Associations between Low to Moderate Consumption of Alcoholic Beverage Types and Health Outcomes: A Systematic Review.

AIMS: There is limited research comparing light to moderate wine, beer and spirits consumption and their impact on long-term health. This systematic review aims to investigate the studies published in the past 10 years and qualitatively assess the similarities and differences between the three main beverages, when consumed at a low to moderate level, for their associations with various health outcomes. METHODS: A systematic search was conducted for comparative studies published in English language (2010 to mid-2021) of beverage-specific low to moderate alcohol consumption associated with all-cause mortality, cancer, cardiovascular disease and diabetes mellitus type II. RESULTS: The search yielded a total of 24 studies (8 meta-analyses; 15 prospective studies and 1 pooled analysis). Overall, most studies showed similar associations of different alcoholic beverages with chronic conditions, including all-cause mortality, many types of cancer, cardiovascular disease and diabetes mellitus type II. Not all data are consistent. Some studies show more beneficial or detrimental effects of wine than other beverage types, whereas other studies show such effects for other beverages. CONCLUSION: Moderate consumption of one specific alcoholic beverage (wine, beer or spirits) may not be consistently associated with higher or lower risks for common health outcomes as compared with moderate consumption of any of the other alcoholic beverages.

Alcohol and Human Health: What Is the Evidence?

Alcohol consumption has long been a part of human culture. However, alcohol consumption levels and alcohol consumption patterns are associated with chronic diseases. Overall, light and moderate alcohol consumption (up to 14 g per day for women and up to 28 g per day for men) may be associated with reduced mortality risk, mainly due to reduced risks for cardiovascular disease and type-2 diabetes. However, chronic heavy alcohol consumption and alcohol abuse lead to alcohol-use disorder, which results in physical and mental diseases such as liver disease, pancreatitis, dementia, and various types of cancer. Risk factors for alcohol-use disorder are largely unknown. Alcohol-use disorder and frequent heavy drinking have detrimental effects on personal health.

Alcohol Consumption, Drinking Patterns, and Cognitive Performance in Young Adults: A Cross-Sectional and Longitudinal Analysis.

Long-term alcohol abuse is associated with poorer cognitive performance. However, the associations between light and moderate drinking and cognitive performance are less clear. We assessed this association via cross-sectional and longitudinal analyses in a sample of 702 Dutch students. At baseline, alcohol consumption was assessed using questionnaires and ecological momentary assessment (EMA) across four weeks ('Wave 1'). Subsequently, cognitive performance, including memory, planning, and reasoning, was assessed at home using six standard cognition tests presented through an online platform. A year later, 436 students completed the four weeks of EMA and online cognitive testing ('Wave 2'). In both waves, there was no association between alcohol consumption and cognitive performance. Further, alcohol consumption during Wave 1 was not related to cognitive performance at Wave 2. In addition, EMA-data-based drinking patterns, which varied widely between persons but were relatively consistent over time within persons, were also not associated with cognitive performance. Post-hoc analyses of cognitive performance revealed higher within-person variance scores (from Wave 1 to Wave 2) than between-person variance scores (both Wave 1 and Wave 2). In conclusion, no association was observed between alcohol consumption and cognitive performance in a large Dutch student sample. However, the online cognitive tests performed at home may not have been sensitive enough to pick up differences in cognitive performance associated with alcohol consumption.

The Effect of an Encapsulated Nutrient Mixture on Food Intake and Satiety: A Double-Blind Randomized Cross-Over Proof of Concept Study.

Activation of the intestinal brake by infusing nutrients into the distal small intestine with catheters inhibits food intake and enhances satiety. Encapsulation of macronutrients, which protects against digestion in the proximal gastrointestinal tract, can be a non-invasive alternative to activate this brake. In this study, we investigate the effect of oral ingestion of an encapsulated casein and sucrose mixture (active) targeting the distal small intestine versus a control product designed to be released in the stomach on food intake, satiety, and plasma glucose concentrations. Fifty-nine volunteers received the active and control product on two separate test days. Food intake was determined during an ad libitum meal 90 min after ingestion of the test product. Visual analogue scale scores for satiety and blood samples for glucose analysis were collected at regular intervals. Ingestion of the active product decreased food intake compared to the control product (655 kcal compared with 699 kcal, respectively, p < 0.05). The area under the curve (AUC) for hunger was decreased (p < 0.05) and AUC for satiety was increased (p < 0.01) after ingestion of the active product compared to the control product. Ingestion of an encapsulated protein-carbohydrate mixture resulted in inhibition of food intake compared to a non-encapsulated control product.

Subjective feelings of appetite of wholegrain breakfasts evaluated under controlled, laboratory and 'at home' conditions.

BACKGROUND: Appetite regulating properties of foods are usually investigated under laboratory conditions, whereas in real life, foods are consumed under at home conditions. The objective of this study was to compare the acute effects of breakfasts when tested in a laboratory condition and in an at home condition. Appetite regulating properties of two bread breakfasts and two cereal breakfasts were also compared. SUBJECTS AND METHODS: In this randomized cross-over trial balanced for laboratory and at home test conditions, thirty-two women consumed five breakfasts, i.e. two bread breakfasts, two cereal breakfasts and one fried-egg breakfast. Visual analogue scales for measuring appetite were captured via an on-line scoring system and were analyzed as incremental area under the curve, as satiation phase and as satiety phase. RESULTS: Location effects were limited to two small effects only. An overall location effect in hunger feelings was observed (p = 0.040), which occurred specifically during the short satiation period (p = 0.0002) where hunger feelings scored higher under laboratory conditions. Similarly, a location effect was observed for desire to eat (p = 0.001); this was again higher under laboratory conditions. No other location effects were observed. Bread breakfasts did not differ in their appetite regulating properties. The Steel Cut oatmeal breakfast was reported to be more satiating (p = 0.001) as compared to the ready-to-eat cereal. CONCLUSIONS: Whereas the five breakfasts varied somewhat in their appetite regulating properties, evaluation under laboratory conditions overall did not result in different appetite scores compared to the at home conditions. This suggests that at home testing may be a useful alternative to laboratory test conditions for nutrition research.

Docosahexaenoyl serotonin emerges as most potent inhibitor of IL-17 and CCL-20 released by blood mononuclear cells from a series of N-acyl serotonins identified in human intestinal tissue.

Fatty acid amides (FAAs), conjugates of fatty acids with ethanolamine, mono-amine neurotransmitters or amino acids are a class of molecules that display diverse functional roles in different cells and tissues. Recently we reported that one of the serotonin-fatty acid conjugates, docosahexaenoyl serotonin (DHA-5-HT), previously found in gut tissue of mouse and pig, attenuates the IL-23-IL-17 signaling axis in LPS-stimulated mice macrophages. However, its presence and effects in humans remained to be elucidated. Here, we report for the first time its identification in human intestinal (colon) tissue, along with a series of related N-acyl serotonins. Furthermore, we tested these fatty acid conjugates for their ability to inhibit the release of IL-17 and CCL-20 by stimulated human peripheral blood mononuclear cells (PBMCs). Serotonin conjugates with palmitic acid (PA-5-HT), stearic acid (SA-5-HT) and oleic acid (OA-5-HT) were detected in higher levels than arachidonoyl serotonin (AA-5-HT) and DHA-5-HT, while eicosapentaenoyl serotonin (EPA-5-HT) could not be quantified. Among these, DHA-5-HT was the most potent in inhibiting IL-17 and CCL-20, typical Th17 pro-inflammatory mediators, by Concanavalin A (ConA)-stimulated human PBMCs. These results underline the idea that DHA-5-HT is a gut-specific endogenously produced mediator with the capacity to modulate the IL-17/Th17 signaling response. Our findings may be of relevance in relation to intestinal inflammatory diseases like Crohn's disease and Ulcerative colitis.

Effects of polydextrose with breakfast or with a midmorning preload on food intake and other appetite-related parameters in healthy normal-weight and overweight females: An acute, randomized, double-blind, placebo-controlled, and crossover study.

Polydextrose (PDX) reduces subsequent energy intake (EI) when administered at midmorning in single-blind trials of primarily normal-weight men. However, it is unclear if this effect also occurs when PDX is given at breakfast time. Furthermore, for ecological validity, it is desirable to study a female population, including those at risk for obesity. We studied the effects of PDX, served as part of a breakfast or midmorning preload, on subsequent EI and other appetite-related parameters in healthy normal-weight and overweight females. Per earlier studies, the primary outcome was defined as the difference in subsequent EI when PDX was consumed at midmorning versus placebo. Thirty-two volunteers were enrolled in this acute, double-blind, placebo-controlled, randomized, and crossover trial to examine the effects of 12.5 g of PDX, administered as part of a breakfast or midmorning preload, on subsequent EI, subjective feelings of appetite, well-being, and mood. Gastric emptying rates and the blood concentrations of glucose, insulin, cholecystokinin, ghrelin, glucagon-like peptide 1 (GLP-1), and peptide tyrosine-tyrosine were measured in the group that received PDX as part of their breakfast. There were no differences in EI between volunteers who were fed PDX and placebo. PDX intake with breakfast tended to elevate blood glucose (P = 0.06) during the postabsorptive phase, significantly lowered insulin by 15.7% (P = 0.04), and increased GLP-1 by 39.9% (P = 0.02); no other effects on blood parameters or gastric emptying rates were observed. PDX intake at midmorning reduced hunger by 31.4% during the satiation period (P = 0.02); all other subjective feelings of appetite were unaffected. Volunteers had a uniform mood profile during the study. PDX was well tolerated, causing one mild adverse event throughout the trial.

Intraileal casein infusion increases plasma concentrations of amino acids in humans: A randomized cross over trial.

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-1ß and TNF-α. 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.

The Noncaloric Sweetener Rebaudioside A Stimulates Glucagon-Like Peptide 1 Release and Increases Enteroendocrine Cell Numbers in 2-Dimensional Mouse Organoids Derived from Different Locations of the Intestine.

BACKGROUND: Glucagon-like peptide 1 (GLP-1) contributes to satiety and plays a pivotal role in insulin secretion and glucose homeostasis. Similar to GLP-1, peptide YY (PYY) and cholecystokinin also influence food intake. The secretion of these hormones by enteroendocrine cells along the intestine is modulated by nutrients. Preparations from the Stevia rebaudiana plant, including rebaudioside A, are increasingly being used as noncaloric sweeteners. OBJECTIVE: We investigated the effects of rebaudioside A on enteroendocrine cells by assessing both cell numbers as well as their secretory capacity in an organoid model. METHODS: A 2-dimensional organoid model derived from duodenal, jejunal, and ileal crypts of a C57BL/6J mouse was developed and characterized with the use of gene expression and immunofluorescence. We stimulated these organoids with 10 mmol/L rebaudioside A for 1 h and measured their GLP-1, PYY, and cholecystokinin release. We also analyzed the effects of rebaudioside A on gene expression in enteroendocrine cells after an 18-h incubation. RESULTS: The 2-dimensional organoids contained crypt cells and differentiated villus cells, including enterocytes and goblet and enteroendocrine cells. These enteroendocrine cells stained positive for GLP-1, PYY, and serotonin. The cultured 2-dimensional organoids maintained their location-specific gene expression patterns. Compared with the control, rebaudioside A induced GLP-1 secretion 1.7-fold in the duodenum (P < 0.01), 2.2-fold in the jejunum (P < 0.01), and 4.3-fold in the ileum (P < 0.001). PYY release was increased by rebaudioside A 3-fold in the ileum compared with the control (P < 0.05). Long-term (18-h) stimulation with the sweetener induced the expression of the enteroendocrine-specific markers chromogranin A, glucagon, Pyy, and cholecystokinin 3.5- (P < 0.001), 3.5- (P < 0.001), 3.8- (P < 0.05), and 6.5-fold (P < 0.001), respectively. CONCLUSIONS: These results show novel ex vivo effects of rebaudioside A on enteroendocrine cells of the mouse small intestine and highlight potentially new applications for rebaudioside A in metabolic diseases.

Moderate Alcohol Consumption and Chronic Disease: The Case for a Long-Term Trial.

Drinking within recommended limits is highly prevalent in much of the world, and strong epidemiological associations exist between moderate alcohol consumption and risk of several major chronic diseases, including coronary heart disease, diabetes, and breast cancer. In many cases, plausible biological mediators for these associations have been identified in randomized trials, but gold standard evidence that moderate drinking causes or prevents any chronic disease remains elusive and important concerns about available evidence have been raised. Although long-term randomized trials to test the observed associations have been termed impossible, clinical investigators have now successfully completed randomized trials of complex nutritional interventions in a variety of settings, along with trials of alcohol consumption itself of up to 2 years duration. The successful completion of these trials suggests that objections to the execution of a full-scale, long-term clinical trial of moderate drinking on chronic disease are increasingly untenable. We present potential lessons learned for such a trial and discuss key features to maximize its feasibility and value.

Feed-forward neural network model for hunger and satiety related VAS score prediction.

BACKGROUND: An artificial neural network approach was chosen to model the outcome of the complex signaling pathways in the gastro-intestinal tract and other peripheral organs that eventually produce the satiety feeling in the brain upon feeding. METHODS: A multilayer feed-forward neural network was trained with sets of experimental data relating concentration-time courses of plasma satiety hormones to Visual Analog Scales (VAS) scores. The network successfully predicted VAS responses from sets of satiety hormone data obtained in experiments using different food compositions. RESULTS: The correlation coefficients for the predicted VAS responses for test sets having i) a full set of three satiety hormones, ii) a set of only two satiety hormones, and iii) a set of only one satiety hormone were 0.96, 0.96, and 0.89, respectively. The predicted VAS responses discriminated the satiety effects of high satiating food types from less satiating food types both in orally fed and ileal infused forms. CONCLUSIONS: From this application of artificial neural networks, one may conclude that neural network models are very suitable to describe situations where behavior is complex and incompletely understood. However, training data sets that fit the experimental conditions need to be available.

Nutrient-induced glucagon like peptide-1 release is modulated by serotonin.

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 (50mM) and rebaudioside A (12.5mM) 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 (0.155µM) further enhanced casein and safflower oil induced-serotonin release. Exposure of ileal tissue segments to serotonin (30µM) stimulated GLP-1 release whereas it did not induce PYY and CCK release. Serotonin (30 and 100µM) also stimulated GLP-1 release from STC-1 cells, which was inhibited by the non-specific 5HT receptor antagonist asenapine (1 and 10µM). These data suggest that nutrient-induced GLP-1 release is modulated by serotonin through a receptor mediated process.

Intraduodenal infusion of a combination of tastants decreases food intake in humans.

BACKGROUND: Taste receptors are expressed not only in taste buds but also in the gastrointestinal tract. It has been hypothesized that these receptors may play a role in satiety and food intake. OBJECTIVE: This study investigated the effect of intraduodenal tastant infusions (bitter, sweet, and umami) on food intake, hunger and fullness, gastrointestinal symptoms, and gastrointestinal peptide release. DESIGN: Fifteen healthy volunteers [6 male; mean ± SEM age: 23.9 ± 2.0 y; mean ± SEM body mass index (in kg/m(2)): 22.4 ± 0.3] received 5 treatments in a double-blind, randomized, placebo-controlled crossover design. Test days started with the insertion of a nasoduodenal catheter followed by a standardized liquid breakfast. Participants received an intraduodenal infusion 150 min after breakfast, containing quinine (bitter), rebaudioside A (sweet), monosodium glutamate (umami), a combination of the 3 tastants, or placebo (tap water) over a period of 60 min. Food intake was measured during an ad libitum meal, and visual analog scales were used to monitor gastrointestinal complaints and hunger and fullness scores. Blood samples were drawn at regular intervals for cholecystokinin, glucagon-like peptide 1 (GLP-1), and peptide YY (PYY) analysis. RESULTS: Infusion of the combination of tastants substantially decreased food intake (422 ± 97 compared with 486 ± 104 kcal for placebo, P < 0.05), whereas both a combination of tastants and umami decreased hunger scores compared with placebo. No change in cholecystokinin, GLP-1, or PYY concentrations was observed during the infusions. Intraduodenal infusions of the tastants did not result in gastrointestinal symptoms. CONCLUSIONS: Intraduodenal infusion of umami and a combination of tastants inhibits feelings of hunger, but only the latter also reduces food intake. However, these alterations were not accompanied by changes in the plasma concentrations of the gut-derived peptides cholecystokinin, GLP-1, or PYY. This trial was registered at clinicaltrials.gov as NCT01956838.

Effects of mood inductions by meal ambiance and moderate alcohol consumption on endocannabinoids and N-acylethanolamines in humans: a randomized crossover trial.

BACKGROUND: The endocannabinoid system is suggested to play a regulatory role in mood. However, the response of circulating endocannabinoids (ECs) to mood changes has never been tested in humans. In the present study, we examined the effects of mood changes induced by ambiance and moderate alcohol consumption on plasma ECs 2-arachidonoylglycerol (2-AG), anandamide (AEA), and some N-acylethanolamine (NAE) congeners in humans. METHODS: Healthy women (n = 28) participated in a randomized cross-over study. They consumed sparkling white wine (340 mL; 30 g alcohol) or alcohol-free sparkling white wine (340 mL; <2 g alcohol) as part of a standard evening meal in a room with either a pleasant or an unpleasant ambiance. RESULTS: Plasma concentrations of palmitoylethanolamide (PEA) and stearoylethanolamide (SEA) increased after 30 min in the unpleasant ambiance, while they decreased in the pleasant ambiance. Changes in ECs and their NAE congeners correlated with mood states, such as happiness and fatigue, but in the pleasant ambiance without alcohol only. ECs and their NAE congeners were correlated with serum free fatty acids and cortisol. CONCLUSION: This is the first human study to demonstrate that plasma NAEs are responsive to an unpleasant meal ambiance. Furthermore, associations between mood states and ECs and their NAE congeners were observed. TRIAL REGISTRATION: Clinicaltrials.gov NCT01426022.

The effect of alcohol consumption on insulin sensitivity and glycemic status: a systematic review and meta-analysis of intervention studies.

OBJECTIVE: Moderate alcohol consumption is associated with a reduced risk of type 2 diabetes. This reduced risk might be explained by improved insulin sensitivity or improved glycemic status, but results of intervention studies on this relation are inconsistent. The purpose of this study was to conduct a systematic review and meta-analysis of intervention studies investigating the effect of alcohol consumption on insulin sensitivity and glycemic status. RESEARCH DESIGN AND METHODS: PubMed and Embase were searched up to August 2014. Intervention studies on the effect of alcohol consumption on biological markers of insulin sensitivity or glycemic status of at least 2 weeks' duration were included. Investigators extracted data on study characteristics, outcome measures, and methodological quality. RESULTS: Fourteen intervention studies were included in a meta-analysis of six glycemic end points. Alcohol consumption did not influence estimated insulin sensitivity (standardized mean difference [SMD] 0.08 [-0.09 to 0.24]) or fasting glucose (SMD 0.07 [-0.11 to 0.24]) but reduced HbA1c (SMD -0.62 [-1.01 to -0.23]) and fasting insulin concentrations (SMD -0.19 [-0.35 to -0.02]) compared with the control condition. Alcohol consumption among women reduced fasting insulin (SMD -0.23 [-0.41 to -0.04]) and tended to improve insulin sensitivity (SMD 0.16 [-0.04 to 0.37]) but not among men. Results were similar after excluding studies with high alcohol dosages (>40 g/day) and were not influenced by dosage and duration of the intervention. CONCLUSIONS: Although the studies had small sample sizes and were of short duration, the current evidence suggests that moderate alcohol consumption may decrease fasting insulin and HbA1c concentrations among nondiabetic subjects. Alcohol consumption might improve insulin sensitivity among women but did not do so overall.

Moderate alcohol consumption stimulates food intake and food reward of savoury foods.

The aim of this study was to investigate whether food reward plays a role in the stimulating effect of moderate alcohol consumption on subsequent food intake. In addition, we explored the role of oral and gut sensory pathways in alcohol's effect on food reward by modified sham feeding (MSF) or consumption of a preload after alcohol intake.In a single-blind crossover design, 24 healthy men were randomly assigned to either consumption of vodka/orange juice (20 g alcohol) or orange juice only, followed by consumption of cake, MSF of cake or no cake. Food reward was evaluated by actual food intake measured by an ad libitum lunch 45 min after alcohol ingestion and by behavioural indices of wanting and liking of four food categories (high fat, low fat, sweet and savoury).Moderate alcohol consumption increased food intake during the ad libitum lunch by 11% (+338 kJ, P = 0.004). Alcohol specifically increased intake (+127 kJ, P <0.001) and explicit liking (P = 0.019) of high-fat savoury foods. Moreover, moderate alcohol consumption increased implicit wanting for savoury (P = 0.013) and decreased implicit wanting for sweet (P = 0.017) before the meal. Explicit wanting of low-fat savoury foods only was higher after alcohol followed by no cake as compared to after alcohol followed by cake MSF (P = 0.009), but not as compared to alcohol followed by cake consumption (P = 0.082). Both cake MSF and cake consumption had no overall effect on behavioural indices of food reward.To conclude, moderate alcohol consumption increased subsequent food intake, specifically of high-fat savoury foods. This effect was related to the higher food reward experienced for savoury foods. The importance of oral and gut sensory signalling in alcohol's effect on food reward remains largely unclear.

Cross-species comparison of genes related to nutrient sensing mechanisms expressed along the intestine.

INTRODUCTION: Intestinal chemosensory receptors and transporters are able to detect food-derived molecules and are involved in the modulation of gut hormone release. Gut hormones play an important role in the regulation of food intake and the control of gastrointestinal functioning. This mechanism is often referred to as "nutrient sensing". Knowledge of the distribution of chemosensors along the intestinal tract is important to gain insight in nutrient detection and sensing, both pivotal processes for the regulation of food intake. However, most knowledge is derived from rodents, whereas studies in man and pig are limited, and cross-species comparisons are lacking. AIM: To characterize and compare intestinal expression patterns of genes related to nutrient sensing in mice, pigs and humans. METHODS: Mucosal biopsy samples taken at six locations in human intestine (n = 40) were analyzed by qPCR. Intestinal scrapings from 14 locations in pigs (n = 6) and from 10 locations in mice (n = 4) were analyzed by qPCR and microarray, respectively. The gene expression of glucagon, cholecystokinin, peptide YY, glucagon-like peptide-1 receptor, taste receptor T1R3, sodium/glucose cotransporter, peptide transporter-1, GPR120, taste receptor T1R1, GPR119 and GPR93 was investigated. Partial least squares (PLS) modeling was used to compare the intestinal expression pattern between the three species. RESULTS AND CONCLUSION: The studied genes were found to display specific expression patterns along the intestinal tract. PLS analysis showed a high similarity between human, pig and mouse in the expression of genes related to nutrient sensing in the distal ileum, and between human and pig in the colon. The gene expression pattern was most deviating between the species in the proximal intestine. Our results give new insights in interspecies similarities and provide new leads for translational research and models aiming to modulate food intake processes in man.

Steviol glycoside rebaudioside A induces glucagon-like peptide-1 and peptide YY release in a porcine ex vivo intestinal model.

Glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are hormones important for satiation and are involved in the process called "ileal brake". The aim of this study was to investigate the GLP-1- and PYY-stimulating efficacy of rebaudioside A, casein, and sucrose. This was studied using tissue segments collected from various regions of the pig small intestine. GLP-1 release was strongest from the distal ileum. There, control release was 0.06 ± 0.01 (GLP-1) and 0.07 ± 0.01 (PYY) pmol/cm(2) of tissue. Rebaudioside A (2.5, 12.5, and 25 mM) stimulated GLP-1 release (0.14 ± 0.02, 0.16 ± 0.02, and 0.13 ± 0.02 pmol/cm(2) of tissue, p < 0.001) and PYY release (0.19 ± 0.02, 0.42 ± 0.06, and 0.27 ± 0.03 pmol/cm(2) of tissue, p < 0.001). Sucrose stimulated GLP-1 release (0.08 ± 0.01 pmol/cm(2) of tissue, p < 0.05) only at 10 mM. Casein (0.5%, 1%, and 2.5%, w/v) stimulated GLP-1 release (0.15 ± 0.03, 0.13 ± 0.02, and 0.14 ± 0.01 pmol/cm(2) of tissue, p < 0.001) and PYY release (0.13 ± 0.02, 0.20 ± 0.03, and 0.27 ± 0.03 pmol/cm(2) of tissue, p < 0.01). These findings may help in developing dietary approaches for weight management.