peptide-yy and Inflammation

Dietary β-glucans are soluble fibers with potentially health-promoting effects. Gut peptides are important signals in the regulation of energy and glucose homeostasis. This article reviews the effects of different enriched β-glucan food consumption on immune responses, inflammation, gut hormone and cancer. Gut hormones are influenced by enriched β-glucan food consumption and levels of such peptide as YY, ghrelin, glucagon-like peptide 1 and 2 in humans influence serum glucose concentration as well as innate and adaptive immunity. Cancer cell development is also regulated by obesity and glucose dishomeostasy that are influenced by β-glucan food consumption that in turn regulated gut hormones.

Topics: Animals; beta-Glucans; Functional Food; Ghrelin; Glucagon-Like Peptide 1; Glucagon-Like Peptide 2; Humans; Inflammation; Neoplasms; Peptide YY

RA is characterized by chronic inflammation in the musculoskeletal system, in which TNF-α is the key cytokine trigger. TNF-α, previously known as cachectin, is implicated in the modulation of body composition and energy expenditure. Gut hormones, including acyl ghrelin, des-acyl ghrelin, GIP, GLP-1 and PYY, have been known to be the major regulators of appetite, nutrition, energy expenditure and body mass formation. Emerging evidence indicates that blockade of TNF-α by biologics not only ameliorates rheumatoid inflammation, but can affect the secretion and action of gut hormones on appetite, body composition, energy expenditure, muscle catabolism and bone remodelling. A link between the gastrointestinal endocrine axis and the immune system may be established through the interaction of proinflammatory cytokines, including TNF-α and these gut hormones. With the ever-increasing understanding of rheumatoid inflammation and the invention of more biologics to modulate the cytokine network, more attention should be given to the possible immunomodulatory roles of gut hormones in autoimmune inflammatory reactions.

Topics: Appetite; Arthritis, Rheumatoid; Biological Products; Energy Metabolism; Gastric Inhibitory Polypeptide; Ghrelin; Glucagon-Like Peptide 1; Humans; Inflammation; Peptide YY; Tumor Necrosis Factor-alpha

The intestine is an important metabolic organ that has gained attention in recent years for the newly identified role that it plays in the pathophysiology of various metabolic diseases including obesity, insulin resistance and diabetes. Recent insights regarding the role of enteroendocrine hormones, such as GIP, GLP-1, and PYY in metabolic diseases, as well as the emerging role of the gut microbial community and gastric bypass bariatric surgeries in modulating metabolic function and dysfunction have sparked a wave of interest in understanding the mechanisms involved, in an effort to identify new therapeutics and novel regulators of metabolism. This review summarizes the current evidence that the gastrointestinal tract has a key role in the development of obesity, inflammation, insulin resistance and diabetes and discusses the possible players that can be targeted for therapeutic intervention.

Topics: Animals; Bariatric Surgery; Diabetes Mellitus, Type 2; Gastric Inhibitory Polypeptide; Gastrointestinal Hormones; Gastrointestinal Tract; Glucagon-Like Peptide 1; Humans; Inflammation; Insulin Resistance; Metabolic Diseases; Metagenome; Obesity; Peptide YY

Topics: Cross-Over Studies; Gastrointestinal Hormones; Gastrointestinal Motility; Glucagon-Like Peptide 1; Humans; Inflammation; Lipopolysaccharides; Male; Nausea; Peptide YY

The prevalence of obesity is increasing worldwide and prevention is needed. Whole grain has shown potential to lower the risk of obesity, cardiovascular disease and type 2 diabetes. One possible mechanism behind the benefits of whole grain is the gut fermentation of dietary fiber (DF), e.g. non-starch polysaccharides and resistant starch (RS), in whole grain. The purpose of the study is to investigate the effect of whole grain rye-based products on glucose- and appetite regulation.. Twenty-one healthy subjects were provided four rye-based evening test meals in a crossover overnight study design. The test evening meals consisted of either whole grain rye flour bread (RFB) or a 1:1 ratio of whole grain rye flour and rye kernels bread (RFB/RKB), with or without added resistant starch (+RS). White wheat flour bread (WWB) was used as reference evening meal. Blood glucose, insulin, PYY, FFA, IL-6 as well as breath H. The evening meal with RFB/RKB + RS decreased postprandial glucose- and insulin responses (iAUC) (P < 0.05) and increased the gut hormone PYY in plasma the following morning 0-120 min after the standardized breakfast, compared to WWB (P = 0.01). Moreover, RFB increased subjective satiety and decreased desire to eat, and both RFB and RFB/RKB decreased feeling of hunger (AUC 0-210 min). All rye-based evening meals decreased or tended to decrease fasting FFA (P < 0.05, RFB/RKB: P = 0.057) and increased breath hydrogen concentration (0-120 min, P < 0.001). No effects were noted on energy intake at lunch or inflammatory marker IL-6 (0 + 180 min) after the rye-based evening meals, compared to WWB.. Whole grain rye bread has the potential to improve cardiometabolic variables in an 11-14.5 h perspective in healthy humans. The combination RFB/RKB + RS positively affected biomarkers of glucose- and appetite regulation in a semi-acute perspective. Meanwhile, RFB and RFB/RKB improved subjective appetite ratings. The effects probably emanate from gut fermentation events.. The study was registered at: ClinicalTrials.gov, register number NCT02347293 ( www.clinicaltrials.gov/ct2/show/NCT02347293 ). Registered 15 January 2015.

Topics: Adult; Appetite; Biomarkers; Blood Glucose; Body Mass Index; Bread; Cholesterol; Cross-Over Studies; Cytokines; Diet; Dietary Carbohydrates; Dietary Fiber; Fatty Acids, Nonesterified; Female; Gastrointestinal Hormones; Glucose Tolerance Test; Healthy Volunteers; Humans; Inflammation; Insulin; Interleukin-6; Male; Peptide YY; Portion Size; Postprandial Period; Secale; Starch; Treatment Outcome; Triglycerides; Whole Grains; Young Adult

Advanced glycation end products (AGEs) formed in food during high-heat cooking may induce overeating and inflammation. We investigated whether AGE contents in a single meal affect postprandial appetite and markers of inflammation, endothelial activation, and oxidative stress.. In total, 19 healthy overweight individuals completed a crossover meal test with two meals of identical ingredients prepared by roasting (H-AGE) or steaming (L-AGE), respectively. Postprandial blood samples were analysed for N(ε)-carboxymethyl-lysine (CML), appetite-regulating gut hormones, glucose, insulin, triacylglycerol, and markers of inflammation and endothelial activation. Subjective appetite ratings and subsequent food intake were also assessed, and urine was analysed for CML, methylglyoxal-derived hydroimidazolone (MG-H1), and F2-isoprostanes.. CML content of the H- and L-AGE meals was 5.0 and 2.8 mg, respectively. Plasma CML and urinary CML and MG-H1 tended to be higher after the H-AGE meal. There was no change in subsequent food intake, appetite sensations, or appetite hormone responses between meals, except for the overall ghrelin response, which was higher after the H-AGE meal compared with the L-AGE meal (p = 0.016). There was an increased glycaemic response to the H-AGE meal (p = 0.027) compared with the L-AGE meal. Inflammatory and endothelial activation markers did not differ between meals, but there was an overall effect on endothelial activation (p = 0.021) and on the oxidative marker, F2-isoprostanes, in urine (p = 0.013).. The present study did not show any pronounced effects of AGEs on appetite and markers of inflammation, but did indicate that AGEs may affect postprandial ghrelin, oxidative stress, and glucose responses.

Topics: Adult; Appetite; Blood Glucose; Body Mass Index; Cross-Over Studies; Diet; Endothelium; Energy Intake; F2-Isoprostanes; Female; Ghrelin; Glucagon-Like Peptide 1; Glycation End Products, Advanced; Hot Temperature; Humans; Inflammation; Insulin; Lysine; Male; Middle Aged; Overweight; Oxidative Stress; Peptide YY; Postprandial Period; Steam; Triglycerides

The disturbance of intestinal microorganisms and the exacerbation of type 2 diabetes (T2D) are mutually influenced. In this study, the effect of exopolysaccharides (EPS) from

Topics: Animals; Bacterial Adhesion; Blood Glucose; Caco-2 Cells; Diabetes Mellitus, Type 2; Energy Metabolism; Gastrointestinal Microbiome; Glucagon-Like Peptide 1; Humans; Inflammation; Interleukin-10; Interleukin-6; Intestines; Lacticaseibacillus paracasei; Lactobacillus plantarum; Liver; Male; Mice; Mice, Inbred C57BL; Pancreas; Peptide YY; Polysaccharides, Bacterial; Random Allocation; Synbiotics; Tumor Necrosis Factor-alpha

Ghrelin and peptide-YY (PYY) are two gut peptides with apparent opposing actions. In normal conditions, ghrelin and PYY work together in synergy to regulate energy homeostasis. During critical illness, series of metabolic, endocrine, and inflammatory changes take place in response to a severe insult. Emerging studies recorded alterations in gut hormone levels in critically ill adults. This study aims to assess the effect of inflammation, nutrition, and feeding status on ghrelin and PYY levels in critically ill children.. In this prospective study, we collected blood samples from critically ill children on days 2 or 3 of pediatric intensive care unit (PICU) admission for the analysis of serum ghrelin, PYY, and inflammatory markers. Data related to the intake anthropometry, as well as other clinical data, were collected from patients' records. Multiple linear regression analysis was used to identify factors affecting serum levels of these hormones.. Forty-two children admitted to the PICU were included in this study. Ghrelin level was influenced by admission nutrition status of the children and age. PYY was influenced by macronutrient intake and age. Inflammatory markers also showed an association with the measured levels of these hormones, with C-reactive protein being positively associated with ghrelin levels and tumor necrosis factor alpha showing a positive association with PYY levels.. Although ghrelin and PYY have been linked to feeding status in healthy patients, during critical illness there might be other factors, such as inflammation and nutrition status, that might contribute to the changes observed in ghrelin/PYY profiles.

Topics: Child; Critical Illness; Ghrelin; Humans; Inflammation; Nutritional Status; Peptide YY; Prospective Studies

Complex interactions between keratinocytes and various cell types, such as inflammatory cells and stromal cells, contribute to the pathogenesis of chronic inflammatory skin lesions. In proinflammatory cytokine‒mediated disease settings, IL-9 plays a pathological role in inflammatory dermatitis. However, IL-9‒related mechanisms remain incompletely understood. In this study, we established tamoxifen-induced keratinocyte-specific IL-9RA-deficient mice (K14

Topics: Animals; Dermatitis; Disease Models, Animal; Imiquimod; Inflammation; Interleukin-9; Keratinocytes; Mice; Peptide YY; Psoriasis; Skin

The central mechanisms underlying the marked beneficial metabolic effects of bariatric surgery are unclear. Here, we characterized global gene expression in the hypothalamic arcuate nucleus (Arc) in diet-induced obese (DIO) rats following Roux-en-Y gastric bypass (RYGB). 60 days post-RYGB, the Arc was isolated by laser-capture microdissection and global gene expression was assessed by RNA sequencing. RYGB lowered body weight and adiposity as compared to sham-operated DIO rats. Discrete transcriptome changes were observed in the Arc following RYGB, including differential expression of genes associated with inflammation and neuropeptide signaling. RYGB reduced gene expression of glial cell markers, including Gfap, Aif1 and Timp1, confirmed by a lower number of GFAP immunopositive astrocyte profiles in the Arc. Sham-operated weight-matched rats demonstrated a similar glial gene expression signature, suggesting that RYGB and dietary restriction have common effects on hypothalamic gliosis. Considering that RYGB surgery also led to increased orexigenic and decreased anorexigenic gene expression, this may signify increased hunger-associated signaling at the level of the Arc. Hence, induction of counterregulatory molecular mechanisms downstream from the Arc may play an important role in RYGB-induced weight loss.

Topics: Adiposity; Animals; Arcuate Nucleus of Hypothalamus; Astrocytes; Biomarkers; Diet, High-Fat; Diet, Reducing; Eating; Gastric Bypass; Gene Expression Profiling; Gene Expression Regulation; Glial Fibrillary Acidic Protein; Gliosis; Glucagon-Like Peptide 1; Inflammation; Laser Capture Microdissection; Male; Neuropeptides; Obesity; Peptide YY; Rats; Rats, Sprague-Dawley; Sequence Analysis, RNA; Weight Loss

The microbial community populating the human digestive tract has been linked to the development of obesity, diabetes and liver diseases. Proposed mechanisms on how the gut microbiota could contribute to obesity and metabolic diseases include: (1) improved energy extraction from diet by the conversion of dietary fibre to SCFA; (2) increased intestinal permeability for bacterial lipopolysaccharides (LPS) in response to the consumption of high-fat diets resulting in an elevated systemic LPS level and low-grade inflammation. Animal studies indicate differences in the physiologic effects of fermentable and non-fermentable dietary fibres as well as differences in long- and short-term effects of fermentable dietary fibre. The human intestinal microbiome is enriched in genes involved in the degradation of indigestible polysaccharides. The extent to which dietary fibres are fermented and in which molar ratio SCFA are formed depends on their physicochemical properties and on the individual microbiome. Acetate and propionate play an important role in lipid and glucose metabolism. Acetate serves as a substrate for de novo lipogenesis in liver, whereas propionate can be utilised for gluconeogenesis. The conversion of fermentable dietary fibre to SCFA provides additional energy to the host which could promote obesity. However, epidemiologic studies indicate that diets rich in fibre rather prevent than promote obesity development. This may be due to the fact that SCFA are also ligands of free fatty acid receptors (FFAR). Activation of FFAR leads to an increased expression and secretion of enteroendocrine hormones such as glucagon-like-peptide 1 or peptide YY which cause satiety. In conclusion, the role of SCFA in host energy balance needs to be re-evaluated.

Topics: Animals; Dietary Fiber; Energy Metabolism; Fatty Acids, Volatile; Gastrointestinal Microbiome; Glucagon-Like Peptide 1; Glucose; Humans; Incretins; Inflammation; Intestinal Mucosa; Intestines; Lipid Metabolism; Lipopolysaccharides; Obesity; Peptide YY; Permeability; Satiation

Cancer-associated anorexia and cachexia are a multifactorial condition described by a loss of body weight and muscle with anorexia, asthenia, and anemia. Moreover, they correlate with a high mortality rate, poor response to chemotherapy, poor performance status, and poor quality of life. Cancer cachexia is regulated by proinflammatory cytokines such as interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor- α (TNF- α). In addition, glucagon like peptide-1 (GIP-1), peptide YY (PYY), ghrelin, and leptin plays a crucial role in food intake. In this study, we investigated the therapeutic effects of one of the traditional herbal medicines, Sipjeondaebo-tang (Juzen-taiho-to in Japanese; SJDBT), on cancer anorexia and cachexia in a fundamental mouse cancer anorexia/cachexia model, CT-26 tumor-bearing mice. SJDBT was more significantly effective in a treatment model where it was treated after anorexia and cachexia than in a prevention model where it was treated before anorexia and cachexia on the basis of parameters such as weights of muscles and whole body and food intakes. Moreover, SJDBT inhibited a production of IL-6, MCP-1, PYY, and GLP-1 and ameliorated cancer-induced anemia. Therefore, our in vivo studies provide evidence on the role of SJDBT in cancer-associated anorexia and cachexia, thereby suggesting that SJDBT may be useful for treating cancer-associated anorexia and cachexia.

Topics: Animals; Anorexia; Body Weight; Cachexia; Cell Line, Tumor; Chemokine CCL2; Drugs, Chinese Herbal; Ghrelin; Glucagon-Like Peptide 1; Inflammation; Interleukin-6; Intestinal Mucosa; Leptin; Male; Mice; Mice, Inbred BALB C; Muscles; Neoplasm Transplantation; Neoplasms; Peptide YY; Plant Preparations; Tumor Necrosis Factor-alpha

Irritable bowel syndrome (IBS) is a common gastrointestinal (GI) disorder that considerably reduces the quality of life. It further represents an economic burden on society due to the high consumption of healthcare resources and the non-productivity of IBS patients. The diagnosis of IBS is based on symptom assessment and the Rome III criteria. A combination of the Rome III criteria, a physical examination, blood tests, gastroscopy and colonoscopy with biopsies is believed to be necessary for diagnosis. Duodenal chromogranin A cell density is a promising biomarker for the diagnosis of IBS. The pathogenesis of IBS seems to be multifactorial, with the following factors playing a central role in the pathogenesis of IBS: heritability and genetics, dietary/intestinal microbiota, low-grade inflammation, and disturbances in the neuroendocrine system (NES) of the gut. One hypothesis proposes that the cause of IBS is an altered NES, which would cause abnormal GI motility, secretions and sensation. All of these abnormalities are characteristic of IBS. Alterations in the NES could be the result of one or more of the following: genetic factors, dietary intake, intestinal flora, or low-grade inflammation. Post-infectious IBS (PI-IBS) and inflammatory bowel disease-associated IBS (IBD-IBS) represent a considerable subset of IBS cases. Patients with PI- and IBD-IBS exhibit low-grade mucosal inflammation, as well as abnormalities in the NES of the gut.

Topics: Adult; Aged; Biomarkers; Cholecystokinin; Chromogranin A; Endocrine Cells; Female; Gastroenterology; Gastrointestinal Tract; Guidelines as Topic; Humans; Inflammation; Intestines; Irritable Bowel Syndrome; Male; Middle Aged; Peptide YY; Prevalence; Serotonin

The aim of the study were to answer the question 1.) Whether circulating pro-inflammatory markers of endothelial dysfunction and due to chronic low-grade inflammation of obesity, are altered in untreated lean, young relatively healthy polycystic ovary syndrome (PCOS) patients in comparison with healthy controls; 2.) Whether postprandial plasma concentration pattern of ghrelin and PYY can be predictable as risk factors for atherosclerosis and depend of obesity. Forty young women with PCOS were divided in two groups: 19 lean and 21 obese. The control group included 20 lean, healthy volunteers. Plasma total and active ghrelin, total PYY and PYY(3-36), serum adiponectin and insulin were measured using RIA technique, serum sCD40L, visfatin, sP-, sE-selectins, resistin by EIA. Composition of test meal was: 527 kcal total and consisted of 24.1% fat, 54.4% carbohydrate and 21.5% protein. Total and active ghrelin and total PYY were significantly lower in obese PCOS women, whereas active ghrelin was also significantly lower in lean PCOS women compared to controls. Postprandial plasma total ghrelin levels decrease were blunted in lean and obese compared to controls (12.8 % and 18.2% vs 28.2 %). Postprandial plasma active ghrelin decreased in lean and obese PCOS groups (49.9 % and 44.1 %) and controls (63.8 %). PCOS subjects exhibited smaller rises in postprandial levels of total PYY. Postprandial plasma PYY(3-36) levels increased in obese PCOS women (30.9 %) and controls (41%), whereas lean PCOS women exhibited blunted increase (11.5%). sCD40L levels increased, whereas adiponectin decreased in PCOS groups independently, whereas rise in visfatin, sE- and sP-selectin and the fall in adiponectin was associated with obesity. sP- and sE -selectins correlated positively with obesity. In summary, our study provides the first evidence that lean untreated young PCOS women contribute to the so called "pancreatic islet adaptation to insulin resistance" because of ghrelin and PYY profiles. We confirmed existing of low-grade chronic inflammation in early stage of visceral obesity in lean PCOS patients. The lost endogenous "islet adaptation to insulin resistance" may lead to endothelial dysfunction and promote acceleration of atherosclerosis.

Topics: Adiponectin; Atherosclerosis; Biomarkers; Body Mass Index; Chronic Disease; Endothelium, Vascular; Female; Ghrelin; Humans; Inflammation; Insulin; Obesity; Peptide YY; Polycystic Ovary Syndrome; Postprandial Period; Risk Factors; Young Adult

It is well documented that neuropeptides participate in local inflammatory reaction and modulate functions of inflammatory cells. The aim of the study was to determine a link between in vivo and in vitro effects of NPY-related peptides on inflammatory response with respect to ageing. Peptide YY (PYY) intraplantarly applied decreases concanavalin A-induced paw edema in 3 and 8 months, but not in 24 months old male rats of Albino Oxford strain. The use of NPY-related receptor-specific peptides and Y1 receptor antagonist revealed that anti-inflammatory effect of PYY is mediated via NPY Y1 receptors. PYY in vitro decreases adherence of macrophages from 8 months, but not from 3 and 24 months old rats and this effect is also mediated via NPY Y1 receptor. Additionally, PYY (10(-6)M) decreases NBT reduction in macrophages from 3 and 8 months old rats, and suppresses NO production in cells from 24 months old rats, albeit regardless of absence of in vivo effect of PYY on inflammation in aged rats. It is concluded that aged rats are less responsive to anti-inflammatory action of PYY compared to adult and young rats, and that ageing is associated with altered NPY Y1 receptor functioning.

Topics: Acute Disease; Aging; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cell Adhesion; Cells, Cultured; Concanavalin A; Dose-Response Relationship, Drug; Edema; Inflammation; Macrophages, Peritoneal; Male; Nitric Oxide; Peptide YY; Rats; Receptors, Neuropeptide Y

Bacillary dysentery arises when Shigella invades the colonic and rectal mucosae of the human gut and elicits a strong inflammatory response, which may lead to life-threatening complications. Hence, downregulation of the host inflammatory response is an appealing therapeutical alternative. The gastrointestinal tract is densely innervated, and nerve endings are often found in the vicinity of leukocytes. We have assessed the impact of experimental Shigella infection on levels of neuropeptides in the intestinal mucosa of rabbits. Ligated small intestinal loops were created in rabbits, and either live, pathogenic Shigella flexneri, a nonpathogenic mutant of Shigella, or NaCl was injected into the loops. Infection was allowed to proceed for 8 or 16 h, after which the rabbits were sacrificed and intestinal biopsies collected. Tissue destruction, fluid secretion and degree of bacterial invasion were monitored. Intestinal biopsies were homogenized, and levels of the neuropeptides calcitonin gene-related peptide, substance P, peptide YY (PYY), vasoactive intestinal peptide, somatostatin, galanin, motilin and neurotensin were measured by radioimmunoassay. Loops exposed to invasive Shigella had 5.7 times lower levels of PYY (P = 0.0095) than loops exposed to NaCl, after 16 h of infection. The levels of the other neuropeptides tested were unchanged. Inhibition of nicotinic cholinergic neurotransmission partly protected the intestinal mucosa from destruction elicited by invasive Shigella. These findings indicate that a tissue-invasive bacterium such as Shigella, which is strictly localized to the intestinal mucosa, activates intramural nerve reflexes that presumably involve a nicotinic synapse as well as the neuropeptide PYY.

Topics: Animals; Calcitonin Gene-Related Peptide; Dysentery, Bacillary; Galanin; Hexamethonium; Inflammation; Intestinal Mucosa; Intestine, Small; Motilin; Neuropeptides; Neurotensin; Nicotinic Antagonists; Peptide YY; Rabbits; Shigella flexneri; Somatostatin; Substance P; Vasoactive Intestinal Peptide

Several lines of evidence suggest that neuropeptide Y (NPY) may exert regulatory effects in local inflammatory responses. Here, we show that intraplantarly (i.pl.) applied NPY, peptide YY (PYY), and an NPY Y5 receptor-selective agonist dose-dependently potentiate concanavalin A (Con A)-induced paw edema in the rat. The NPY Y1 receptor antagonist BIBO 3304 abolishes the pro-inflammatory action of both NPY and PYY while the dipeptidyl-peptidase IV (CD26) inhibitor Ile-thiazolidide exerted synergistic and potentiating effects in vivo. Taken together, the present data reveal an NPY Y1/Y5 receptor interplay and an involvement of CD26 in the NPY-induced potentiation of paw edema in the rat.

Topics: Animals; Arginine; Cells, Cultured; Concanavalin A; Dipeptidyl Peptidase 4; Dose-Response Relationship, Drug; Edema; Hydrogen Peroxide; Inflammation; Isoleucine; Macrophages; Male; Neuropeptide Y; Peptide Fragments; Peptide YY; Rats; Rats, Wistar; Receptors, Neuropeptide Y; Thiazoles

The effect of potential mediators of mucus secretion was investigated in the isolated vascularly perfused rat colon by using a sandwich enzyme-linked immunosorbent assay for rat colonic mucin and by histochemical analysis. Bethanechol (100-200 microM), bombesin (100 nM), and vasoactive intestinal peptide (VIP, 100 nM) provoked a dramatic mucin discharge (maximal response at 900, 900, and 600% of control loops, respectively). VIP-stimulated mucin secretion was abolished by tetrodotoxin, whereas atropine was without effect. In contrast, both tetrodotoxin and atropine significantly decreased mucin release induced by bombesin. Isoproterenol or calcitonin gene-related peptide was without effect. Serotonin (1-5 microM) and peptide YY (10 nM) evoked mucin discharge, whereas glucagon-like peptide-1 did not release mucin. Finally, bromolasalocid (20 microM), interleukin-1beta (0.25 nM), sodium nitroprusside (1 mM), and dimethyl-PGE2 (2.5 microM) induced mucus discharge. The results demonstrated a good correlation between the immunological method and histological analysis. In conclusion, these findings suggest a role for the enteric nervous system, the enteroendocrine cells, and resident immune cells in mediation of colonic mucus release.

Topics: 16,16-Dimethylprostaglandin E2; Animals; Atropine; Bethanechol; Bombesin; Calcitonin Gene-Related Peptide; Colon; Enteric Nervous System; Gastrointestinal Hormones; Glucagon; Glucagon-Like Peptide 1; Inflammation; Interleukin-1; Intestinal Mucosa; Isoproterenol; Lasalocid; Male; Mucus; Neurotransmitter Agents; Nitroprusside; Peptide Fragments; Peptide YY; Protein Precursors; Rats; Rats, Wistar; Serotonin; Tetrodotoxin; Vasoactive Intestinal Peptide