scholarly journals A Review on the Role of Food-Derived Bioactive Molecules and the Microbiota–Gut–Brain Axis in Satiety Regulation

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 632
Author(s):  
Nuria A. Pizarroso ◽  
Pablo Fuciños ◽  
Catarina Gonçalves ◽  
Lorenzo Pastrana ◽  
Isabel R. Amado
Keyword(s):  
Metabolic Diseases ◽  
Environmental Changes ◽  
Peptide Yy ◽  
Brain Regions ◽  
Nutrient Sensing ◽  
Bioactive Molecules ◽  
Intestinal Hormones ◽  
Signaling Systems ◽  
Chip Technology ◽  
Glucagon Like Peptide 1

Obesity is a chronic disease resulting from an imbalance between energy intake and expenditure. The growing relevance of this metabolic disease lies in its association with other comorbidities. Obesity is a multifaceted disease where intestinal hormones such as cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1), and peptide YY (PYY), produced by enteroendocrine cells (EECs), have a pivotal role as signaling systems. Receptors for these hormones have been identified in the gut and different brain regions, highlighting the interconnection between gut and brain in satiation mechanisms. The intestinal microbiota (IM), directly interacting with EECs, can be modulated by the diet by providing specific nutrients that induce environmental changes in the gut ecosystem. Therefore, macronutrients may trigger the microbiota–gut–brain axis (MGBA) through mechanisms including specific nutrient-sensing receptors in EECs, inducing the secretion of specific hormones that lead to decreased appetite or increased energy expenditure. Designing drugs/functional foods based in bioactive compounds exploiting these nutrient-sensing mechanisms may offer an alternative treatment for obesity and/or associated metabolic diseases. Organ-on-a-chip technology represents a suitable approach to model multi-organ communication that can provide a robust platform for studying the potential of these compounds as modulators of the MGBA.

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.

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 orlistat improves release of gut hormones increasing satiety in obese women

2014 ◽  
Vol 11 (4) ◽  
pp. 64
Author(s):  
Teona Albertovna Shvangiradze
Keyword(s):  
Impact Analysis ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Metabolic Effects ◽  
Obese Women ◽  
Fat Absorption ◽  
Intestinal Hormones ◽  
Glucose And Lipid Metabolism ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Orlistat, which reduces fat absorption by inhibiting intestinal lipase is a registered drug for obesity pharmacotherapy. Meta-analyzes indicate various positive metabolic effects of orlistat, including improvements in glucose and lipid metabolism, lowering both systolic and diastolic blood pressure. It is assumed that orlistat can reduce postprandial satiety by inhibiting the release of intestinal hormones (incretins), especially glucagon-like peptide-1 (GLP-1). Impact analysis of the secretion of incretins, with prolonged use of orlistat was conducted. The aim of the study M.Olszanecka-Glinianowicz et al. was to evaluate the effect of 8 weeks of treatment with orlistat as part of a weight loss program for preprandialnye levels of peptide YY and GLP-1.

scholarly journals Intestinal SGLT1 in metabolic health and disease

2016 ◽  
Vol 310 (11) ◽  
pp. G887-G898 ◽  
Author(s):  
Anders Lehmann ◽  
Pamela J. Hornby
Keyword(s):  
Metabolic Diseases ◽  
Apical Membrane ◽  
Peptide Yy ◽  
Metabolic Effects ◽  
New Class ◽  
Health And Disease ◽  
Glucose Exposure ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The Na+-glucose cotransporter 1 (SGLT1/SLC5A1) is predominantly expressed in the small intestine. It transports glucose and galactose across the apical membrane in a process driven by a Na+ gradient created by Na+-K+-ATPase. SGLT2 is the major form found in the kidney, and SGLT2-selective inhibitors are a new class of treatment for type 2 diabetes mellitus (T2DM). Recent data from patients treated with dual SGLT1/2 inhibitors or SGLT2-selective drugs such as canagliflozin (SGLT1 IC50 = 663 nM) warrant evaluation of SGLT1 inhibition for T2DM. SGLT1 activity is highly dynamic, with modulation by multiple mechanisms to ensure maximal uptake of carbohydrates (CHOs). Intestinal SGLT1 inhibition lowers and delays the glucose excursion following CHO ingestion and augments glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) secretion. The latter is likely due to increased glucose exposure of the colonic microbiota and formation of metabolites such as L cell secretagogues. GLP-1 and PYY secretion suppresses food intake, enhances the ileal brake, and has an incretin effect. An increase in colonic microbial production of propionate could contribute to intestinal gluconeogenesis and mediate positive metabolic effects. On the other hand, a threshold of SGLT1 inhibition that could lead to gastrointestinal intolerability is unclear. Altered Na+ homeostasis and increased colonic CHO may result in diarrhea and adverse gastrointestinal effects. This review considers the potential mechanisms contributing to positive metabolic and negative intestinal effects. Compounds that inhibit SGLT1 must balance the modulation of these mechanisms to achieve therapeutic efficacy for metabolic diseases.

scholarly journals Amino Acid Sensing in Metabolic Homeostasis and Health

2020 ◽  
Author(s):  
Xiaoming Hu ◽  
Feifan Guo
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Metabolic Regulation ◽  
Metabolic Diseases ◽  
Nutrient Sensing ◽  
The Body ◽  
Bioactive Molecules ◽  
Metabolic Homeostasis ◽  
Amino Acid Availability ◽  
Amino Acid Sensing

Abstract Sensing and responding to changes in nutrient levels, including those of glucose, lipids, and amino acids, by the body is necessary for survival. Accordingly, perturbations in nutrient sensing are tightly linked with human pathologies, particularly metabolic diseases such as obesity, type 2 diabetes mellitus, and other complications of metabolic syndromes. The conventional view is that amino acids are fundamental elements for protein and peptide synthesis, while recent studies have revealed that amino acids are also important bioactive molecules that play key roles in signaling pathways and metabolic regulation. Different pathways that sense intracellular and extracellular levels of amino acids are integrated and coordinated at the organismal level, and, together, these pathways maintain whole metabolic homeostasis. In this review, we discuss the studies describing how important sensing signals respond to amino acid availability and how these sensing mechanisms modulate metabolic processes, including energy, glucose, and lipid metabolism. We further discuss whether dysregulation of amino acid sensing signals can be targeted to promote metabolic disorders, and discuss how to translate these mechanisms to treat human diseases. This review will help to enhance our overall understanding of the correlation between amino acid sensing and metabolic homeostasis, which have important implications for human health.

GLP-1 slows solid gastric emptying and inhibits insulin, glucagon, and PYY release in humans

1999 ◽  
Vol 277 (3) ◽  
pp. R910-R916 ◽  
Author(s):  
Erik Näslund ◽  
Jesper Bogefors ◽  
Staffan Skogar ◽  
Per Grybäck ◽  
Hans Jacobsson ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Plasma Glucose ◽  
Peptide Yy ◽  
Plasma Concentrations ◽  
Lag Phase ◽  
Intestinal Hormones ◽  
C Peptide ◽  
Lower Plasma Glucose ◽  
C And N ◽  
Glucagon Like Peptide 1

The aim of the present study was to assess the effect of glucagon-like peptide-1 (GLP-1) on solid gastric emptying and the subsequent release of pancreatic and intestinal hormones. In eight men [age 33.6 ± 2.5 yr, body mass index 24.1 ± 0.9 (means ± SE)], scintigraphic solid gastric emptying during infusion of GLP-1 (0.75 pmol ⋅ kg−1 ⋅ min−1) or saline was studied for 180 min. Concomitantly, plasma concentrations of C- and N-terminal GLP-1, glucose, insulin, C-peptide, glucagon, and peptide YY (PYY) were assessed. Infusion of GLP-1 resulted in a profound inhibition of both the lag phase (GLP-1: 91.5, range 73.3–103.6 min vs. saline: 19.5, range 10.2–43.4 min) and emptying rate (GLP-1: 0.34, range 0.06–0.56 %/min vs. saline: 0.84, range 0.54–1.33 %/min; P< 0.01 for both) of solid gastric emptying. Concentrations of both intact and total GLP-1 were elevated to supraphysiological levels. Plasma glucose and glucagon concentrations were below baseline during infusion of GLP-1 in contrast to saline infusion, where concentrations were elevated above baseline (both P< 0.001). The insulin and C-peptide responses were lower during infusion with GLP-1 than with saline ( P < 0.004 and P < 0.001, respectively). Plasma PYY concentrations decreased below baseline during GLP-1 infusion in contrast to saline, where concentrations were elevated above baseline ( P = 0.04). Infusion of GLP-1 inhibits solid gastric emptying with secondary effects on the release of insulin, C-peptide, and glucagon, resulting in lower plasma glucose concentrations. In addition, the release of PYY into the circulation is inhibited by GLP-1 infusion, suggesting a negative feedback of GLP-1 on the function of the L-cell.

scholarly journals Lipid-rich diet enhances L-cell density in obese subjects and in mice through improved L-cell differentiation

2015 ◽  
Vol 4 ◽  
Author(s):  
Thomas Aranias ◽  
Alexandra Grosfeld ◽  
Christine Poitou ◽  
Amal Ait Omar ◽  
Maude Le Gall ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Cell Density ◽  
Environmental Changes ◽  
Peptide Yy ◽  
High Fat ◽  
L Cell ◽  
Fat Consumption ◽  
Severely Obese ◽  
Obese Subjects ◽  
Glucagon Like Peptide 1

AbstractThe enterohormone glucagon-like peptide-1 (GLP-1) is required to amplify glucose-induced insulin secretion that facilitates peripheral glucose utilisation. Alteration in GLP-1 secretion during obesity has been reported but is still controversial. Due to the high adaptability of intestinal cells to environmental changes, we hypothesised that the density of GLP-1-producing cells could be modified by nutritional factors to prevent the deterioration of metabolic condition in obesity. We quantified L-cell density in jejunum samples collected during Roux-en-Y gastric bypass in forty-nine severely obese subjects analysed according to their fat consumption. In mice, we deciphered the mechanisms by which a high-fat diet (HFD) makes an impact on enteroendocrine cell density and function. L-cell density in the jejunum was higher in obese subjects consuming >30 % fat compared with low fat eaters. Mice fed a HFD for 8 weeks displayed an increase in GLP-1-positive cells in the jejunum and colon accordingly to GLP-1 secretion. The regulation by the HFD appears specific to GLP-1-producing cells, as the number of PYY (peptide YY)-positive cells remained unchanged. Moreover, genetically obese ob/ob mice did not show alteration of GLP-1-positive cell density in the jejunum or colon, suggesting that obesity per se is not sufficient to trigger the mechanism. The higher L-cell density in HFD-fed mice involved a rise in L-cell terminal differentiation as witnessed by the increased expression of transcription factors downstream of neurogenin3 (Ngn3). We suggest that the observed increase in GLP-1-positive cell density triggered by high fat consumption in humans and mice might favour insulin secretion and therefore constitute an adaptive response of the intestine to balance diet-induced insulin resistance.

scholarly journals Hormonal and Metabolic Mechanisms of Diabetes Remission after Gastrointestinal Surgery

Endocrinology ◽  
2009 ◽  
Vol 150 (6) ◽  
pp. 2518-2525 ◽  
Author(s):  
Joshua P. Thaler ◽  
David E. Cummings
Keyword(s):  
Weight Loss ◽  
Time Course ◽  
Gastrointestinal Surgery ◽  
Specific Weight ◽  
Diabetes Remission ◽  
Nutrient Sensing ◽  
Diabetic Patients ◽  
Intestinal Hormones ◽  
Glucagon Like Peptide 1 ◽  
Altered Physiology

Bariatric surgery is the most effective available treatment for obesity. The most frequently performed operation, Roux-en-Y gastric bypass (RYGB), causes profound weight loss and ameliorates obesity-related comorbid conditions, especially type 2 diabetes mellitus (T2DM). Approximately 84% of diabetic patients experience complete remission of T2DM after undergoing RYGB, often before significant weight reduction. The rapid time course and disproportional degree of T2DM improvement after RYGB compared with equivalent weight loss from other interventions suggest surgery-specific, weight-independent effects on glucose homeostasis. Potential mechanisms underlying the direct antidiabetic impact of RYGB include enhanced nutrient stimulation of lower intestinal hormones (e.g. glucagon-like peptide-1), altered physiology from excluding ingested nutrients from the upper intestine, compromised ghrelin secretion, modulations of intestinal nutrient sensing and regulation of insulin sensitivity, and other changes yet to be fully characterized. Research aimed at determining the relative importance of these effects and identifying additional mechanisms promises not only to improve surgical design but also to identify novel targets for diabetes medications.

The Role of Neuropeptide Y and Peptide YY in the Development of Obesity via Gut-brain Axis

2019 ◽  
Vol 20 (7) ◽  
pp. 750-758 ◽  
Author(s):  
Yi Wu ◽  
Hengxun He ◽  
Zhibin Cheng ◽  
Yueyu Bai ◽  
Xi Ma
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuropeptide Y ◽  
Metabolic Diseases ◽  
Peptide Yy ◽  
Vital Role ◽  
Gut Peptides ◽  
Nonalcoholic Fatty Liver ◽  
The Central Nervous System

Obesity is one of the main challenges of public health in the 21st century. Obesity can induce a series of chronic metabolic diseases, such as diabetes, dyslipidemia, hypertension and nonalcoholic fatty liver, which seriously affect human health. Gut-brain axis, the two-direction pathway formed between enteric nervous system and central nervous system, plays a vital role in the occurrence and development of obesity. Gastrointestinal signals are projected through the gut-brain axis to nervous system, and respond to various gastrointestinal stimulation. The central nervous system regulates visceral activity through the gut-brain axis. Brain-gut peptides have important regulatory roles in the gut-brain axis. The brain-gut peptides of the gastrointestinal system and the nervous system regulate the gastrointestinal movement, feeling, secretion, absorption and other complex functions through endocrine, neurosecretion and paracrine to secrete peptides. Both neuropeptide Y and peptide YY belong to the pancreatic polypeptide family and are important brain-gut peptides. Neuropeptide Y and peptide YY have functions that are closely related to appetite regulation and obesity formation. This review describes the role of the gutbrain axis in regulating appetite and maintaining energy balance, and the functions of brain-gut peptides neuropeptide Y and peptide YY in obesity. The relationship between NPY and PYY and the interaction between the NPY-PYY signaling with the gut microbiota are also described in this review.

Roux-en-Y Gastrointestinal Bypass Promotes Activation of TGR5 and Peptide YY

2020 ◽  
Vol 20 (8) ◽  
pp. 1262-1267
Author(s):  
Haojun Yang ◽  
Hanyang Liu ◽  
YuWen Jiao ◽  
Jun Qian
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Metabolic Diseases ◽  
Peptide Yy ◽  
The Body ◽  
Wild Type ◽  
L Cells ◽  
Body Weights ◽  
Gastrointestinal Bypass ◽  
G Protein Coupled

Background: G protein-coupled bile acid receptor (TGR5) is involved in a number of metabolic diseases. The aim of this study was to identify the role of TGR5 after Roux-en-Y gastric bypass (GBP). Methods: Wild type and TGR5 knockout mice (tgr5-/-) were fed a high-fat diet (HFD) to establish the obesity model. GBP was performed. The changes in body weight and food intake were measured. The levels of TGR5 and peptide YY (PYY) were evaluated by RT-PCR, Western blot, and ELISA. Moreover, the L-cells were separated from wild type and tgr5-/- mice. The levels of PYY in L-cells were evaluated by ELISA. Results: The body weights were significantly decreased after GBP in wild type mice (p<0.05), but not tgr5-/- mice (p>0.05). Food intake was reduced after GBP in wild type mice, but also not significantly affected in tgr5-/- mice (p>0.05). The levels of PYY were significantly increased after GBP compared with the sham group (p<0.05); however, in tgr5-/- mice the expression of PYY was not significantly affected (p>0.05). After INT-777 stimulation in L-cells obtained from murine intestines, the levels of PYY were significantly increased in L-cells tgr5+/+ (p<0.05). Conclusion: Our study suggests that GBP up-regulated the expression of TGR5 in murine intestines, and increased the levels of PYY, which further reduced food intake and decreased the body weight.

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