scholarly journals Nutrient sensing and signalling by the gut

2012 ◽  
Vol 71 (4) ◽  
pp. 446-455 ◽  
Author(s):  
Rojo Rasoamanana ◽  
Nicolas Darcel ◽  
Gilles Fromentin ◽  
Daniel Tomé
Keyword(s):  
Peptide Yy ◽  
Nutrient Sensing ◽  
Vagal Afferents ◽  
Adaptive Responses ◽  
Gut Peptides ◽  
Intestinal Peptides ◽  
Nutrient Transporter ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Brain

Recent advances highlight that nutrient receptors (such as T1R1/T1R3 heterodimer, Ca sensing receptor and GPR93 for amino acids and protein, GPR40, GPR41, GPR43 and GPR120 for fatty acids, T1R2/T1R3 heterodimer for monosaccharides) are expressed in the apical face of the gut and sense nutrients in the lumen. They transduce signals for the regulation of nutrient transporter expressions in the apical face. Interestingly, they are also localised in enteroendocrine cells (EEC) and mainly exert a direct control on the secretion in the lamina propria of gastro-intestinal peptides such as cholecystokinin, glucagon-like peptide-1 and peptide YY in response to energy nutrient transit and absorption in the gut. This informs central nuclei involved in the control of feeding such as the hypothalamus and nucleus of the solitary tract of the availability of these nutrients and thus triggers adaptive responses to maintain energy homoeostasis. These nutrient receptors then have a prominent position since they manage nutrient absorption and are principally the generator of the first signal of satiation mechanisms mainly transmitted to the brain by vagal afferents. Moreover, tastants are also able to elicit gut peptides secretion via chemosensory receptors expressed in EEC. Targeting these nutrient and tastant receptors in EEC may thus be helpful to promote satiation and so to fight overfeeding and its consequences.

scholarly journals Regulation of Appetite and Satiety by Gastrointestinal Peptides

2021 ◽  
Vol 30 (1) ◽  
pp. 14-21
Author(s):  
Sarah H. Mhaibes ◽  
Najwan K. Fakree ◽  
Sonia I. Naser
Keyword(s):  
Food Consumption ◽  
Energy Homeostasis ◽  
Peptide Yy ◽  
Brain Regions ◽  
Gut Peptides ◽  
Major Health Problem ◽  
Vital Functions ◽  
Gastrointestinal Peptides ◽  
Glucagon Like Peptide 1 ◽  
The Brain

In recent decades, global obesity has increased significantly, causing a major health problem with associated complications and major socioeconomic issues. The central nervous system (CNS), particularly the hypothalamus, regulates food intake through sensing the metabolic signals of peripheral organs and modulating feeding behaviors.  The hypothalamus interacts with other brain regions such as the brain stem to perform these vital functions. The gut plays a crucial role in controlling food consumption and energy homeostasis. The gut releases orexigenic and anorexigenic hormones that interact directly with the CNS or indirectly through vagal afferent neurons. Gastrointestinal peptides (GIP) including cholecystokinin, peptide YY, Nesfatin-1, glucagon-like peptide 1, and oxyntomodulin send satiety signals to the brain and ghrelin transmit hunger signals to the brain. The GIP is essential for the control of food consumption; thus, explain the link between the gastrointestinal tract (GIT) and the brain is important for managing obesity and its associated diseases. This review aimed to explain the role of gut peptides in satiety and hunger control.

Loss of cholecystokinin and glucagon-like peptide-1-induced satiation in mice lacking serotonin 2C receptors

2009 ◽  
Vol 296 (1) ◽  
pp. R51-R56 ◽  
Author(s):  
Lori Asarian
Keyword(s):  
Neural Mechanisms ◽  
Wild Type ◽  
Gut Peptides ◽  
Serotonin Signaling ◽  
The Central Nervous System ◽  
Fos Expression ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Brain

To investigate the role of serotonin 2C receptors (2CR), which are expressed only in the central nervous system, in the satiating actions of the gut peptides CCK and glucagon-like peptide 1 (GLP-1), we examined 1) the effect of null mutations of serotonin 2CR (2CR KO) on the eating-inhibitory potencies of dark-onset intraperitoneal injections of 0.9, 1.7, or 3.5 nmol/kg (1, 2, or 4 μg/kg) CCK and 100, 200, and 400 nmol/kg (33, 66, or 132 μg/kg) GLP-1, and 2) the effects of intraperitoneal injections of 1.7 nmol//kg CCK and 100 nmol/kg GLP-1 on neuronal activation in the brain, as measured by c-Fos expression. All CCK and GLP-1 doses decreased 30-min food intake in wild-type (WT) mice, but none of them did in 2CR KO mice. CCK increased the number of cells expressing c-Fos in the nucleus tractus solitarii (NTS) of WT, but not 2CR KO mice. CCK induced similar degrees of c-Fos expression in the paraventricular (PVN) and arcuate (Arc) nuclei of the hypothalamus of both genotypes. GLP-1, on the other hand, increased c-Fos expression similarly in the NTS of both genotypes and increased c-Fos expression more in the PVN and Arc of 2CR KO mice, but not WT mice. These results indicate that serotonin signaling via serotonin 2CR is necessary for the full satiating effects of CCK and GLP-1. In addition, they suggest that the satiating effects of the two peptides are mediated by different neural mechanisms.

Changes in Satiety Hormones in Response to Leptin Treatment in a Patient with Leptin Deficiency

2018 ◽  
Vol 90 (6) ◽  
pp. 424-430 ◽  
Author(s):  
Christian L. Roth ◽  
Julia von Schnurbein ◽  
Clinton Elfers ◽  
Anja Moss ◽  
Martin Wabitsch
Keyword(s):  
Energy Homeostasis ◽  
Peptide Yy ◽  
Hormone Secretion ◽  
Calorie Intake ◽  
Strong Increase ◽  
Morbidly Obese ◽  
Gut Peptides ◽  
Treatment Results ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Background: We tested whether leptin treatment affects secretion of satiety-related gut peptides and brain-derived neurotrophic factor (BDNF), which is a regulator of energy homeostasis downstream of hypothalamic leptin signaling. Methods: We report the case of a morbidly obese 14.7-year-old girl with a novel previously reported homozygous leptin gene mutation, in whom hormone secretion was evaluated in 30-min intervals for 10 h (07.30–17.30) to assess BDNF, insulin, glucagon-like peptide-1 (GLP-1), ghrelin, and peptide YY (PYY) secretion before as well as 11 and 46 weeks after start of metreleptin treatment. Results: Leptin substitution resulted in strong reductions of body fat and calorie intake. Insulin secretion increased by 58.9% after 11 weeks, but was reduced by –44.8% after 46 weeks compared to baseline. Similarly, GLP-1 increased after 11 weeks (+15.2%) and decreased after 46 weeks. PYY increased consistently (+5%/ +13.2%, after 11/46 weeks). Ghrelin decreased after 46 weeks (–11%). BDNF secretion was not affected by leptin treatment. Conclusion: The strong increase in insulin and GLP-1 secretion after 11 weeks of metreleptin treatment cannot be explained by reduced adiposity and might contribute to improved central satiety. Observed changes of PYY can lead to increased satiety as well. However, leptin replacement does not seem to affect circulating BDNF levels.

scholarly journals Minireview: Gut Peptides Regulating Satiety

Endocrinology ◽  
2004 ◽  
Vol 145 (6) ◽  
pp. 2660-2665 ◽  
Author(s):  
Maralyn R. Druce ◽  
Caroline J. Small ◽  
Stephen R. Bloom
Keyword(s):  
Body Weight ◽  
Gastrointestinal Tract ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Premature Death ◽  
Gut Peptides ◽  
The United Kingdom ◽  
Glucagon Like Peptide ◽  
Low Levels ◽  
Glucagon Like Peptide 1

Abstract The gastrointestinal tract and the pancreas release hormones regulating satiety and body weight. Ghrelin stimulates appetite, and glucagon-like peptide-1, oxyntomodulin, peptide YY, cholecystokinin, and pancreatic polypeptide inhibit appetite. These gut hormones act to markedly alter food intake in humans and rodents. Obesity is the current major cause of premature death in the United Kingdom, killing almost 1000 people per week. Worldwide, its prevalence is accelerating. There is currently no effective answer to the pandemic of obesity, but replacement of the low levels of peptide YY observed in the obese may represent an effective antiobesity therapy.

scholarly journals Learning of food preferences: mechanisms and implications for obesity & metabolic diseases

2021 ◽  
Author(s):  
Hans-Rudolf Berthoud ◽  
Christopher D. Morrison ◽  
Karen Ackroff ◽  
Anthony Sclafani
Keyword(s):  
Metabolic Diseases ◽  
Food Preferences ◽  
Reward System ◽  
Nutrient Sensing ◽  
Vagal Afferents ◽  
Dietary Knowledge ◽  
Ongoing Work ◽  
Brain Reward ◽  
The Brain ◽  
Vagal Function

AbstractOmnivores, including rodents and humans, compose their diets from a wide variety of potential foods. Beyond the guidance of a few basic orosensory biases such as attraction to sweet and avoidance of bitter, they have limited innate dietary knowledge and must learn to prefer foods based on their flavors and postoral effects. This review focuses on postoral nutrient sensing and signaling as an essential part of the reward system that shapes preferences for the associated flavors of foods. We discuss the extensive array of sensors in the gastrointestinal system and the vagal pathways conveying information about ingested nutrients to the brain. Earlier studies of vagal contributions were limited by nonselective methods that could not easily distinguish the contributions of subsets of vagal afferents. Recent advances in technique have generated substantial new details on sugar- and fat-responsive signaling pathways. We explain methods for conditioning flavor preferences and their use in evaluating gut–brain communication. The SGLT1 intestinal sugar sensor is important in sugar conditioning; the critical sensors for fat are less certain, though GPR40 and 120 fatty acid sensors have been implicated. Ongoing work points to particular vagal pathways to brain reward areas. An implication for obesity treatment is that bariatric surgery may alter vagal function.

scholarly journals Failure of the Brain Glucagon-Like Peptide-1-Mediated Control of Intestinal Redox Homeostasis in a Rat Model of Sporadic Alzheimer’s Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1118
Author(s):  
Jan Homolak ◽  
Ana Babic Perhoc ◽  
Ana Knezovic ◽  
Jelena Osmanovic Barilar ◽  
Melita Salkovic-Petrisic
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Redox Homeostasis ◽  
Brain State ◽  
Gastrointestinal Hormone ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Brain

The gastrointestinal system may be involved in the etiopathogenesis of the insulin-resistant brain state (IRBS) and Alzheimer’s disease (AD). Gastrointestinal hormone glucagon-like peptide-1 (GLP-1) is being explored as a potential therapy as activation of brain GLP-1 receptors (GLP-1R) exerts neuroprotection and controls peripheral metabolism. Intracerebroventricular administration of streptozotocin (STZ-icv) is used to model IRBS and GLP-1 dyshomeostasis seems to be involved in the development of neuropathological changes. The aim was to explore (i) gastrointestinal homeostasis in the STZ-icv model (ii) assess whether the brain GLP-1 is involved in the regulation of gastrointestinal redox homeostasis and (iii) analyze whether brain-gut GLP-1 axis is functional in the STZ-icv animals. Acute intracerebroventricular treatment with exendin-3(9-39)amide was used for pharmacological inhibition of brain GLP-1R in the control and STZ-icv rats, and oxidative stress was assessed in plasma, duodenum and ileum. Acute inhibition of brain GLP-1R increased plasma oxidative stress. TBARS were increased, and low molecular weight thiols (LMWT), protein sulfhydryls (SH), and superoxide dismutase (SOD) were decreased in the duodenum, but not in the ileum of the controls. In the STZ-icv, TBARS and CAT were increased, LMWT and SH were decreased at baseline, and no further increment of oxidative stress was observed upon central GLP-1R inhibition. The presented results indicate that (i) oxidative stress is increased in the duodenum of the STZ-icv rat model of AD, (ii) brain GLP-1R signaling is involved in systemic redox regulation, (iii) brain-gut GLP-1 axis regulates duodenal, but not ileal redox homeostasis, and iv) brain-gut GLP-1 axis is dysfunctional in the STZ-icv model.

scholarly journals PET evaluation of light-induced modulation of microglial activation and GLP-1R expression in depressive rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yu Liu ◽  
Lizhen Wang ◽  
Donghui Pan ◽  
Mingzhu Li ◽  
Yaoqi Li ◽  
...  
Keyword(s):  
Microglial Activation ◽  
Light Therapy ◽  
Emission Tomography ◽  
Noninvasive Evaluation ◽  
Mild Stress ◽  
Positron Emission ◽  
Therapeutic Choice ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Brain

AbstractLight therapy has been accepted as a promising therapeutic choice for depression. Positron emission tomography (PET) combined with specific radiotracers has great benefits for revealing pathogenesis and developing therapeutics. This study aimed to investigate the influences of light therapy on microglial activation and glucagon-like peptide-1 receptor (GLP-1R) expression in the brain of depressive rats using [18F]DPA-714 and [18F]exendin-4 PET. The results showed that chronic unpredictable mild stress (CUMS)-induced depressive rats had poorer performance in behavioral tests compared to normal rats (p < 0.05) and the depressive-like behavior could be ameliorated by light therapy. Besides, depressive rats had significantly higher [18F]DPA-714 uptake and lower [18F]FDG uptake compare to normal rats in 11 and 9 regions of interest (ROIs) of the brain, respectively (p < 0.05). After 5 weeks of light therapy, higher [18F]FDG and [18F]exendin-4 uptake was observed in most ROIs of light therapy-treated depressive rats compared to untreated depressive rats (p < 0.05) and no significant differences existed in [18F]DPA-714 uptake between the two groups. This study demonstrated that light therapy can ameliorate depressive-like behavior, improve glucose metabolism, and halt the decline of brain GLP-1R expression of depressive rats, but have no effects on microglial activation caused by CUMS. Besides, this study validated that [18F]DPA-714 and [18F]exendin-4 PET have the potential for noninvasive evaluation of microglial activation and GLP-1R expression in the brain of depression.

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 Ileal short-chain fatty acids inhibit gastric motility by a humoral pathway

2000 ◽  
Vol 279 (5) ◽  
pp. G925-G930 ◽  
Author(s):  
G. Cuche ◽  
J. C. Cuber ◽  
C. H. Malbert
Keyword(s):  
Gastric Motility ◽  
Short Chain Fatty Acid ◽  
Peptide Yy ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Maximal Amplitude ◽  
Inhibiting Factor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The aim of this study was to evaluate the nervous and humoral pathways involved in short-chain fatty acid (SCFA)-induced ileal brake in conscious pigs. The role of extrinsic ileal innervation was evaluated after SCFA infusion in innervated and denervated Babkin's ileal loops, and gastric motility was measured with strain gauges. Peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) concentrations were evaluated in both situations. The possible involvement of absorbed SCFA was tested by using intravenous infusion of acetate. Ileal SCFA infusion in the intact terminal ileum decreased the amplitude of distal and terminal antral contractions (33 ± 1.2 vs. 49 ± 1.2% of the maximal amplitude recorded before infusion) and increased their frequency (1.5 ± 0.11 vs. 1.3 ± 0.10/min). Similar effects were observed during SCFA infusion in ileal innervated and denervated loops (amplitude, 35 ± 1.0 and 34 ± 0.8 vs. 47 ± 1.3 and 43 ± 1.2%; frequency, 1.4 ± 0.07 and 1.6 ± 0.06 vs. 1.1 ± 0.14 and 1.0 ± 0.12/min). Intravenous acetate did not modify the amplitude and frequency of antral contractions. PYY but not GLP-1 concentrations were increased during SCFA infusion in innervated and denervated loops. In conclusion, ileal SCFA inhibit distal gastric motility by a humoral pathway involving the release of an inhibiting factor, which is likely PYY.

scholarly journals Glucagon-Like Peptide 1 in the Brain: Where Is It Coming From, Where Is It Going?

Diabetes ◽  
2018 ◽  
Vol 68 (1) ◽  
pp. 15-17 ◽  
Author(s):  
Derek Daniels ◽  
Elizabeth G. Mietlicki-Baase
Keyword(s):  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Brain
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