The Role of the Gastrointestinal Hormones Ghrelin, Peptide YY, and Glucagon-like Peptide-1 in the Regulation of Energy Balance

2007 ◽  
pp. 107-123
Author(s):  
Ruben Nogueiras ◽  
Hilary Wilson ◽  
Diego Perez-Tilve ◽  
Matthias H. Tschöp
Keyword(s):  
Energy Balance ◽  
Peptide Yy ◽  
Gastrointestinal Hormones ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

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 The Role of the Vagal Nerve in Peripheral PYY3–36-Induced Feeding Reduction in Rats

Endocrinology ◽  
2005 ◽  
Vol 146 (5) ◽  
pp. 2369-2375 ◽  
Author(s):  
Shuichi Koda ◽  
Yukari Date ◽  
Noboru Murakami ◽  
Takuya Shimbara ◽  
Takeshi Hanada ◽  
...  
Keyword(s):  
Peptide Yy ◽  
Gastrointestinal Hormones ◽  
Blood Stream ◽  
Afferent Nerve ◽  
Solitary Tract ◽  
Afferent Fibers ◽  
Vagal Afferent ◽  
Glucagon Like Peptide 1 ◽  
The Brain

Abstract Peptide YY (PYY), an anorectic peptide, is secreted postprandially from the distal gastrointestinal tract. PYY3–36, the major form of circulating PYY, binds to the hypothalamic neuropeptide Y Y2 receptor (Y2-R) with a high-affinity, reducing food intake in rodents and humans. Additional gastrointestinal hormones involved in feeding, including cholecystokinin, glucagon-like peptide 1, and ghrelin, transmit satiety or hunger signals to the brain via the vagal afferent nerve and/or the blood stream. Here we determined the role of the afferent vagus nerve in PYY function. Abdominal vagotomy abolished the anorectic effect of PYY3–36 in rats. Peripheral administration of PYY3–36 induced Fos expression in the arcuate nucleus of sham-operated rats but not vagotomized rats. We showed that Y2-R is synthesized in the rat nodose ganglion and transported to the vagal afferent terminals. PYY3–36 stimulated firing of the gastric vagal afferent nerve when administered iv. Considering that Y2-R is present in the vagal afferent fibers, PYY3–36 could directly alter the firing rate of the vagal afferent nerve via Y2-R. We also investigated the effect of ascending fibers from the nucleus of the solitary tract on the transmission of PYY3–36-mediated satiety signals. In rats, bilateral midbrain transections rostral to the nucleus of the solitary tract also abolished PYY3–36-induced reductions in feeding. This study indicates that peripheral PYY3–36 may transmit satiety signals to the brain in part via the vagal afferent pathway.

scholarly journals Role of Gastrointestinal Hormones in the Proliferation of Normal and Neoplastic Tissues

2003 ◽  
Vol 24 (5) ◽  
pp. 571-599 ◽  
Author(s):  
Robert P. Thomas ◽  
Mark R. Hellmich ◽  
Courtney M. Townsend ◽  
B. Mark Evers
Keyword(s):  
Peptide Yy ◽  
Gastrointestinal Hormones ◽  
Physiological Effects ◽  
Future Perspectives ◽  
Therapeutic Implications ◽  
Gastrin Releasing Peptide ◽  
Gi Cancers ◽  
Glucagon Like Peptide ◽  
Breast And Prostate Cancer

Abstract Gastrointestinal (GI) hormones are chemical messengers that regulate the physiological functions of the intestine and pancreas, including secretion, motility, absorption, and digestion. In addition to these well-defined physiological effects, GI hormones can stimulate proliferation of the nonneoplastic intestinal mucosa and pancreas. Furthermore, in an analogous fashion to breast and prostate cancer, certain GI cancers possess receptors for GI hormones; growth can be altered by administration of these hormones or by blocking their respective receptors. The GI hormones that affect proliferation, either stimulatory or inhibitory, include gastrin, cholecystokinin, gastrin-releasing peptide, neurotensin, peptide YY, glucagon-like peptide-2, and somatostatin. The effects of these peptides on normal and neoplastic GI tissues will be described. Also, future perspectives and potential therapeutic implications will be discussed.

scholarly journals Role of the glucagon-like-peptide-1 receptor in the control of energy balance

2010 ◽  
Vol 100 (5) ◽  
pp. 503-510 ◽  
Author(s):  
Matthew R. Hayes ◽  
Bart C. De Jonghe ◽  
Scott E. Kanoski
Keyword(s):  
Energy Balance ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Oxyntomodulin and Glicentin May Predict the Effect of Bariatric Surgery on Food Preferences and Weight Loss

2020 ◽  
Vol 105 (4) ◽  
pp. e1064-e1074 ◽  
Author(s):  
Mette S Nielsen ◽  
Christian Ritz ◽  
Nicolai J Wewer Albrechtsen ◽  
Jens Juul Holst ◽  
Carel W le Roux ◽  
...  
Keyword(s):  
Weight Loss ◽  
Energy Density ◽  
Energy Intake ◽  
Peptide Yy ◽  
Food Preferences ◽  
Gastrointestinal Hormones ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Additional Support ◽  
Surgical Treatments

Abstract Background Alterations in several gastrointestinal hormones are implicated in the postoperative suppression of food intake leading to weight loss after Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG). The aim was to evaluate changes in responses of gastrointestinal hormones after RYGB and SG and the associations of these changes with weight loss, energy intake, and food preferences. Methods Forty-two subjects with severe obesity were included (32 RYGB; 10 SG). Postprandial responses of glicentin, oxyntomodulin, glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and ghrelin were measured before and 6 months after surgery. Energy intake and energy density were assessed before and 6 months after surgery using a buffet meal test and weight loss was assessed 18 months after surgery. Results Postprandial concentrations of glicentin, oxyntomodulin, GLP-1, and ghrelin differed between RYGB and SG (all P ≤ .02). Enhanced responses of glicentin and oxyntomodulin predicted a greater weight loss (both P < .01) and were associated with a larger decrease in energy density (P ≤ .04). No associations were found for GLP-1, PYY, and ghrelin, and changes were not associated with changes in energy intake. When combing all hormones, 60%, 19%, and 33% of the variations in weight loss, energy intake, and energy density, respectively, could be explained. Conclusion Postprandial responses of gastrointestinal hormones differed between RYGB and SG. Enhanced responses of glicentin and oxyntomodulin predicted a better weight loss and were associated with a decreased preference for energy-dense foods. Replication of these results could imply an opportunity to identify patients in need of additional support after surgical treatments of obesity.

scholarly journals Glucagon-like peptide-1 regulates brown adipose tissue thermogenesis via the gut-brain axis in rats

2018 ◽  
Vol 315 (4) ◽  
pp. R708-R720 ◽  
Author(s):  
Jean-Philippe Krieger ◽  
Ellen Paula Santos da Conceição ◽  
Graciela Sanchez-Watts ◽  
Myrtha Arnold ◽  
Klaus G. Pettersen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Balance ◽  
Brown Adipose Tissue ◽  
Body Weight Gain ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Sympathetic Regulation ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Endogenous intestinal glucagon-like peptide-1 (GLP-1) controls satiation and glucose metabolism via vagal afferent neurons (VANs). Recently, VANs have received increasing attention for their role in brown adipose tissue (BAT) thermogenesis. It is, however, unclear whether VAN GLP-1 receptor (GLP-1R) signaling affects BAT thermogenesis and energy expenditure (EE) and whether this VAN mechanism contributes to energy balance. First, we tested the effect of the GLP-1R agonist exendin-4 (Ex4, 0.3 μg/kg ip) on EE and BAT thermogenesis and whether these effects require VAN GLP-1R signaling using a rat model with a selective Glp1r knockdown (kd) in VANs. Second, we examined the role of VAN GLP-1R in energy balance during chronic high-fat diet (HFD) feeding in VAN Glp1r kd rats. Finally, we used viral transsynaptic tracers to identify the possible neuronal substrates of such a gut-BAT interaction. VAN Glp1r kd attenuated the acute suppressive effects of Ex4 on EE and BAT thermogenesis. Consistent with this finding, the VAN Glp1r kd increased EE and BAT activity, diminished body weight gain, and improved insulin sensitivity compared with HFD-fed controls. Anterograde transsynaptic viral tracing of VANs infected major hypothalamic and hindbrain areas involved in BAT sympathetic regulation. Moreover, retrograde tracing from BAT combined with laser capture microdissection revealed that a population of VANs expressing Glp1r is synaptically connected to the BAT. Our findings reveal a novel role of VAN GLP-1R signaling in the regulation of EE and BAT thermogenesis and imply that through this gut-brain-BAT connection, intestinal GLP-1 plays a role in HFD-induced metabolic syndrome.

scholarly journals Role of Bile Acids in the Regulation of Food Intake, and Their Dysregulation in Metabolic Disease

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1104
Author(s):  
Cong Xie ◽  
Weikun Huang ◽  
Richard L. Young ◽  
Karen L. Jones ◽  
Michael Horowitz ◽  
...  
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Peptide Yy ◽  
Glycogen Synthesis ◽  
Hormone Secretion ◽  
Gastrointestinal Hormones ◽  
Farnesoid X Receptor ◽  
Gastrointestinal Hormone ◽  
Bile Acid Sequestrants

Bile acids are cholesterol-derived metabolites with a well-established role in the digestion and absorption of dietary fat. More recently, the discovery of bile acids as natural ligands for the nuclear farnesoid X receptor (FXR) and membrane Takeda G-protein-coupled receptor 5 (TGR5), and the recognition of the effects of FXR and TGR5 signaling have led to a paradigm shift in knowledge regarding bile acid physiology and metabolic health. Bile acids are now recognized as signaling molecules that orchestrate blood glucose, lipid and energy metabolism. Changes in FXR and/or TGR5 signaling modulates the secretion of gastrointestinal hormones including glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), hepatic gluconeogenesis, glycogen synthesis, energy expenditure, and the composition of the gut microbiome. These effects may contribute to the metabolic benefits of bile acid sequestrants, metformin, and bariatric surgery. This review focuses on the role of bile acids in energy intake and body weight, particularly their effects on gastrointestinal hormone secretion, the changes in obesity and T2D, and their potential relevance to the management of metabolic disorders.

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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