scholarly journals Effects of neurotransmitters, gut hormones, and inflammatory mediators on mucus discharge in rat colon

1998 ◽  
Vol 275 (5) ◽  
pp. G1073-G1084 ◽  
Author(s):  
Pascale Plaisancié ◽  
Aline Barcelo ◽  
Frederic Moro ◽  
Jean Claustre ◽  
Jean-Alain Chayvialle ◽  
...  
Keyword(s):  
Peptide Yy ◽  
Gut Hormones ◽  
Rat Colon ◽  
Maximal Response ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Loops ◽  
Colonic Mucin ◽  
Calcitonin Gene ◽  
Glucagon Like Peptide 1 ◽  
Mucin Release

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 μM), 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 μM) and peptide YY (10 nM) evoked mucin discharge, whereas glucagon-like peptide-1 did not release mucin. Finally, bromolasalocid (20 μM), interleukin-1β (0.25 nM), sodium nitroprusside (1 mM), and dimethyl-PGE2(2.5 μM) 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.

scholarly journals Bile acids drive colonic secretion of glucagon-like-peptide 1 and peptide-YY in rodents

2019 ◽  
Vol 316 (5) ◽  
pp. G574-G584 ◽  
Author(s):  
Charlotte Bayer Christiansen ◽  
Samuel Addison Jack Trammell ◽  
Nicolai Jacob Wewer Albrechtsen ◽  
Kristina Schoonjans ◽  
Reidar Albrechtsen ◽  
...  
Keyword(s):  
Bile Acids ◽  
G Protein ◽  
Peptide Yy ◽  
Whole Body ◽  
Rat Colon ◽  
G Protein Coupled Receptor ◽  
L Cells ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
G Protein Coupled

A large number of glucagon-like-peptide-1 (GLP-1)- and peptide-YY (PYY)-producing L cells are located in the colon, but little is known about their contribution to whole body metabolism. Since bile acids (BAs) increase GLP-1 and PYY release, and since BAs spill over from the ileum to the colon, we decided to investigate the ability of BAs to stimulate colonic GLP-1 and PYY secretion. Using isolated perfused rat/mouse colon as well as stimulation of the rat colon in vivo, we demonstrate that BAs significantly enhance secretion of GLP-1 and PYY from the colon with average increases of 3.5- and 2.9-fold, respectively. Furthermore, we find that responses depend on BA absorption followed by basolateral activation of the BA-receptor Takeda-G protein-coupled-receptor 5. Surprisingly, the apical sodium-dependent BA transporter, which serves to absorb conjugated BAs, was not required for colonic conjugated BA absorption or conjugated BA-induced peptide secretion. In conclusion, we demonstrate that BAs represent a major physiological stimulus for colonic L-cell secretion.NEW & NOTEWORTHY By the use of isolated perfused rodent colon preparations we show that bile acids are potent and direct promoters of colonic glucagon-like-peptide 1 and peptide-YY secretion. The study provides convincing evidence that basolateral Takeda-G protein-coupled-receptor 5 activation is mediating the effects of bile acids in the colon and thus add to the existing literature described for L cells in the ileum.

scholarly journals Neurotensin Is Coexpressed, Coreleased, and Acts Together With GLP-1 and PYY in Enteroendocrine Control of Metabolism

Endocrinology ◽  
2016 ◽  
Vol 157 (1) ◽  
pp. 176-194 ◽  
Author(s):  
Kaare V. Grunddal ◽  
Cecilia F. Ratner ◽  
Berit Svendsen ◽  
Felix Sommer ◽  
Maja S. Engelstoft ◽  
...  
Keyword(s):  
Peptide Yy ◽  
Secretory Granules ◽  
Gut Hormones ◽  
Distal Small Intestine ◽  
Cell Ablation ◽  
Target Organs ◽  
Gut Hormone ◽  
Toxin Receptor ◽  
Functional Consequences ◽  
Glucagon Like Peptide 1

Abstract The 2 gut hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are well known to be coexpressed, costored, and released together to coact in the control of key metabolic target organs. However, recently, it became clear that several other gut hormones can be coexpressed in the intestinal-specific lineage of enteroendocrine cells. Here, we focus on the anatomical and functional consequences of the coexpression of neurotensin with GLP-1 and PYY in the distal small intestine. Fluorescence-activated cell sorting analysis, laser capture, and triple staining demonstrated that GLP-1 cells in the crypts become increasingly multihormonal, ie, coexpressing PYY and neurotensin as they move up the villus. Proglucagon promoter and pertussis toxin receptor-driven cell ablation and reappearance studies indicated that although all the cells die, the GLP-1 cells reappear more quickly than PYY- and neurotensin-positive cells. High-resolution confocal fluorescence microscopy demonstrated that neurotensin is stored in secretory granules distinct from GLP-1 and PYY storing granules. Nevertheless, the 3 peptides were cosecreted from both perfused small intestines and colonic crypt cultures in response to a series of metabolite, neuropeptide, and hormonal stimuli. Importantly, neurotensin acts synergistically, ie, more than additively together with GLP-1 and PYY to decrease palatable food intake and inhibit gastric emptying, but affects glucose homeostasis in a more complex manner. Thus, neurotensin is a major gut hormone deeply integrated with GLP-1 and PYY, which should be taken into account when exploiting the enteroendocrine regulation of metabolism pharmacologically.

DIFFERENTIAL EFFECTS OF BILE ACIDS ON THE POST-PRANDIAL SECRETION OF GUT HORMONES: a randomised crossover study

2021 ◽  
Author(s):  
Emma Rose McGlone ◽  
Khalefah Malallah ◽  
Joyceline Cuenco ◽  
Nicolai J. Wewer Albrechtsen ◽  
Jens J. Holst ◽  
...  
Keyword(s):  
Bile Acids ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Mixed Meal ◽  
Gut Hormone ◽  
Mixed Meal Test ◽  
Hormone Responses ◽  
Glucagon Like Peptide 1 ◽  
Fibroblast Growth Factor 19 ◽  
Insulinotropic Peptide

AIMS Bile acids (BA) regulate post-prandial metabolism directly and indirectly by affecting the secretion of gut hormones like glucagon-like peptide-1 (GLP-1). The post-prandial effects of BA on the secretion of other metabolically active hormones are not well understood. The objective of this study was to investigate the effect of oral ursodeoxycholic acid (UDCA) and chenodeoxycholic acid (CDCA) on post-prandial secretion of GLP-1, oxyntomodulin (OXM), peptide YY (PYY), glucose-dependent insulinotropic peptide (GIP), glucagon and ghrelin. METHODS Twelve healthy volunteers underwent a mixed meal test 60 minutes after ingestion of UDCA (12-16 mg/kg), CDCA (13-16 mg/kg) or no BA in a randomised cross-over study. Glucose, insulin, GLP-1, OXM, PYY, GIP, glucagon, ghrelin and fibroblast growth factor 19 were measured prior to BA administration at -60, 0 (just prior to mixed meal) and 15, 30, 60, 120, 180 and 240 minutes after the meal. RESULTS UDCA and CDCA provoked differential gut hormone responses: UDCA did not have any significant effects, but CDCA provoked significant increases in GLP-1 and OXM and a profound reduction in GIP. CDCA increased fasting GLP-1 and OXM secretion in parallel with an increase in insulin. On the other hand, CDCA reduced post-prandial secretion of GIP, with an associated reduction in post-prandial insulin secretion. CONCLUSIONS Exogenous CDCA can exert multiple salutary effects on the secretion of gut hormones; if these effects are confirmedin obesity and type 2 diabetes, CDCA may be a potential therapy for these conditions.

Gut microbiome, metabolic syndrome, and atherosclerosis

ESC CardioMed ◽  
2018 ◽  
pp. 1082-1085
Author(s):  
Eduard F. Stange
Keyword(s):  
Metabolic Syndrome ◽  
Gut Microbiome ◽  
Peptide Yy ◽  
Endocannabinoid System ◽  
Gut Hormones ◽  
Adenosine Monophosphate ◽  
Farnesoid X Receptor ◽  
Glucagon Like Peptide 1 ◽  
G Protein Coupled ◽  
Definite Role

The link between the gut microbiome and metabolic syndrome is complicated and reaches far beyond energy conservation from dietary fibre through bacterial glycosidases. Involved mechanisms include fasting-induced adipose factor affecting lipoprotein lipase, adenosine monophosphate-activated protein kinase regulating lipogenesis, and G protein-coupled receptors acting through the gut hormones peptide YY and glucagon-like peptide-1. In addition, farnesoid X receptor via ceramide secretion as well as the endocannabinoid system may induce obesity. Finally, there appears to be a definite role for gut bacteria-induced chronic (subclinical) inflammation. This state of metabolic syndrome, insulin resistance, and obesity clearly is a major risk factor for atherosclerosis.

scholarly journals MON-589 Studying Mechanisms of Satiety in the Human Ileum and Colon

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Anya Ramgulam ◽  
Martina Tashkova ◽  
Maeve O’Driscoll ◽  
Georgia Franco Becker ◽  
Hannah Stephens ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Glucose Homeostasis ◽  
Peptide Yy ◽  
Gut Hormones ◽  
16S Rrna Gene Sequencing ◽  
Gut Contents ◽  
Rrna Gene ◽  
Clinical Research Facility ◽  
Glucagon Like Peptide 1 ◽  
Rrna Gene Sequencing

Abstract Background The gut-brain axis plays important roles in the regulation of appetite and glucose homeostasis. The presence of nutrients and their digestive products in specific regions of the gastrointestinal tract modulates neuronal and hormonal signalling, including the release of the appetite-suppressing gut hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY). While there has been significant research into the upper gut mechanisms behind satiation, i.e. the termination of meal, the role of the ileum and colon in satiety, i.e. the process which delays a subsequent meal, has been relatively little investigated, particularly in humans. Methods Ten healthy volunteers attended our Clinical Research Facility for two visits of four days each. At each visit they had either a nasoileal or a nasocolonic tube inserted under fluoroscopy. They were then provided a diet rich in protein and fibre to promote satiety. Gut contents and blood samples were taken before and during test meals at the start and end of the visit, and visual analogue scales were used to measure subjective feelings of appetite. Metabonomic analysis of gut fluid was carried out using a combination of in-house NMR and LC-MS-based methods. 16S rRNA gene sequencing was used to investigate effects on the colonic microbiome. Circulating levels of glucose, the gut hormones GLP-1 and PYY, and the pancreatic hormones insulin and glucagon were measured. Results and discussion The test meals resulted in sustained suppression of appetite and release of GLP-1 and PYY. Ileal and colonic microbial profiles were distinct from those identified in stool samples, and changed with adaptation to the high protein and fibre diet. Integrating hormonal, metabonomic and bacterial datasets from these human studies gives insight into how nutrient and metabolite sensing in the gastrointestinal tract regulates appetite and glucose homeostasis, and may suggest novel therapeutic targets for metabolic disease.

scholarly journals A Plant-Based Meal Increases Gastrointestinal Hormones and Satiety More Than an Energy- and Macronutrient-Matched Processed-Meat Meal in T2D, Obese, and Healthy Men: A Three-Group Randomized Crossover Study

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 157 ◽  
Author(s):  
Marta Klementova ◽  
Lenka Thieme ◽  
Martin Haluzik ◽  
Renata Pavlovicova ◽  
Martin Hill ◽  
...  
Keyword(s):  
Repeated Measures ◽  
Peptide Yy ◽  
Plasma Concentrations ◽  
Gastrointestinal Hormones ◽  
Gut Hormones ◽  
Acute Effect ◽  
Processed Meat ◽  
Healthy Men ◽  
Meat Meal ◽  
Glucagon Like Peptide 1

Gastrointestinal hormones are involved in regulation of glucose metabolism and satiety. We tested the acute effect of meal composition on these hormones in three population groups. A randomized crossover design was used to examine the effects of two energy- and macronutrient-matched meals: a processed-meat and cheese (M-meal) and a vegan meal with tofu (V-meal) on gastrointestinal hormones, and satiety in men with type 2 diabetes (T2D, n = 20), obese men (O, n = 20), and healthy men (H, n = 20). Plasma concentrations of glucagon-like peptide -1 (GLP-1), amylin, and peptide YY (PYY) were determined at 0, 30, 60, 120 and 180 min. Visual analogue scale was used to assess satiety. We used repeated-measures Analysis of variance (ANOVA) for statistical analysis. Postprandial secretion of GLP-1 increased after the V-meal in T2D (by 30.5%; 95%CI 21.2 to 40.7%; p < 0.001) and H (by 15.8%; 95%CI 8.6 to 23.5%; p = 0.01). Postprandial plasma concentrations of amylin increased in in all groups after the V-meal: by 15.7% in T2D (95%CI 11.8 to 19.6%; p < 0.001); by 11.5% in O (95%CI 7.8 to 15.3%; p = 0.03); and by 13.8% in H (95%CI 8.4 to 19.5%; p < 0.001). An increase in postprandial values of PYY after the V-meal was significant only in H (by 18.9%; 95%CI 7.5 to 31.3%; p = 0.03). Satiety was greater in all participants after the V-meal: by 9% in T2D (95%CI 4.4 to 13.6%; p = 0.004); by 18.7% in O (95%CI 12.8 to 24.6%; p < 0.001); and by 25% in H (95%CI 18.2 to 31.7%; p < 0.001). Our results indicate there is an increase in gut hormones and satiety, following consumption of a single plant-based meal with tofu when compared with an energy- and macronutrient-matched processed-meat meat and cheese meal, in healthy, obese and diabetic men.

scholarly journals Plant-rich mixed meals based on Palaeolithic diet principles have a dramatic impact on incretin, peptide YY and satiety response, but show little effect on glucose and insulin homeostasis: an acute-effects randomised study

2015 ◽  
Vol 113 (4) ◽  
pp. 574-584 ◽  
Author(s):  
H. Frances J. Bligh ◽  
Ian F. Godsland ◽  
Gary Frost ◽  
Karl J. Hunter ◽  
Peter Murray ◽  
...  
Keyword(s):  
Peptide Yy ◽  
Blood Glucose Control ◽  
Gut Hormones ◽  
Acute Effects ◽  
Randomised Study ◽  
Satiety Response ◽  
Gut Hormone ◽  
Palaeolithic Diet ◽  
Glucagon Like Peptide 1 ◽  
Few Data

There is evidence for health benefits from ‘Palaeolithic’ diets; however, there are a few data on the acute effects of rationally designed Palaeolithic-type meals. In the present study, we used Palaeolithic diet principles to construct meals comprising readily available ingredients: fish and a variety of plants, selected to be rich in fibre and phyto-nutrients. We investigated the acute effects of two Palaeolithic-type meals (PAL 1 and PAL 2) and a reference meal based on WHO guidelines (REF), on blood glucose control, gut hormone responses and appetite regulation. Using a randomised cross-over trial design, healthy subjects were given three meals on separate occasions. PAL2 and REF were matched for energy, protein, fat and carbohydrates; PAL1 contained more protein and energy. Plasma glucose, insulin, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP) and peptide YY (PYY) concentrations were measured over a period of 180 min. Satiation was assessed using electronic visual analogue scale (EVAS) scores. GLP-1 and PYY concentrations were significantly increased across 180 min for both PAL1 (P= 0·001 and P< 0·001) and PAL2 (P= 0·011 and P= 0·003) compared with the REF. Concomitant EVAS scores showed increased satiety. By contrast, GIP concentration was significantly suppressed. Positive incremental AUC over 120 min for glucose and insulin did not differ between the meals. Consumption of meals based on Palaeolithic diet principles resulted in significant increases in incretin and anorectic gut hormones and increased perceived satiety. Surprisingly, this was independent of the energy or protein content of the meal and therefore suggests potential benefits for reduced risk of obesity.

scholarly journals Peptide YY, appetite and food intake

2005 ◽  
Vol 64 (2) ◽  
pp. 213-216 ◽  
Author(s):  
C. W. le Roux ◽  
S. R. Bloom
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Energy Content ◽  
Peak Plasma ◽  
Evolutionary Relationship ◽  
Gut Hormones ◽  
Amino Acid Peptide ◽  
Control Food ◽  
Glucagon Like Peptide 1 ◽  
Control Food Intake

Obesity is taking on pandemic proportions. The laws of thermodynamics, however, remain unchanged, as energy will be stored if less energy is expended than consumed; the storage is usually in the form of adipose tissue. Several neural, humeral and psychological factors control the complex process known as appetite. Recently, a close evolutionary relationship between the gut and brain has become apparent. The gut hormones regulate important gastrointestinal functions such as motility, secretion, absorption, provide feedback to the central nervous system on availability of nutrients and may play a part in regulating food intake. Peptide YY (PYY) is a thirty-six amino acid peptide related to neuropeptide Y (NPY) and is co-secreted with glucagon-like peptide 1. Produced by the intestinal L-cells, the highest tissue concentrations of PYY are found in distal segments of the gastrointestinal tract, although it is present throughout the gut. Following food intake PYY is released into the circulation. PYY concentrations are proportional to meal energy content and peak plasma levels appear postprandially after 1 h. PYY3-36 is a major form of PYY in both the gut mucosal endocrine cells and the circulation. Peripheral administration of PYY3-36 inhibits food intake for several hours in both rodents and man. The binding of PYY3-36 to the Y2 receptor leads to an inhibition of the NPY neurones and a possible reciprocal stimulation of the pro-opiomelanocortin neurones. Thus, PYY3-36 appears to control food intake by providing a powerful feedback on the hypothalamic circuits. The effect on food intake has been demonstrated at physiological concentrations and, therefore, PYY3-36 may be important in the everyday regulation of food intake.

Inhibition of gastric emptying by acarbose is correlated with GLP-1 response and accompanied by CCK release

2001 ◽  
Vol 281 (3) ◽  
pp. G752-G763 ◽  
Author(s):  
Feruze Y. Enç ◽  
Neşe I˙meryüz ◽  
Levent Akin ◽  
Turgut Turoğlu ◽  
Fuat Dede ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Peptide Yy ◽  
Area Under The Curve ◽  
Gut Hormones ◽  
Random Order ◽  
Mixed Meal ◽  
Carbohydrate Absorption ◽  
Plasma Response ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

We investigated the effect of acarbose, an α-glucosidase and pancreatic α-amylase inhibitor, on gastric emptying of solid meals of varying nutrient composition and plasma responses of gut hormones. Gastric emptying was determined with scintigraphy in healthy subjects, and all studies were performed with and without 100 mg of acarbose, in random order, at least 1 wk apart. Acarbose did not alter the emptying of a carbohydrate-free meal, but it delayed emptying of a mixed meal and a carbohydrate-free meal given 2 h after sucrose ingestion. In meal groups with carbohydrates, acarbose attenuated responses of plasma insulin and glucose-dependent insulinotropic polypeptide (GIP) while augmenting responses of CCK, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY). With mixed meal + acarbose, area under the curve (AUC) of gastric emptying was positively correlated with integrated plasma response of GLP-1 ( r = 0.68 , P < 0.02). With the carbohydrate-free meal after sucrose and acarbose ingestion, AUC of gastric emptying was negatively correlated with integrated plasma response of GIP, implying that prior alteration of carbohydrate absorption modifies gastric emptying of a meal. The results demonstrate that acarbose delays gastric emptying of solid meals and augments release of CCK, GLP-1, and PYY mainly by retarding/inhibiting carbohydrate absorption. Augmented GLP-1 release by acarbose appears to play a major role in the inhibition of gastric emptying of a mixed meal, whereas CCK and PYY may have contributory roles.

scholarly journals Combination gut hormones: prospects and questions for the future of obesity and diabetes therapy

2020 ◽  
Vol 246 (3) ◽  
pp. R65-R74 ◽  
Author(s):  
Bernard Khoo ◽  
Tricia Mei-Mei Tan
Keyword(s):  
Peptide Yy ◽  
Gut Hormones ◽  
Clinical Results ◽  
Therapeutic Effects ◽  
Physiological Basis ◽  
Obesity And Diabetes ◽  
Gut Hormone ◽  
Glucagon Like Peptide 1 ◽  
Treatment Of Obesity ◽  
Insulinotropic Peptide

Obesity represents an important public health challenge for the twenty-first century: globalised, highly prevalent and increasingly common with time, this condition is likely to reverse some of the hard-won gains in mortality accomplished in previous centuries. In the search for safe and effective therapies for obesity and its companion, type 2 diabetes mellitus (T2D), the gut hormone glucagon-like peptide-1 (GLP-1) has emerged as a forerunner and analogues thereof are now widely used in treatment of obesity and T2D, bringing proven benefits in improving glycaemia and weight loss and, notably, cardiovascular outcomes. However, GLP-1 alone is subject to limitations in terms of efficacy, and as a result, investigators are evaluating other gut hormones such as glucose-dependent insulinotropic peptide (GIP), glucagon and peptide YY (PYY) as possible partner hormones that may complement and enhance GLP-1’s therapeutic effects. Such combination gut hormone therapies are in pharmaceutical development at present and are likely to make it to market within the next few years. This review examines the physiological basis for combination gut hormone therapy and presents the latest clinical results that underpin the excitement around these treatments. We also pose, however, some hard questions for the field which need to be answered before the full benefit of such treatments can be realised.

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