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IntroductionMalnutrition is prevalent after stroke, particularly if post-stroke oropharyngeal dysphagia (OD) reduces nutritional intake. To further understand stroke-related malnutrition, a thorough nutritional assessment was performed in ischemic stroke patients with or without OD during sub-acute inpatient rehabilitation.MethodsIn this exploratory, observational, cross-sectional, multi-center study in Germany (NTR6802), ischemic stroke patients with (N = 36) or without (N = 49) OD were age- and sex-matched to healthy reference subjects. Presence of (risk of) malnutrition (MNA-SF), blood concentration of stroke-relevant nutritional compounds and metabolites, nutritional intake, quality of life (EQ-5D-5L), and activities of daily living (Barthel index) were assessed.ResultsMore than half of the stroke patients displayed (risk of) malnutrition, with higher prevalence in patient with OD vs. without OD. Fasted blood concentrations of vitamins B1, B2, B6, A, D, and E, selenium, choline, coenzyme Q10, albumin, pre-albumin, transferrin, docosahexaenoic acid, and eicosapentaenoic acid were all lower in stroke patients compared to their matched healthy reference subjects, irrespective of OD status. Reported energy, macronutrient, and water intake were lower in stroke patients vs. healthy reference subjects. As expected, quality of life and activities of daily living scores were lower in stroke vs. healthy reference subjects, with OD scoring worse than non-OD patients.DiscussionThis study shows that malnutrition is highly prevalent in sub-acute stroke patients during rehabilitation. Even though patients with OD were more likely to be malnourished, blood levels of specific nutritional compounds were similarly lower in stroke patients with or without OD compared to healthy reference subjects. Furthermore, subgroup analysis showed similarly lower blood levels of specific nutritional compounds in patients that are normal nourished vs. patients with (risk of) malnutrition. This might imply disease-specific changes in blood levels on top of overall protein-energy malnutrition. The results of the current study underline that it is important to screen for nutritional impairments in every stroke patient, either with or without OD.

Glucagon like peptide-1 (GLP-1) and serotonin are both involved in food intake regulation. GLP-1 release is stimulated upon nutrient interaction with G-protein coupled receptors by enteroendocrine cells (EEC), whereas serotonin is released from enterochromaffin cells (ECC). The central hypothesis for the current study was that nutrient-induced GLP-1 release from EECs is modulated by serotonin through a process involving serotonin receptor interaction. This was studied by assessing the effects of serotonin reuptake inhibition by fluoxetine on nutrient-induced GLP-1, PYY and CCK release from isolated pig intestinal segments. Next, serotonin-induced GLP-1 release was studied in enteroendocrine STC-1 cells, where effects of serotonin receptor inhibition were studied using specific and non-specific antagonists.Casein (1% w/v), safflower oil (3.35% w/v), sucrose (50 mM) and rebaudioside A (12.5 mM) stimulated GLP-1 release from intestinal segments, whereas casein only stimulated PYY and CCK release. Combining nutrients with fluoxetine further increased nutrient-induced GLP-1, PYY and CCK release.Serotonin release from intestinal tissue segments was stimulated by casein and safflower oil while sucrose and rebaudioside A had no effect. The combination with fluoxetine (0.155 μM) further enhanced casein and safflower oil induced-serotonin release.Exposure of ileal tissue segments to serotonin (30 μM) stimulated GLP-1 release whereas it did not induce PYY and CCK release. Serotonin (30 and 100 μM) also stimulated GLP-1 release from STC-1 cells, which was inhibited by the non-specific 5HT receptor antagonist asenapine (1 and 10 μM). These data suggest that nutrient-induced GLP-1 release is modulated by serotonin through a receptor mediated process. © 2016 The Authors.

Background Increasing viscosity with thickening agents is a valid therapeutic strategy for oropharyngeal dysphagia (OD). To assess the therapeutic effect of a xanthan gum‐based thickener (Nutilis Clear®) at six viscosities compared with thin liquid in poststroke OD (PSOD) patients. Methods A total of 120 patients with PSOD were studied in this controlled, multiple‐dose, fixed‐order, and single‐blind study using videofluoroscopy (VFSS). A series of boluses of 10 mL thin liquid and 2000, 1400, 800, 450, 250, and 150 mPa s viscosities were given in duplicate, interrupted in case of aspiration. We assessed the safety and efficacy of swallow and the kinematics of the swallow response. Key Results A total of 41.2% patients had safe swallow at thin liquid which significantly increased for all viscosities from 71.9% at 150 mPa s to 95.6% at 1400 mPa s (P, This study shows a strong therapeutic effect of a gum‐based thickener on safety of swallow in post‐stroke dysphagia that depends on shear viscosity levels, and a therapeutic range of 150‐800 mPa s. Increasing viscosity shortened time to laryngeal vestibule closure at all viscosities and reduced bolus velocity at ≥450 mPa s.

BACKGROUND: Activation of the ileal brake by casein induces satiety signals and reduces energy intake. However, adverse effects of intraileal casein administration have not been studied before. These adverse effects may include impaired amino acid digestion, absorption and immune activation. OBJECTIVE: To investigate the effects of intraileal infusion of native casein on plasma amino acid appearance, immune activation and gastrointestinal (GI) symptoms. DESIGN: A randomized single-blind cross over study was performed in 13 healthy subjects (6 male; mean age 26 +/- 2.9 years; mean body mass index 22.8 +/- 0.4 kg/m-2), who were intubated with a naso-ileal feeding catheter. Thirty minutes after intake of a standardized breakfast, participants received an ileal infusion, containing either control (C) consisting of saline, a low-dose (17.2 kcal) casein (LP) or a high-dose (51.7 kcal) of casein (HP) over a period of 90 min. Blood samples were collected for analysis of amino acids (AAs), C-reactive protein (CRP), pro-inflammatory cytokines and oxylipins at regular intervals. Furthermore, GI symptom questionnaires were collected before, during and after ileal infusion. RESULTS: None of the subjects reported any GI symptoms before, during or after ileal infusion of C, LP and HP. Plasma concentrations of all AAs analyzed were significantly increased after infusion of HP as compared to C (p < 0.001), and most AAs were increased after infusion of LP (p < 0.001). In total, 12.49 +/- 1.73 and 3.18 +/- 0.87 g AAs were found in plasma after intraileal infusion of HP and LP, corresponding to 93 +/- 13% (HP) and 72 +/- 20% (LP) of AAs infused as casein, respectively. Ileal casein infusion did not affect plasma concentrations of CRP, IL-6, IL-8, IL-1beta and TNF-alpha. Infusion of HP resulted in a decreased concentration of 11,12-dihydroxyeicosatrienoic acid whereas none of the other oxylipins analyzed were affected. CONCLUSIONS: A single intraileal infusion of native casein results in a concentration and time dependent increase of AAs in plasma, suggesting an effective digestion and absorption of AAs present in casein. Also, ileal infusion did not result in immune activation nor in GI symptoms. CLINICALTRIALS.GOV: NCT01509469.

BACKGROUND: Activation of the ileal brake, by infusing lipid directly into the distal part of the small intestine, alters gastrointestinal (GI) motility and inhibits food intake. The ileal brake effect on eating behavior of the other macronutrients is currently unknown. OBJECTIVE: The objective of this study was to investigate the effects of ileal infusion of sucrose and casein on food intake, release of GI peptides, gastric emptying rate and small-bowel transit time with safflower oil as positive control. DESIGN: This randomized, single-blind, crossover study was performed in 13 healthy subjects (6 male; mean age 26.4 ± 2.9 years; mean body mass index 22.8 ± 0.4 kgm-2) who were intubated with a naso-ileal catheter. Thirty minutes after the intake of a standardized breakfast, participants received an ileal infusion, containing control ((C) saline), safflower oil ((HL) 51.7 kcal), low-dose casein ((LP) 17.2 kcal) or high-dose casein ((HP) 51.7 kcal), low-dose sucrose ((LC) 17.2 kcal) and high-dose sucrose ((HC) 51.7 kcal), over a period of 90 min. Food intake was determined during an ad libitum meal. Visual analogue score questionnaires for hunger and satiety and blood samples were collected at regular intervals. RESULTS: Ileal infusion of lipid, protein and carbohydrate resulted in a significant reduction in food intake compared with control (HL: 464.3 ± 90.7 kcal, P < 0.001; HP: 458.0 ± 78.6 kcal, P < 0.005; HC: 399.0 ± 57.0 kcal, P < 0.0001 vs control: 586.7 ± 70.2 kcal, P < 0.001, respectively). A reduction in energy intake was still apparent when the caloric amount of infused nutrients was added to the amount eaten during the ad libitum meal. Secretion of cholecystokinin and peptide YY but not of glucagon-like peptide-1 (7-36) was increased during ileal perfusion of fat, carbohydrates and protein. During ileal perfusion of all macronutrients, a delay in gastric emptying and intestinal transit was observed, but differences were not significant compared with control. CONCLUSION: Apart from lipids, also sucrose and casein reduce food intake on ileal infusion, thereby activating the ileal brake. In addition to food intake, also satiety and GI peptide secretion were affected. Chemicals/CAS: casein, 9000-71-9; cholecystokinin, 9011-97-6, 93443-27-7; glucagon like peptide 1, 89750-14-1; peptide YY, 81858-94-8; safflower oil, 8001-23-8; sucrose, 122880-25-5, 57-50-1

The vagal nerve and gut hormones CCK and GLP-1 play important roles in the control of food intake. However, it is not clear to what extent CCK and GLP-1 increase satiation by stimulating receptors located on abdominal vagal nerve endings or via receptors located elsewhere. This study aimed to further explore the relative contribution of the abdominal vagal nerve in mediating the satiating effects of endogenous CCK and GLP-1. Total subdiaphragmatic vagotomy or sham operation was combined with administration of CCK1 and GLP-1 receptor antagonists devazepide and exendin (9-39) in 12 pigs, applying an unbalanced Latin Square within-subject design. Furthermore, effects of vagotomy on preprandial and postprandial acetaminophen absorption, glucose, insulin, GLP-1 and CCK plasma concentrations were investigated.Ad libitum liquid meal intake (mean±SEM) was similar in sham and vagotomized pigs (4180±435 and 3760±810g/meal). Intake increased by about 20% after blockade of CCK1 receptors, independently of the abdominal vagal nerve. Food intake did not increase after blockade of GLP-1 receptors. Blockade of CCK1 and GLP-1 receptors increased circulating CCK and GLP-1 concentrations in sham pigs only, suggesting the existence of a vagal reflex mechanism in the regulation of plasma CCK1 and GLP-1 concentrations. Vagotomy decreased acetaminophen absorption and changed glucose, insulin, CCK and GLP-1 concentrations indicating a delay in gastric emptying. Our data show that at liquid feeding, satiation is decreased effectively by pharmacological blockade of CCK1 receptors. We conclude that regulation of liquid meal intake appears to be primarily regulated by CCK1 receptors not located on abdominal vagal nerve endings. Chemicals/CAS: cholecystokinin, 9011-97-6, 93443-27-7; devazepide, 103420-77-5; glucagon like peptide 1, 89750-14-1; glucose, 50-99-7, 84778-64-3; insulin, 9004-10-8; paracetamol, 103-90-2