, modestly affected some appetite-related gastrointestinal functions, but had no detectable effects when given in the lower dose or intragastrically. Thus, BHE, at none of the doses or routes of administration tested, has appetite- or energy intake-suppressant effects.

A surprising culprit for delayed gastrointestinal bleeding after endoscopic ultrasound-guided cholecystoduodenostomy: the double-pigtail stent.

Endoscopic ultrasound-guided gallbladder drainage using a lumen-apposing metal stent has emerged as an accepted option for the treatment of acute cholecystitis in patients unfit for surgery. While metal stents carry a risk of intra- and post-procedural bleeding, the coaxial placement of a double-pigtail stents through lumen-apposing metal stents has been proposed to lower the bleeding risk by preventing tissue abrasion against the stent flanges. We present a case of an 83year-old male who had previously undergone uncomplicated endoscopic ultrasound-guided cholecystoduodenostomy with this technique. Six months later, he presented with upper gastrointestinal bleeding due to a duodenal pressure ulcer from the coaxial 10-Fr double-pigtail stent originally employed to prevent such bleeding. The 10-Fr stent was replaced with two 7-Fr stents whose increased flexibility and distribution of pressure across multiple points of contact with the duodenal wall was theorized to reduce the likelihood of erosion or perforation. Following the procedure, the patient's clinical course improved significantly with complete resolution of his symptoms of choledocholithiasis and cholecystitis. While 10-Fr double-pigtail stents are generally preferred for this indication due to their stiffness that reduces out-migration, use of more flexible 7-Fr stents may be advisable in thin-walled structures such as the duodenum.

Effect of oat β-glucan of different molecular weights on fecal bile acids, urine metabolites and pressure in the digestive tract – A human cross over trial

While the development of oat products often requires altered molecular weight (MW) of β-glucan, the resulting health implications are currently unclear. This 3-leg crossover trial (n = 14) investigated the effects of the consumption of oat bran with High, Medium and Low MW β-glucan (average > 1000, 524 and 82 kDa respectively) with 3 consequent meals on oat-derived phenolic compounds in urine (UHPLC-MS/MS), bile acids in feces (UHPLC-QTOF), gastrointestinal conditions (ingestible capsule), and perceived gut well-being. Urine excretion of ferulic acid was higher (p < 0.001, p < 0.001), and the fecal excretion of deoxycholic (p < 0.03, p < 0.02) and chenodeoxycholic (p < 0.06, p < 0.02) acids lower after consumption of Low MW β-glucan compared with both Medium and High MW β-glucan. Duodenal pressure was higher after consumption of High MW β-glucan compared to Medium (p < 0.041) and Low (p < 0.022) MW β-glucan. The MW of β-glucan did not affect gut well-being, but the perceptions between females and males differed.

2731 Duodenal Pressure Ulcer Secondary to Migratory PEG Tube

INTRODUCTION: Percutaneous endoscopic gastrostomy (PEG) tubes allow for long-term nutritional support in patients with preserved gastrointestinal function and dysphagia. The procedure and long-term presence of a PEG tube is well tolerated, with a complication rate of 0.4% to 4.4%. Adverse events include infection, skin breakdown, and aspiration. Upper GI bleeding, secondary to gastric or duodenal pressure ulcers is a rare complication. We present a case of duodenal pressure ulcers secondary to a PEG tube, along with a review of the literature and a proposed mechanism for this injury. CASE DESCRIPTION/METHODS: A 94-year-old non-verbal woman with a history of dementia and oral squamous cell carcinoma presented to the ED for RLQ abdominal pain. She was found to have leakage around the replacement PEG tube. Given comorbidities, patient was initially managed conservatively, but eventually underwent an endoscopy (EGD) due to persistent melena and down trending hemoglobin. The EGD demonstrated that the intragastric retention balloon had migrated beyond the pyloric channel resulting in a partial gastric outlet obstruction. The balloon was deflated revealing a large nonbleeding duodenal pressure ulcer. Since no stigmata of bleeding were identified, the replacement PEG was removed and new mushroom catheter and internal bumper was placed through the original tract. The patient was placed on an IV PPI to allow for adequate healing and melena resolved. DISCUSSION: Standard replacement PEG tubes are secured with an external bumper on the skin with an intragastric saline filled balloon. Ideal distance between the retainer and skin is 1-2 cm. If a PEG balloon is pulled too tightly there is a risk for pressure ulcer formation at the gastrostomy site. Conversely, if the PEG tube is too loose there is the risk of PEG balloon migration. With intense gastric peristalsis, the saline-filled balloon can migrate through the stomach, pylorus, and into the duodenum. While this is rare, case reports of gastric and duodenal outlet obstruction have been observed. In this case, the migration of the balloon into the duodenum led to a partial gastric outlet obstruction leading the patient to present with leakage, pain, melena, and anemia due to a large duodenal pressure ulcer. Proper PEG placement and care should be the main source of pressure ulcer prevention, and this rare complication should be considered in patients with melena and anemia.

Effects of Intraduodenal Infusion of the Bitter Tastant, Quinine, on Antropyloroduodenal Motility, Plasma Cholecystokinin, and Energy Intake in Healthy Men.

Background/AimsNutrient-induced gut hormone release (eg, cholecystokinin [CCK]) and the modulation of gut motility (particularly pyloric stimulation) contribute to the regulation of acute energy intake. Non-caloric bitter compounds, including quinine, have recently been shown in cell-line and animal studies to stimulate the release of gastrointestinal hormones by activating bitter taste receptors expressed throughout the gastrointestinal tract, and thus, may potentially suppress energy intake without providing additional calories. This study aims to evaluate the effects of intraduodenally administered quinine on antropyloroduodenal pressures, plasma CCK and energy intake.MethodsFourteen healthy, lean men (25 ± 5 years; BMI: 22.5 ± 2.0 kg/m2) received on 4 separate occasions, in randomized, double-blind fashion, 60-minute intraduodenal infusions of quinine hydrochloride at doses totaling 37.5 mg (“Q37.5”), 75 mg (“Q75”) or 225 mg (“Q225”), or control (all 300 mOsmol). Antropyloroduodenal pressures (high-resolution manometry), plasma CCK (radioimmunoassay), and appetite perceptions/gastrointestinal symptoms (visual analog questionnaires) were measured. Ad libitum energy intake (buffet-meal) was quantified immediately post-infusion. Oral quinine taste-thresholds were assessed on a separate occasion using 3-alternative forced-choice procedure.ResultsAll participants detected quinine orally (detection-threshold: 0.19 ± 0.07 mmol/L). Intraduodenal quinine did not affect antral, pyloric or duodenal pressures, plasma CCK (pmol/L [peak]; control: 3.6 ± 0.4, Q37.5: 3.6 ± 0.4, Q75: 3.7 ± 0.3, Q225: 3.9 ± 0.4), appetite perceptions, gastrointestinal symptoms or energy intake (kcal; control: 1088 ± 90, Q37.5: 1057 ± 69, Q75: 1029 ±70, Q225: 1077 ± 88).ConclusionQuinine, administered intraduodenally over 60 minutes, even at moderately high doses, but low infusion rates, does not modulate appetite-related gastrointestinal functions or energy intake.

Intraduodenal Administration of L-Valine Has No Effect on Antropyloroduodenal Pressures, Plasma Cholecystokinin Concentrations or Energy Intake in Healthy, Lean Men.

Whey protein is rich in the branched-chain amino acids, L-leucine, L-isoleucine and L-valine. Thus, branched-chain amino acids may, at least in part, mediate the effects of whey to reduce energy intake and/or blood glucose. Notably, 10 g of either L-leucine or L-isoleucine, administered intragastrically before a mixed-nutrient drink, lowered postprandial blood glucose, and intraduodenal infusion of L-leucine (at a rate of 0.45 kcal/min, total: 9.9 g) lowered fasting blood glucose and reduced energy intake from a subsequent meal. Whether L-valine affects energy intake, and the gastrointestinal functions involved in the regulation of energy intake, as well as blood glucose, in humans, is currently unknown. We investigated the effects of intraduodenally administered L-valine on antropyloroduodenal pressures, plasma cholecystokinin, blood glucose and energy intake. Twelve healthy lean men (age: 29 ± 2 years, BMI: 22.5 ± 0.7 kg/m2) were studied on 3 separate occasions in randomised, double-blind order. Antropyloroduodenal pressures, plasma cholecystokinin, blood glucose, appetite perceptions and gastrointestinal symptoms were measured during 90-min intraduodenal infusions of L-valine at 0.15 kcal/min (total: 3.3 g) or 0.45 kcal/min (total: 9.9 g), or 0.9% saline (control). Energy intake from a buffet-meal immediately after the infusions was quantified. L-valine did not affect antral, pyloric (mean number; control: 14 ± 5; L-Val-0.15: 21 ± 9; L-Val-0.45: 11 ± 4), or duodenal pressures, plasma cholecystokinin (mean concentration, pmol/L; control: 3.1 ± 0.3; L-Val-0.15: 3.2 ± 0.3; L-Val-0.45: 3.0 ± 0.3), blood glucose, appetite perceptions, symptoms or energy intake (kcal; control: 1040 ± 73; L-Val-0.15: 1040 ± 81; L-Val-0.45: 1056 ± 100), at either load (p > 0.05 for all). In conclusion, intraduodenal infusion of L-valine, at loads that are moderately (3.3 g) or substantially (9.9 g) above World Health Organization valine requirement recommendations, does not appear to have energy intake- or blood glucose-lowering effects.

Дуоденальная гипертензия и декомпрессия у пациентов с некротическим панкреатитом билиарного происхождения

Duodenomanometrical parameters and clinical results of active duodenal decompression on 65 operated patients with middle severe and severe biliary pancreatitis in 1st A-B phase, were studied. Revealed, that duodenal decompression provided duodenal pressure normalization towards 5 postoperative day, and decreased the frequency of necrotic pancreatitis infection and its widespread suppurative complications since 2-4 times.

Acute effects of the glucagon-like peptide-1 receptor agonist, exenatide, on blood pressure and heart rate responses to intraduodenal glucose infusion in type 2 diabetes.

To evaluate the effects of the glucagon-like peptide-1 receptor agonist, exenatide, on blood pressure and heart rate during an intraduodenal glucose infusion in type 2 diabetes. Nine subjects with type 2 diabetes were randomised to receive intravenous exenatide or saline control in a crossover design. Glucose (3 kcal min-1) was infused via an intraduodenal manometry catheter for 60 min. Blood pressure, heart rate, and the frequency and amplitude of duodenal pressure waves were measured at regular intervals. Gastrointestinal symptoms were monitored using 100 mm visual analogue scales. During intraduodenal glucose infusion (0-60 min), diastolic (p(0-60) = 0.03) and mean arterial (p(0-60) = 0.03) blood pressures and heart rate (p(0-60) = 0.06; p(0-120) = 0.03)) were higher with exenatide compared to placebo. The increase in the area under the curve for diastolic blood pressure and mean arterial blood pressure was related directly to the suppression of the duodenal motility index with exenatide compared to control (p = 0.007 and 0.04, respectively). In type 2 diabetes, intravenous exenatide increases mean arterial blood pressure and heart rate during an intraduodenal glucose infusion, supporting the need for further research with exenatide for its potential use in postprandial hypotension.

Contributions of upper gut hormones and motility to the energy intake-suppressant effects of intraduodenal nutrients in healthy, lean men - a pooled-data analysis.

We have previously identified pyloric pressures and plasma cholecystokinin (CCK) concentrations as independent determinants of energy intake following administration of intraduodenal lipid and intravenous CCK. We evaluated in healthy men whether these parameters also determine energy intake in response to intraduodenal protein, and whether, across the nutrients, any predominant gastrointestinal (GI) factors exist, or many factors make small contributions. Data from nine published studies, in which antropyloroduodenal pressures, GI hormones, and GI /appetite perceptions were measured during intraduodenal lipid or protein infusions, were pooled. In all studies energy intake was quantified immediately after the infusions. Specific variables for inclusion in a mixed‐effects multivariable model for determination of independent predictors of energy intake were chosen following assessment for collinearity, and within‐subject correlations between energy intake and these variables were determined using bivariate analyses adjusted for repeated measures. In models based on all studies, or lipid studies, there were significant effects for amplitude of antral pressure waves, premeal glucagon‐like peptide‐1 (GLP‐1) and time‐to‐peak GLP‐1 concentrations, GLP‐1 AUC and bloating scores (P < 0.05), and trends for basal pyloric pressure (BPP), amplitude of duodenal pressure waves, peak CCK concentrations, and hunger and nausea scores (0.05 < P ≤ 0.094), to be independent determinants of subsequent energy intake. In the model including the protein studies, only BPP was identified as an independent determinant of energy intake (P < 0.05). No single parameter was identified across all models, and effects of the variables identified were relatively small. Taken together, while GI mechanisms contribute to the regulation of acute energy intake by lipid and protein, their contribution to the latter is much less. Moreover, the effects are likely to reflect small, cumulative contributions from a range of interrelated factors.

The consequences of cholecystectomy

to analyze the consequences of cholecystectomy. 348 patients were under observation within 10 years after cholecystectomy. Surgery for destructive and chronic cholecystitis was performed in 115 and 233 patients respectively. The consequences of cholecystectomy were assessed using bile acids level in blood plasma, stomach and duodenal pressure, pancreatic and stomach changes. It was established that lithocholic, deoxycholic, taurodeoxycholic acids were increased by 44% within 10 years after surgery. At the same time glycocholic and tauroursodeoxycholic acids were decreased by 21.5% in 5 years after surgery. Bile acids level changes were associated with changes of stomach and duodenal pressure. The most pronounced disorders were observed in distal duodenum. There was more than 2.8-fold excess of normal pressure in this area. Duodenal hypertension was accompanied by pancreatic ducts enlargement in 9.5% of cases and increased echogenicity in 93% of cases. Changes of the level and proportion of blood plasma bile acids and hypertension in upper gastrointestinal tract are the most important in chronic pancreatitis pathogenesis after cholecystectomy. Such conditions occur within first 3 years after surgery.

Comparative effects of intraduodenal whey protein hydrolysate on antropyloroduodenal motility, gut hormones, glycemia, appetite, and energy intake in lean and obese men

In lean individuals, intraduodenal protein and lipid modulate gastrointestinal motor and hormone functions and reduce energy intake in a load-dependent manner; protein also stimulates insulin, with modest effects on reducing blood glucose. The effect of intraduodenal lipid on gastrointestinal motor and hormone responses is diminished in obesity; whether the effects of protein are also attenuated remains unclear. The objectives of this study were to characterize the load-dependent effects of intraduodenal whey protein hydrolysate on antropyloroduodenal pressures, gut hormones, glycemia, appetite, and energy intake in obese subjects and to compare the responses to the higher protein load with those in lean subjects. We measured antropyloroduodenal pressures, plasma cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), glucagon, insulin, blood glucose, appetite, and energy intake in 12 nondiabetic obese men on 3 separate occasions, in a double-blind, randomized order, during 60-min intraduodenal infusions of hydrolyzed whey protein at either 0 (saline control), 1.5, or 3 kcal/min. Twelve age-matched lean individuals received a 3-kcal/min infusion only. Immediately after the infusions, energy intake from a buffet lunch was quantified. In obese subjects, protein suppressed antral and duodenal pressures; stimulated plasma CCK, GLP-1, GIP, insulin, and glucagon (all r > 0.57, P < 0.01); and tended to reduce energy intake (r = -10.38, P = 0.057) in a dose-dependent manner. In response to the 3-kcal/min protein load, antropyloroduodenal pressures, CCK, GLP-1, and glucagon did not differ between lean and obese subjects. Insulin release was greater, and GIP release less, in obese than in lean subjects (both P < 0.05), whereas the reduction in glucose was comparable. Energy intake tended to be higher in obese subjects (P = 0.08). The gastrointestinal effects of hydrolyzed whey protein remain relatively intact in obesity; however, the observed changes in insulin and GIP suggest early disturbances in the insulin-incretin axis. This study was registered at www.anzctr.org.au as ACTRN 12612000203853.

The Glucagon-Like Peptide 1 Receptor Agonist Exenatide Inhibits Small Intestinal Motility, Flow, Transit, and Absorption of Glucose in Healthy Subjects and Patients With Type 2 Diabetes: A Randomized Controlled Trial.

The short-acting glucagon-like peptide 1 receptor agonist exenatide reduces postprandial glycemia, partly by slowing gastric emptying, although its impact on small intestinal function is unknown. In this study, 10 healthy subjects and 10 patients with type 2 diabetes received intravenous exenatide (7.5 μg) or saline (-30 to 240 min) in a double-blind randomized crossover design. Glucose (45 g), together with 5 g 3-O-methylglucose (3-OMG) and 20 MBq (99m)Tc-sulfur colloid (total volume 200 mL), was given intraduodenally (t = 0-60 min; 3 kcal/min). Duodenal motility and flow were measured using a combined manometry-impedance catheter and small intestinal transit using scintigraphy. In both groups, duodenal pressure waves and antegrade flow events were fewer, and transit was slower with exenatide, as were the areas under the curves for serum 3-OMG and blood glucose concentrations. Insulin concentrations were initially lower with exenatide than with saline and subsequently higher. Nausea was greater in both groups with exenatide, but suppression of small intestinal motility and flow was observed even in subjects with little or no nausea. The inhibition of small intestinal motor function represents a novel mechanism by which exenatide can attenuate postprandial glycemia.

Effects of intraduodenal infusion of the branched-chain amino acid leucine on ad libitum eating, gut motor and hormone functions, and glycemia in healthy men

Branched-chain amino acids (BCAAs), particularly leucine, act as nutrient signals regulating protein synthesis and degradation as well as glucose metabolism. In addition, leucine has been demonstrated in animal experiments to modulate eating and energy homeostasis. We aimed to characterize the effects of physiologic and supraphysiologic loads of intraduodenal leucine on eating, gut hormone and motor functions, and blood glucose in humans. Twelve lean men were studied on 3 occasions in a randomized, double-blind order. Antropyloroduodenal motility, plasma ghrelin, cholecystokinin, glucagon-like peptide 1, peptide YY, insulin, glucagon, blood glucose, appetite perceptions, and gastrointestinal symptoms were measured during 90-min intraduodenal infusions of leucine at 0.15 kcal/min (total 3.3 g, 13.5 kcal), 0.45 kcal/min (total 9.9 g, 40.5 kcal), or saline (control). Ad libitum eating from a buffet lunch was quantified immediately after the infusions. Leucine at 0.45 kcal/min inhibited eating (energy intake by ∼13%, P < 0.05), increased plasma cholecystokinin, slightly reduced blood glucose and increased plasma insulin, and decreased antral pressures (all P < 0.05). Leucine at 0.15 kcal/min had no effect on food intake, blood glucose, or antral pressures but also slightly increased plasma cholecystokinin (P < 0.05). Neither dose affected plasma ghrelin, glucagon, glucagon-like peptide 1 and peptide YY, or pyloric and duodenal pressures. Plasma leucine concentrations were related to the dose of intraduodenal leucine, with substantial increases during both 0.15 and 0.45 kcal/min. The effects of intraduodenal infusions of free leucine on eating are probably not primarily mediated by changes in gut motor and hormone functions, with perhaps the exception of cholecystokinin. Instead, increased plasma leucine concentrations may be a potential signal mediating the eating-inhibitory effect of leucine. The study was registered as a clinical trial with the Australia and New Zealand Clinical Trial Registry (www.anzctr.org.au) as ACTRN12613000899741.

Effects of Intraduodenal Infusions of L-phenylalanine and L-glutamine on Antropyloroduodenal Motility and Plasma Cholecystokinin in Healthy Men.

Background/AimsDietary proteins have potent eating-inhibitory and glucose-lowering effects, which may be mediated via effects of amino acids on gastrointestinal hormone and motor function, although little information is available. We have now evaluated the effects of L-phenylalanine (L-Phe) and L-glutamine (L-Gln) on antropyloroduodenal motility and plasma cholecystokinin (CCK) concentrations.MethodsTwo double-blind, 3-way cross-over studies were performed, each including 10 healthy, normal-weight men. We determined the antropyloroduodenal motor and plasma CCK responses to 90-minute intraduodenal infusions of L-Phe (study A) or L-Gln (study B), each at 0.15 kcal/min (total 13.5 kcal), or 0.45 kcal/min (total 40.5 kcal), or saline (control), in randomized fashion.ResultsIntraduodenal L-Phe at 0.45 kcal/min, but not at 0.15 kcal/min, suppressed antral (P < 0.01), and stimulated phasic (P < 0.01), but not tonic, pyloric, or duodenal pressures, while L-Phe at both 0.15 kcal/min and 0.45 kcal/min stimulated plasma CCK. In contrast, L-Gln had no effect on antral, duodenal or pyloric pressures, or plasma CCK.ConclusionsIntraduodenal infusions of L-Phe and L-Gln, in doses of 0.15 kcal/min and 0.45 kcal/min for 90 minutes, have different effects on antropyloroduodenal motility and CCK in normal-weight men. The modulation of antral and pyloric pressures and CCK may contribute to the eating-inhibitory effects of oral L-Phe, possibly through the slowing of gastric emptying.

Effects of intraduodenal protein on appetite, energy intake, and antropyloroduodenal motility in healthy older compared with young men in a randomized trial

Protein-rich supplements are used widely for the prevention and management of undernutrition in older people. The use of protein supplements in older people could, however, be counterproductive by reducing appetite and overall energy intake. The objective was to determine whether aging influences the effects of protein loads, administered directly into the small intestine, on energy intake, antropyloroduodenal motility, and appetite. Intraduodenal infusions (240 mL, 60 min) of saline (0 kcal, control) and protein (hydrolyzed whey) loads of 30, 90, and 180 kcal were followed by an ad libitum buffet meal in 10 young (19-29 y) and 10 healthy older (68-81 y) men. Suppression of energy intake (kcal) at the meal by protein infusion compared with control was calculated. In young subjects, a dose-responsive suppression (±SEM) of energy intake was found at the buffet meal by protein (suppression at 30 kcal: 7 ± 8%, P = 0.189; 90 kcal: 17 ± 8%, P = 0.054; 180 kcal: 33 ± 7%, P = 0.002), whereas suppression was observed only after the 180-kcal load in older subjects (30 kcal: 7 ± 4% increase, P = 0.126; 90 kcal: 6 ± 7% increase, P = 0.291; 180 kcal: 17 ± 6% suppression, P = 0.016). Suppression of energy intake by protein was less in older than in young subjects (P < 0.005). In young subjects, total energy intake (meal + infusion) on the 180-kcal protein-infusion day was lower than that on the control day (P = 0.041), whereas in older subjects it was greater on the 30-kcal (P = 0.033) and 90-kcal (P = 0.016) infusion days. Energy intake was inversely related to isolated pyloric pressure waves (r = -0.32, P = 0.013) and positively related to antral (r = 0.30, P = 0.021) and duodenal (r = 0.35, P = 0.006) pressure waves. Suppression of energy intake by protein was inversely related to the change in isolated pyloric pressure waves (r = -0.35, P = 0.027) and positively related to duodenal pressure waves (r = 0.32, P = 0.044). Intraduodenal protein suppresses appetite and energy intake less in healthy older than in young adults. In older subjects, intraduodenal protein at low doses increased overall energy intake, which supports the use of protein supplements in undernourished older people. This trial was registered at www.anzctr.org.au as 12612000906853.

Numerical and experimental analysis of factors leading to suture dehiscence after Billroth II gastric resection

The main goal of this study was to numerically quantify risk of duodenal stump blowout after Billroth II (BII) gastric resection. Our hypothesis was that the geometry of the reconstructed tract after BII resection is one of the key factors that can lead to duodenal dehiscence. We used computational fluid dynamics (CFD) with finite element (FE) simulations of various models of BII reconstructed gastrointestinal (GI) tract, as well as non-perfused, ex vivo, porcine experimental models. As main geometrical parameters for FE postoperative models we have used duodenal stump length and inclination between gastric remnant and duodenal stump. Virtual gastric resection was performed on each of 3D FE models based on multislice Computer Tomography (CT) DICOM. According to our computer simulation the difference between maximal duodenal stump pressures for models with most and least preferable geometry of reconstructed GI tract is about 30%. We compared the resulting postoperative duodenal pressure from computer simulations with duodenal stump dehiscence pressure from the experiment. Pressure at duodenal stump after BII resection obtained by computer simulation is 4–5 times lower than the dehiscence pressure according to our experiment on isolated bowel segment. Our conclusion is that if the surgery is performed technically correct, geometry variations of the reconstructed GI tract by themselves are not sufficient to cause duodenal stump blowout. Pressure that develops in the duodenal stump after BII resection using omega loop, only in the conjunction with other risk factors can cause duodenal dehiscence. Increased duodenal pressure after BII resection is risk factor. Hence we recommend the routine use of Roux en Y anastomosis as a safer solution in terms of resulting intraluminal pressure. However, if the surgeon decides to perform BII reconstruction, results obtained with this methodology can be valuable.

Deep-sea water containing selenium provides intestinal protection against duodenal ulcers through the upregulation of Bcl-2 and thioredoxin reductase 1.

Deep-sea water (DSW), which is rich in micronutrients and minerals and with antioxidant and anti-inflammatory qualities, may be developed as marine drugs to provide intestinal protection against duodenal ulcers. We determined several characteristics in the modified DSW. We explored duodenal pressure, oxygenation, microvascular blood flow, and changes in pH and oxidative redox potential (ORP) values within the stomach and duodenum in response to tap water (TW, hardness: 2.48 ppm), DSW600 (hardness: 600 ppm), and DSW1200 (hardness: 1200 ppm) in Wistar rats and analyzed oxidative stress and apoptosis gene expressions by cDNA and RNA microarrays in the duodenal epithelium. We compared the effects of drinking DSW, MgCl2, and selenium water on duodenal ulcers using pathologic scoring, immunohistochemical analysis, and Western blotting. Our results showed DSW has a higher pH value, lower ORP value, higher scavenging H2O2 and HOCl activity, higher Mg2+ concentrations, and micronutrients selenium compared with TW samples. Water infusion significantly increased intestinal pressure, O2 levels, and microvascular blood flow in DSW and TW groups. Microarray showed DSW600, DSW1200, selenium water upregulated antioxidant and anti-apoptotic genes and downregulated pro-apoptotic gene expression compared with the TW group. Drinking DSW600, DSW1200, and selenium water but not Mg2+ water significantly enhanced Bcl-2 and thioredoxin reductase 1 expression. Bax/Bcl-2/caspase 3/poly-(ADP-ribose)-polymerase signaling was activated during the pathogenesis of duodenal ulceration. DSW drinking reduced ulcer area as well as apoptotic signaling in acetic acid-induced duodenal ulcers. DSW, which contains selenium, provides intestinal protection against duodenal ulcers through the upregulation of Bcl-2 and thioredoxin reductase 1.