Disease relevance of PYY

• In eight conscious dogs with chronic gastric and pancreatic fistulas, we compared the action of intravenous infusion of 200 and 400 pmol/kg/h of the Y receptor agonists PYY 1-36, PYY 3-36, PYY 13-36, Pro34PYY 1-36, and NPY 1-36 on the pancreatic secretory response to secretin (20.5 pmol/kg/h) and cerulein (29.6 pmol/kg/h) [1].
• The purpose of this investigation was to examine the effect of PYY on gastric inhibitory polypeptide (GIP)-stimulated insulin release in conscious dogs with gastric and duodenal fistulas [2].
• In contrast, only serum PP concentrations (mean delta PP = 294 +/- 36 pg/ml) increased significantly (p less than 0.01) in response to insulin hypoglycemia, demonstrating differences in the sensitivity of the PP and PYY cells to vagal stimulation [3].
• In athymic-nude mice, implantation of a human gastrinoma resulted in an elevation of serum gastrin concentrations and a concomitant depression of colonic PYY mRNA levels [4].
• In contrast, obesity decreases both basal and meal-stimulated PYY levels [5].

Psychiatry related information on PYY

• Our findings strongly suggest that the inhibitory effect of PYY on gastric secretion is in part mediated by a non-vagal pathway and the inhibitory effect of PYY on gastric motor activities is completely dependent on vagal innervation, but the vagus nerve acts as an inhibitory modulator of the inhibitory effect of PYY on gastric secretion [6].
• The plasma peptide YY, ghrelin, and growth hormone (GH) concentrations increased due to food deprivation, while the T4 and Acrp30 concentrations decreased [7].

High impact information on PYY

• The present study seeks to determine the mechanism by which PYY inhibits acid secretion by examining the effects of PYY on gastric acid stimulated by pentagastrin, histamine, and bethanechol [8].
• A dose of PYY (400 pmol X kg-1 X h-1) was employed that reproduced blood levels observed after intestinal perfusion with oleic acid and inhibited the acid secretory response to an intragastric meal by 35 +/- 6% [8].
• This same dose of PYY maximally inhibited histamine- and pentagastrin-stimulated acid secretion by 28 +/- 7% (P less than 0.05), and 17 +/- 4% (P less than 0.05), respectively [8].
• Although PYY had no effect on bethanechol-stimulated secretion it markedly inhibited the secretory response to sham feeding, maximally reducing secretion by 90 +/- 4% (P less than 0.01) [8].
• We speculate that PYY acts by inhibiting acetylcholine release from vagal nerve fibers rather than by inhibiting acetylcholine's action on the parietal cell [8].

Chemical compound and disease context of PYY

• METHODS: In conscious rats, plasma PYY was determined in response to oral ingestion of a 6-mL meal and intravenous infusion of PYY; small intestinal transit time was measured by phenol red as a nonabsorbable marker, and pancreatic secretory studies were performed in rats with pancreatic fistulas and jugular vein catheters [9].
• The objective of this study was to determine the effect of PYY on insulin release stimulated by either 2-deoxyglucose (2-DG) or neuropeptides in conscious dogs with gastric and duodenal fistulas [10].
• Six mongrel dogs with chronic gastric and duodenal fistulas were given an intravenous infusion of pentagastrin (0.5 microgram . kg-1 . h-1), histamine (18 micrograms . kg-1 . h-1), or bethanechol (80 micrograms . kg-1 . h-1) either alone or simultaneously with intravenous PYY (100, 200, 400, pmol . kg-1 . h-1) [11].
• Plasma levels of peptide YY correlate with cisplatin-induced emesis in dogs [12].

Biological context of PYY

• Ileal or colonic perfusion of Ensure delayed phase 3 [migrating motor complexes (MMC)] in the duodenum, inhibited ileal motility, and increased plasma levels of PYY and GLP-1 [13].
• BACKGROUND: Peptide YY (PYY), a hormone released following a meal, is one potential mediator of intestinal absorption [14].
• Although the mediator of this response is not established, peptide YY (PYY) has been considered the most likely peptide candidate because inhibition of intestinal motility by fat in the distal gut correlated with the release of PYY but not other distal gut peptides such as enteroglucagon or neurotensin [15].
• We conclude that exogenous PYY or endogenous PYY released by ileal oleate inhibits pancreatic secretory responses to exogenous secretin, cholecystokinin, or a meal and causes pancreatic vasoconstriction [16].
• Competition studies revealed a higher affinity of the binding sites for PYY than NPY (inhibition constants were 118 +/- 17 pM and 300 +/- 53 pM, respectively, P < or = 0.001) [17].

Anatomical context of PYY

• PYY was purified from canine colonic mucosa by sequential steps of reverse phase HPLC and ion-exchange FPLC [18].
• This study re-examined the anatomical locations of PYY in the canine gastrointestinal tract [19].
• These studies demonstrate that PYY is not confined to distal intestinal endocrine cells in the dog but is also an enteric neuropeptide with maximal concentrations being present in the intestinal myenteric plexus [19].
• Individual synaptosomal preparations obtained from canine intestinal and gastric myenteric plexus, and intestinal deep muscular plexus and submucous plexus, contained considerable quantities of PYY-LI which, on reverse-phase HPLC, co-eluted with a synthetic canine/porcine PYY standard [19].
• PYY: a neuropeptide in the canine enteric nervous system [19].

Associations of PYY with chemical compounds

• On the other hand, PYY (400 pmol/kg.h) had no effect on insulin secretion induced by intravenous glucose (0.6 g/kg.h) alone [2].
• These inhibitory effects of PYY on pancreatic secretion and blood flow were abolished in the presence of combined phentolamine and propranolol [16].
• The cephalic phase of gastric acid secretion, stimulated by the intravenous injection of 2-deoxyglucose (75 mg/kg), was found to be inhibited by intravenous PYY (100, 200, 400 pmol/kg X h) in a dose-related fashion [20].
• RESULTS: Oral ingestion of the meal (containing phenol red, 1.6 mg/100 mL) significantly increased plasma PYY within 30 minutes [9].
• After intravenous administration of PYY, there was a dose-dependent inhibition of pancreatic HCO3 and protein responses to secretin, cholecystokinin, and feeding in conscious dogs and a reduction in pancreatic blood flow in anesthetized animals [16].

Other interactions of PYY

• Intravenous infusions of 50 pmol/kg x h GLP-1 or PYY, which reproduced plasma elevations after intraduodenal fat, inhibited gastric acid secretion by 66 +/- 5% and 51 +/- 6%, respectively (both P < 0.01); coinfusions of GLP-1 and PYY abolished gastric acid secretion (P < 0.001) without influencing plasma gastrin or somatostatin [21].
• In addition, serum levels of motilin and PYY were determined before and during the administration of 1500 cGy in four separate dogs instrumented to record upper gut contractile activity [22].
• Glucagon-like peptide-1-(7-36) amide and peptide YY mediate intraduodenal fat-induced inhibition of acid secretion in dogs [21].

Analytical, diagnostic and therapeutic context of PYY

• The concentration and distribution of PYY was highest in the ileum and colon as determined by both radioimmunoassay of rat tissue extracts and immunocytochemistry [23].
• After all, vagal denervation enhanced the inhibitory effect of PYY on gastric secretion, but abolished the inhibitory effect on phase III contractile activity [6].
• In the ileal reservoir dogs, postprandial PYY levels reached 238 +/- 31 pmol/liter compared with 93 +/- 33 pmol/liter in sham operated controls (P less than 0.001) [24].
• Ileal luminal PYY recovery increased significantly after both OGTT and IVGT [25].
• PYY opposed the action of CCK-8 to a greater extent than that of nicotine and transmural electrical stimulation [26].

References