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

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.

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Modulation of Food Intake by Differential TAS2R Stimulation in Rat

Nutrients ◽

10.3390/nu12123784 ◽

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.

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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

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00024.2014 ◽

2014 ◽

Vol 307 (8) ◽

pp. E619-E629 ◽

Cited By ~ 9

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.

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Effect of a protein preload on food intake and satiety feelings in response to duodenal fat perfusions in healthy male subjects

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00039.2005 ◽

2005 ◽

Vol 289 (4) ◽

pp. R1042-R1047 ◽

Cited By ~ 6

Author(s):

Sibylle Oesch ◽

Lukas Degen ◽

Christoph Beglinger

Keyword(s):

Food Intake ◽

Synergistic Effect ◽

Peptide Yy ◽

Caloric Intake ◽

Healthy Male ◽

Double Blind ◽

Control Food ◽

Initial Hypothesis ◽

Glucagon Like Peptide 1 ◽

Control Food Intake

The control of food intake and satiety requires a coordinated interplay. Oral protein and duodenal fat inhibit food intake and induce satiety, but their interactive potential is unclear. Our aim was therefore to investigate the interactions between an oral protein preload and intraduodenal (ID) fat on food intake and satiety feelings. Twenty healthy male volunteers were studied in a randomized, double-blind, four-period crossover design. On each study day, subjects underwent one of the following treatments: 1) water preload plus ID saline perfusion, 2) water preload plus ID fat perfusion, 3) protein preload plus ID saline perfusion, or 4) protein preload plus ID fat perfusion. Subjects were free to eat and drink as much as they wished. An oral protein preload significantly reduced caloric intake (19%, P < 0.01). Simultaneous administration of an oral protein preload and ID fat did not result in a positive synergistic effect with respect to caloric consumption, rejecting the initial hypothesis that the two nutrients exert a positive synergistic effect on food intake. An oral protein preload but not ID fat altered the feelings of hunger and fullness. These data indicate that the satiety effect of an oral protein preload is not amplified by ID fat; indeed, the effect of a protein preload does not seem to be mediated by cholecystokinin, glucagon-like peptide-1, or peptide YY. Much more information is necessary to understand the basic physiological mechanisms that control food intake and satiety.

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