scholarly journals Appetite and Satiety Effects of the Acute and Regular Consumption of Green Coffee Phenols and Green Coffee Phenol/Oat β-Glucan Nutraceuticals in Subjects with Overweight and Obesity

Foods ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2511
Author(s):  
Mónica Redondo-Puente ◽  
Raquel Mateos ◽  
Miguel A. Seguido ◽  
Joaquín García-Cordero ◽  
Susana González ◽  
...  
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Overweight And Obesity ◽  
Ghrelin Level ◽  
Green Coffee ◽  
Visual Analog Scales ◽  
Regular Consumption ◽  
Phenolic Extract ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Green coffee has weight management properties, yet its effects on appetite and satiety remain unclear as few, mainly acute, studies perform objective measurements. Therefore, the influence on appetite/satiety of acute and regular consumption of two nutraceuticals, a decaffeinated green coffee phenolic extract (GC) alone or combined with oat β-glucans (GC/BG), with known satiating properties, has been analysed subjectively using visual analog scales (VAS) and objectively measuring actual food intake and postprandial appetite and satiety hormones. A randomised, cross-over, blind trial was carried out in 29 overweight volunteers who consumed GC or GC/BG twice a day for 8 weeks. After acute (day = 0) and regular consumption (day = 56) of the nutraceuticals, satiety was measured at 30, 60, 90, 150, and 210 min, as well as food intake at breakfast (30 min) and lunch (300 min). Additionally, in a subgroup of participants (n = 9), cholecystokinin, peptide-YY, glucagon-like-peptide-1, ghrelin and leptin concentrations were analysed in blood samples taken at the same time-points. According to VAS results, GC/BG reduced hunger more efficiently than GC. However, there were no statistically significant differences in food intake. Comparing the effects of the acute consumption of GC/BG and GC, leptin concentration at 150 min was higher after GC/BG intake vs. GC. Moreover, when comparing the effects of regularly consuming the two nutraceuticals, maximum ghrelin level decreased with GC/BG vs. GC. In conclusion, acute and regular effects of the nutraceuticals on appetite/satiety differed, and subjective and objective results partially agreed; GC/BG may reduce hunger more efficiently than GC.

Peptide YY and glucagon-like peptide-1 contribute to decreased food intake after Roux-en-Y gastric bypass surgery

2016 ◽  
Vol 40 (11) ◽  
pp. 1699-1706 ◽  
Author(s):  
M S Svane ◽  
N B Jørgensen ◽  
K N Bojsen-Møller ◽  
C Dirksen ◽  
S Nielsen ◽  
...  
Keyword(s):  
Gastric Bypass ◽  
Food Intake ◽  
Bypass Surgery ◽  
Peptide Yy ◽  
Gastric Bypass Surgery ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Mechanisms of oleoylethanolamide-induced changes in feeding behavior and motor activity

2005 ◽  
Vol 289 (3) ◽  
pp. R729-R737 ◽  
Author(s):  
Karine Proulx ◽  
Daniela Cota ◽  
Tamara R. Castañeda ◽  
Matthias H. Tschöp ◽  
David A. D'Alessio ◽  
...  
Keyword(s):  
Food Intake ◽  
Motor Activity ◽  
Peptide Yy ◽  
Metabolic Effects ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Apolipoprotein A ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Induced Changes

Oleoylethanolamide (OEA), a lipid synthesized in the intestine, reduces food intake and stimulates lipolysis through peroxisome proliferator-activated receptor-α. OEA also activates transient receptor potential vanilloid type 1 (TRPV1) in vitro. Because the anorexigenic effect of OEA is associated with delayed feeding onset and reduced locomotion, we examined whether intraperitoneal administration of OEA results in nonspecific behavioral effects that contribute to the anorexia in rats. Moreover, we determined whether circulating levels of other gut hormones are modulated by OEA and whether CCK is involved in OEA-induced anorexia. Our results indicate that OEA reduces food intake without causing a conditioned taste aversion or reducing sodium appetite. It also failed to induce a conditioned place aversion. However, OEA induced changes in posture and reduced spontaneous activity in the open field. This likely underlies the reduced heat expenditure and sodium consumption observed after OEA injection, which disappeared within 1 h. The effects of OEA on motor activity were similar to those of the TRPV1 agonist capsaicin and were also observed with the peroxisome proliferator-activated receptor-α agonist Wy-14643. Plasma levels of ghrelin, peptide YY, glucagon-like peptide 1, and apolipoprotein A-IV were not changed by OEA. Finally, antagonism of CCK-1 receptors did not affect OEA-induced anorexia. These results suggest that OEA suppresses feeding without causing visceral illness and that neither ghrelin, peptide YY, glucagon-like peptide 1, apolipoprotein A-IV, nor CCK plays a critical role in this effect. Despite that OEA-induced anorexia is unlikely to be due to impaired motor activity, our data raise a cautionary note in how specific behavioral and metabolic effects of OEA should be interpreted.

scholarly journals Modulation of Food Intake by Differential TAS2R Stimulation in Rat

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3784
Author(s):  
Carme Grau-Bové ◽  
Alba Miguéns-Gómez ◽  
Carlos González-Quilen ◽  
José-Antonio Fernández-López ◽  
Xavier Remesar ◽  
...  
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Reduce Food Intake ◽  
Intestinal Segments ◽  
Regulate Food Intake ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Specific Stimulation ◽  
Ghrelin Secretion ◽  
Stimulation Of

Metabolic surgery modulates the enterohormone profile, which leads, among other effects, to changes in food intake. Bitter taste receptors (TAS2Rs) have been identified in the gastrointestinal tract and specific stimulation of these has been linked to the control of ghrelin secretion. We hypothesize that optimal stimulation of TAS2Rs could help to modulate enteroendocrine secretions and thus regulate food intake. To determine this, we have assayed the response to specific agonists for hTAS2R5, hTAS2R14 and hTAS2R39 on enteroendocrine secretions from intestinal segments and food intake in rats. We found that hTAS2R5 agonists stimulate glucagon-like peptide 1 (GLP-1) and cholecystokinin (CCK), and reduce food intake. hTAS2R14 agonists induce GLP1, while hTASR39 agonists tend to increase peptide YY (PYY) but fail to reduce food intake. The effect of simultaneously activating several receptors is heterogeneous depending on the relative affinity of the agonists for each receptor. Although detailed mechanisms are not clear, bitter compounds can stimulate differentially enteroendocrine secretions that modulate food intake in rats.

scholarly journals Role of capsaicin-sensitive peripheral sensory neurons in anorexic responses to intravenous infusions of cholecystokinin, peptide YY-(3–36), and glucagon-like peptide-1 in rats

2014 ◽  
Vol 307 (8) ◽  
pp. E619-E629 ◽  
Author(s):  
Roger Reidelberger ◽  
Alvin Haver ◽  
Krista Anders ◽  
Bettye Apenteng
Keyword(s):  
Food Intake ◽  
Sensory Neurons ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Intravenous Infusions ◽  
Peripheral Sensory Neurons ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Peripheral Sensory ◽  
Infusion Period

Cholecystokinin (CCK)-induced suppression of feeding is mediated by vagal sensory neurons that are destroyed by the neurotoxin capsaicin (CAP). Here we determined whether CAP-sensitive neurons mediate anorexic responses to intravenous infusions of gut hormones peptide YY-(3–36) [PYY-(3–36)] and glucagon-like peptide-1 (GLP-1). Rats received three intraperitoneal injections of CAP or vehicle (VEH) in 24 h. After recovery, non-food-deprived rats received at dark onset a 3-h intravenous infusion of CCK-8 (5, 17 pmol·kg−1·min−1), PYY-(3–36) (5, 17, 50 pmol·kg−1·min−1), or GLP-1 (17, 50 pmol·kg−1·min−1). CCK-8 was much less effective in reducing food intake in CAP vs. VEH rats. CCK-8 at 5 and 17 pmol·kg−1·min−1 reduced food intake during the 3-h infusion period by 39 and 71% in VEH rats and 7 and 18% in CAP rats. In contrast, PYY-(3–36) and GLP-1 were similarly effective in reducing food intake in VEH and CAP rats. PYY-(3–36) at 5, 17, and 50 pmol·kg−1·min−1 reduced food intake during the 3-h infusion period by 15, 33, and 70% in VEH rats and 13, 30, and 33% in CAP rats. GLP-1 at 17 and 50 pmol·kg−1·min−1 reduced food intake during the 3-h infusion period by 48 and 60% in VEH rats and 30 and 52% in CAP rats. These results suggest that anorexic responses to PYY-(3–36) and GLP-1 are not primarily mediated by the CAP-sensitive peripheral sensory neurons (presumably vagal) that mediate CCK-8-induced anorexia.

scholarly journals Oral administration of glucagon-like peptide 1 or peptide YY 3-36 affects food intake in healthy male subjects

2010 ◽  
Vol 92 (4) ◽  
pp. 810-817 ◽  
Author(s):  
Robert E Steinert ◽  
Birk Poller ◽  
M Cristina Castelli ◽  
Juergen Drewe ◽  
Christoph Beglinger
Keyword(s):  
Food Intake ◽  
Oral Administration ◽  
Peptide Yy ◽  
Healthy Male ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Male Subjects

Central glucagon-like peptide 1 receptor-induced anorexia requires glucose metabolism-mediated suppression of AMPK and is impaired by central fructose

2013 ◽  
Vol 304 (7) ◽  
pp. E677-E685 ◽  
Author(s):  
Melissa A. Burmeister ◽  
Jennifer Ayala ◽  
Daniel J. Drucker ◽  
Julio E. Ayala
Keyword(s):  
Food Intake ◽  
Glucose Metabolism ◽  
Dependent Manner ◽  
Anorectic Effect ◽  
Dependent Inhibition ◽  
Glycolytic Inhibitor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Amp Activated Protein Kinase ◽  
Mediated Reduction

Glucagon-like peptide-1 (GLP-1) suppresses food intake via activation of a central (i.e., brain) GLP-1 receptor (GLP-1R). Central AMP-activated protein kinase (AMPK) is a nutrient-sensitive regulator of food intake that is inhibited by anorectic signals. The anorectic effect elicited by hindbrain GLP-1R activation is attenuated by the AMPK stimulator AICAR. This suggests that central GLP-1R activation suppresses food intake via inhibition of central AMPK. The present studies examined the mechanism(s) by which central GLP-1R activation inhibits AMPK. Supporting previous findings, AICAR attenuated the anorectic effect elicited by intracerebroventricular (icv) administration of the GLP-1R agonist exendin-4 (Ex-4). We demonstrate that Ex-4 stimulates glycolysis and suppresses AMPK phosphorylation in a glucose-dependent manner in hypothalamic GT1-7 cells. This suggests that inhibition of AMPK and food intake by Ex-4 requires central glucose metabolism. Supporting this, the glycolytic inhibitor 2-deoxyglucose (2-DG) attenuated the anorectic effect of Ex-4. However, icv glucose did not enhance the suppression of food intake by Ex-4. AICAR had no effect on Ex-4-mediated reduction in locomotor activity. We also tested whether other carbohydrates affect the anorectic response to Ex-4. Intracerebroventricular pretreatment with the sucrose metabolite fructose, an AMPK activator, attenuated the anorectic effect of Ex-4. This potentially explains the increased food intake observed in sucrose-fed mice. In summary, we propose a model whereby activation of the central GLP-1R reduces food intake via glucose metabolism-dependent inhibition of central AMPK. We also suggest that fructose stimulates food intake by impairing central GLP-1R action. This has significant implications given the correlation between sugar consumption and obesity.

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.

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