Biomedical subjects

G H Greeley

Publications and source records attributed to G H Greeley.

At least 55 records · Page 3Linked to original sources

PubMed1993

Pituitary adenylate cyclase activating polypeptide stimulates release of peptide YY.

The purpose of these experiments was to examine the effects of the recently discovered gastrointestinal peptide, pituitary adenylate cyclase activating polypeptide (PACAP), and two structurally related peptides, vasoactive intestinal polypeptide and secretin, on release of peptide YY (PYY) in conscious dogs. Intravenous administration of PACAP-27 or -38 stimulated a dose-related release of PYY; PACAP-27 was more potent than PACAP-38. PACAP-stimulated release of PYY was inhibited significantly by atropine, whereas ganglionic or beta-adrenergic blockade with hexamethonium and propranolol treatment, respectively, did not affect PACAP-induced release of PYY significantly (P > 0.05). These results indicate that PACAP-induced release of PYY is cholinergic dependent and that beta-adrenergic tone and ganglionic transmission do not participate in PACAP-induced release of PYY. PACAP may play a role in the neural regulation of PYY release.

Animals↗

PubMed1993

Age-related changes in gallbladder contractility and cytoplasmic Ca2+ concentration in the guinea pig.

Gallbladder (GB) motility diminishes with aging. This study was performed to characterize mechanisms that are involved in changes in GB contractility that occur during aging. Cytoplasmic Ca2+ concentrations ([Ca2+]i) and the contractile force of guinea pig GB muscle strips were simultaneously measured using fura-2 and force-displacement transducers. The binding ability of the Ca2+ channel antagonist and GB muscle compliance were also examined. The COOH-terminal octapeptide of cholecystokinin (CCK-8) evoked a dose-dependent increase in force and [Ca2+]i. Changes of [Ca2+]i and contractile force of muscle strips in response to CCK-8 were significantly greater in young (2 mo old) compared with mature and aged (12 and 24 mo old) guinea pigs (changes in [Ca2+]i, ED50: 46.1 nM at 2 mo, 6.1 microM at 12 mo, and 2.8 mM at 24 mo; changes of contractile force, ED50: 24.8 microM at 2 mo, 2.1 mM at 12 mo, and 357 mM at 24 mo). However, the magnitude of the contraction at each percent change in [Ca2+]i was actually similar in young and aged guinea pigs. In a Ca(2+)-free buffer, the responses of [Ca2+]i and force to CCK-8 in both young and aged GB muscles decreased, but those were still dose and age dependent. Binding ability of the Ca2+ channel antagonist did not differ in the young and aged groups, but the compliance of the GB muscle strip decreased with aging. These results suggest that both a reduced mobilization of intracellular Ca2+ and a decreased muscle compliance are responsible, at least in part, for age-related reduced contraction of guinea pig GB in response to CCK.

Aging↗

PubMed1993

Effects of peptide YY on the growth of the pancreas and intestine.

The effects of Peptide YY (PYY) on pancreatic and intestinal growth have been investigated in conscious rats. Male Wistar rats equipped with jugular vein cannulas were randomly assigned to five groups. All rats received continuous i.v. infusion of gut peptides for 4 days, rats were then killed, and the pancreas and intestine were analyzed. Infusion of PYY alone at the dose of 400 pmol/kg.h affected neither pancreatic weight, DNA and RNA contents, or the duodenal weight, protein, DNA and RNA contents. Infusion of caerulein at the dose of 0.25 microgram/kg.h significantly increased pancreatic weight, DNA, RNA, and protein contents by 202%, 109%, 171%, 183% above control values, but it did not affect duodenal weight, DNA, RNA, and protein contents. PYY, 400 pmol/kg.h, infused simultaneously with caerulein significantly reduced by 39%, 35%, and 45% increases in pancreatic weight, RNA and DNA contents stimulated by caerulein, respectively. Surprisingly, administration of PYY antiserum also resulted in a small but significant reduction in caerulein-stimulated pancreatic weight, protein, and DNA contents. In conclusion, PYY has an inhibitory effect on cholecystokinin-stimulated pancreatic growth and may play a physiological role as an inhibitor of pancreatic growth.

Animals↗

PubMed1993

Characterization of peptide-YY release in response to intracolonic infusion of amino acids.

Peptide-YY-(1-36) [PYY-(1-36)] is an endocrine peptide that is found primarily in the mucosal layer of the colon. We reported previously that a direct intracolonic (IC) infusion of amino acids in dogs resulted in a robust release of PYY compared to other nutrients (fat, glucose, and protein). The objective of this study was to investigate the possible mechanisms underlying the release of PYY in response to IC infusion of amino acids. Intracolonic infusion of a mixture of tryptophan and phenylalanine (Trp+Phe; 100 mM; 200 ml/h) resulted in a significant release of PYY [integrated PYY release, 74.5 +/- 14.0 ng (0-120 min)/ml], which was not affected by iv atropine, hexamethonium, or propranolol treatment. Intravenous infusion of Trp+Phe failed to release PYY [integrated PYY release, -0.6 +/- 0.9 ng (0-120 min)/ml]. Intracolonic infusion of aromatic amino acids (Trp+Phe) was more potent in releasing PYY than aliphatic (leucine and glycine) and charged (arginine) amino acids. PYY release in response to IC infusion of the deamino and decarboxylated forms of Phe was significantly (P < 0.05) decreased [integrated PYY release, 17.5 +/- 2.6 and 12.1 +/- 2.8 ng (0-120 min)/ml, respectively] compared to that in response to intact Phe [integrated PYY release, 39.4 +/- 4.3 ng (0-120 min)/ml]. These results suggest that 1) PYY release in response to IC administered amino acids is independent of ganglionic, cholinergic, and beta-adrenergic transmission; 2) PYY release in response to IC amino acids is due to a direct contact of amino acids with the luminal pole of PYY cells in the colon and is not the result of a stimulatory action of amino acids via the general circulation; and 3) the amino and carboxylic groups of an amino acid as well as the ring structures of aromatic amino acids are structural requirements for PYY release.

Animals↗

PubMed1993

Parastatin (porcine chromogranin A347-419), a novel chromogranin A-derived peptide, inhibits parathyroid cell secretion.

Chromogranin A (CgA), previously referred to as secretory protein-I, is a 50-kilodalton protein present in secretory granules of many endocrine and neuroendocrine cells. In the parathyroid it is present and cosecreted with PTH in response to hypocalcemia. CgA appears to be a precursor of bioactive peptides including pancreastatin, beta-granin, vasostatin, and chromostatin. The presence of several highly conserved pairs of basic amino acids, putative cleavage sites, in the CgA molecule suggests that other yet unidentified bioactive peptides might exist within the molecule. We tested this speculation by subjecting porcine parathyroid CgA to digestion by endoproteinase Lys-C. Resulting CgA-derived peptides were isolated by reverse-phase C18 HPLC and tested for their ability to affect low-Ca2+ stimulated secretion by porcine parathyroid cells. We characterized one peptide, which we named parastatin, that inhibited secretion of both PTH and CgA in a dose-dependent fashion over the range of 0.2-0.6 microM. Parastatin migrated as a single band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis with an apparent mol wt of 11,000. Edman degradation yielded the sequence L-S-F-R-A-P-A-Y-G-F-R-G-P-G-L corresponding to residues 347-361 of porcine CgA. Amino acid analysis of endoproteinase Lys-C and endoproteinase Asp-N-generated fragments indicated that parastatin corresponds to residues 347-419 of CgA. A synthetic NH2-terminal fragment of rat parastatin corresponding to residues 1-19 was an inhibitory as intact porcine parastatin on parathyroid gland secretion. These results extend the concept that CgA is a precursor of biologically active peptides.

Amino Acid Sequence↗

PubMed1992

Receptor-mediated autocrine growth-stimulatory effect of 5-hydroxytryptamine on cultured human pancreatic carcinoid cells.

5-hydroxytryptamine (5-HT) is a mitogen for fibroblasts, vascular smooth muscle cells, renal mesangial cells, and jejunal crypt cells. The human carcinoid cell line (termed BON) that we established in our laboratory from a pancreatic carcinoid tumor produces and secretes 5-HT. In this study, therefore, we examined the effect of 5-HT on growth of BON cells. Furthermore, by use of selective 5-HT receptor antagonists, we examined receptor and post-receptor mechanisms by which 5-HT-induced responses were produced. 5-HT stimulated growth of BON cells. 5-HT stimulated phosphatidylinositol (PI) hydrolysis in a dose-dependent fashion and inhibited cyclic AMP production in a dose-dependent fashion. The 5-HT1A/1B receptor antagonist, SDZ 21-009, prevented the reduction of cyclic AMP production evoked by 5-HT and inhibited the mitogenic action of 5-HT. The 5-HT1C/2 receptor antagonist, mesulergine, competitively inhibited PI hydrolysis, but did not affect the mitogenic action of 5-HT. The mitogenic action of 5-HT and the reduction of cyclic AMP production evoked by 5-HT were also inhibited by pertussis toxin. These results suggest that 5-HT is an autocrine growth factor for BON cells and that mitogenic mechanism of 5-HT involves receptor-mediated inhibition of the production of cyclic AMP which may be linked to pertussis toxin-sensitive GTP binding protein. 8-bromo-cyclic AMP inhibited growth of BON cells whereas 8-bromo-cyclic GMP had no effect on cell growth. Involvement of protein kinase A in BON cell growth regulation was confirmed by the observation that a cAMP-dependent protein kinase antagonist (Rp-cAMPS) could stimulate BON cell growth.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1992

Neurotensin stimulates growth of colonic mucosa in young and aged rats.

Neurotensin, a tridecapeptide widely distributed in the gut, stimulates growth of small bowel mucosa in young and aged rats. In the present study, the effect of long-term neurotensin administration on the growth of colonic mucosa was examined in young (2-month-old) and aged (24-month-old) rats. Subcutaneous injections of saline (control) or neurotensin (300 micrograms/kg) in gelatin were given to the groups of rats every 8 hours for 10 days. During treatment, all rats were maintained on a regular chow diet. Rats were killed on day 11; the entire colon was removed, mucosa was scraped and weighed, and DNA, RNA, and protein contents were determined. Neurotensin induced growth of colonic mucosa in both age groups. In young rats, neurotensin increased weight and DNA, RNA, and protein contents of colonic mucosa. The ratio of DNA content, an index of cellular hyperplasia, was increased significantly in the neurotensin-treated young rats compared with age-matched controls, indicating an overall increase in mucosal cellularity. In the aged rats, growth was characterized by an increase in weight and RNA and protein contents, but not DNA content, thus suggesting cellular hypertrophy. These results suggest that neurotensin has an important regulatory function in the growth of colonic mucosa; however, the mode of action, at the cellular level, appears to be different depending on age.

Aging↗

PubMed1992

Chronic effect of oral cholestyramine, a bile salt sequestrant, and exogenous cholecystokinin on insulin release in rats.

Oral cholestyramine, a bile salt sequestrant, stimulates pancreatic exocrine secretion and growth chiefly by increasing cholecystokinin (CCK) release. In this report, we examine pancreatic insulin content and insulin release from the isolated perfused pancreas in rats given oral cholestyramine (4%, wt/wt) or subcutaneous CCK-8 (1 micrograms/kg every 8 h) for 2 weeks. Cholestyramine significantly increased pancreatic weight by 32%. CCK administration significantly increased pancreatic weight by 15%. Total pancreatic content of protein and DNA were also increased significantly by cholestyramine and pancreatic protein content was increased significantly by CCK administration. Total pancreatic insulin content was not affected by cholestyramine or CCK. Both cholestyramine and CCK significantly increased the first phase of glucose (8.4 mM)-stimulated release of insulin [mean insulin output (ng/min): control, 2.0 +/- 0.1; cholestyramine, 2.7 +/- 0.2; CCK, 2.6 +/- 0.2]. Cholestyramine also significantly enhanced the second phase of glucose-stimulated release of insulin. Insulin release stimulated by CCK-8 (10(-10) M) was not affected by oral cholestyramine or CCK treatment. These findings indicate that oral cholestyramine and exogenous CCK have a stimulatory effect on beta cell function. Since pancreatic insulin content was not affected by cholestyramine and CCK treatment, cholestyramine and CCK may increase the sensitivity of beta cells to glucose. The absence of a stimulatory effect of cholestyramine and CCK administration on insulin release in response to CCK-8 may be related to a down-regulation of CCK receptors on beta cells.

Administration, Oral↗

PubMed1992

Release of peptide-YY from the dog pancreas.

The objectives of this study were to characterize the distribution of immunoreactive peptide-YY (PYY) in the dog pancreas and to examine whether vagal stimulation can release PYY from the pancreas. Levels of pancreatic polypeptide (PP) were also measured. PYY levels in extracts of the right lobe (0.43 +/- 0.03 ng/mg tissue) and head (0.35 +/- 0.12 ng/mg tissue) of the pancreas were approximately 10- to 20-fold higher than those in extracts of the stomach (0.03 +/- 0.01 ng/mg tissue; P less than 0.05) and left lobe of the pancreas (0.02 +/- 0.01 ng/mg tissue). However, PYY levels in extracts of the pancreas and stomach were significantly lower than PYY levels in extracts of the colonic mucosa (7.63 +/- 0.71 ng/mg tissue). PP levels were significantly (300-fold) higher in pancreatic extracts than in stomach and colonic extracts. Immunoreactive PYY and PP in pancreatic and colonic mucosal extracts coeluted with synthetic PYY and PP standards on HPLC. Electrical vagal stimulation of dogs resulted in a significant (P less than 0.05) release of PYY and PP, which was abolished by atropine treatment (2 mg/kg, iv). PYY levels in the pancreatic veins increased more quickly than in the peripheral veins. The integrated levels of PYY in the pancreatic veins [1.63 +/- 0.30 ng (0-30 min)/ml] were significantly (P less than 0.05) higher than those in peripheral veins [0.86 +/- 0.16 ng (0-30 min)/ml], but lower than those in colonic veins [3.14 +/- 0.22 ng (0-30 min)/ml]. Our results indicate that PYY is primarily produced in the colon; however, the pancreas contains a measurable amount of PYY, which is mainly distributed in the right lobe and head of the pancreas. In addition, PYY can be released from the pancreas in response to vagal stimulation. These data suggest that pancreatic PYY may participate in the regulation of pancreatic and gastrointestinal functions through endocrine and paracrine actions.

Animals↗

PubMed1991

Effects of pancreastatin and chromogranin A on insulin release stimulated by various insulinotropic agents.

The effects of porcine pancreastatin on insulin release stimulated by insulinotropic agents, glucagon, cholecystokinin-octapeptide (CCK-8), gastric inhibitory polypeptide (GIP) and L-arginine, were compared to those of bovine chromogranin A (CGA) using the isolated perfused rat pancreas. Pancreastatin significantly potentiated glucagon-stimulated insulin release (first phase: 12.5 +/- 0.9 ng/8 min; second phase: 34.5 +/- 1.6 ng/25 min in controls; 16.5 +/- 1.1 ng/8 min and 44.0 +/- 2.2 ng/25 min in pancreastatin group), whereas CGA was ineffective. The first phase of L-arginine-stimulated insulin release was also potentiated by pancreastatin (6.9 +/- 0.5 ng/5 min in controls, 8.4 +/- 0.6 ng/5 min in pancreastatin group), but not by CGA. Pancreastatin did not affect CCK-8 or GIP-stimulated insulin release. Similarly, CGA did not affect insulin release stimulated by CCK-8 or GIP. These findings suggest that pancreastatin stimulates insulin release in the presence of glucagon. Because pancreastatin can have multiple effects on insulin release, which are dependent upon the local concentration of insulin effectors, pancreastatin may participate in the fine tuning of insulin release from B cells.

Animals↗

PubMed1991

Intracolonic fat inhibits gastric acid secretion independent of gastrin release in the dog.

The purpose of this study was to examine the effect of perfusion of the colon with a fatty acid (oleic acid) on peptone-stimulated gastric acid secretion and release of gastrin in conscious dogs. Gastric acid secretion was monitored by continuous intragastric titration. Perfusion of the colon with sodium oleate (24 mmol/hr) inhibited gastric acid secretion (14.2 +/- 2.6 meq/hr) stimulated by a peptone meal (1%) significantly (P less than 0.05) when compared to perfusion of the colon with saline alone (20.1 +/- 1.6 meq/hr). The serum elevation in gastrin in response to intragastric instillation of the peptone meal was not affected by the colonic perfusion of oleic acid. Plasma concentrations of peptide YY (PYY) increased significantly in response to perfusion of the colon with saline or sodium oleate, and the integrated release of PYY in response to sodium oleate [6.9 +/- 2.8 ng (60-120) min/ml] was significantly greater than the response to saline [3.1 +/- 0.7 ng (60-120) min/ml]. The results of this study indicate that inhibition of gastric acid secretion by perfusion of the colon with fat is not due to an inhibition of gastrin release. In addition, because PYY is an inhibitor of gastric acid secretion, it is possible that PYY participates as an inhibitor of gastric acid secretion by the colon.

Animals↗

PubMed1991

Characterization of secretin release in response to food and intraduodenal administration of fat and hydrochloric acid.

The development and validation of a radioimmunoassay that detects release of secretin in plasma in response to low doses of secretagogues [intraduodenal HCl (0.033 meq/min); intraduodenal sodium oleate (0.04 mmol/min)] or an oral mixed meal in conscious dogs is described. Plasma secretin levels increased significantly (P less than 0.05) in response to an oral mixed meal in conscious dogs from a basal level of 4.0 to a peak level of 12.3 pg/ml at 15 min. Infusion of graded doses of HCl (2, 4, 8, 16, meq/hr for 30 min) intraduodenally in six dogs resulted in significant elevation of plasma secretin levels in a dose-dependent manner. The pancreatic bicarbonate and volume outputs correlated with the dosage of HCl administered and with the elevations in plasma secretin concentrations. Intraduodenal infusion of increasing doses of sodium oleate (2.4, 4.8, 9.6, and 19.2 mmol in 15-min periods) resulted in a significant (P less than 0.05) elevation of plasma levels of secretin.

Animals↗

PubMed1991

Peptide YY, a new gut hormone (a mini-review).

This report describes our current knowledge of a new gut peptide hormone, peptide YY. The localization, action, and possible mechanisms that control release of peptide YY are described.

Amino Acid Sequence↗

PubMed1991

Stimulation of calcitonin secretion in the pig by calcitonin gene-related peptide.

Pig thyroid glands were surgically isolated in situ and perfused with autologous blood to which was added known concentrations of calcitonin gene-related peptide (alpha CGRP). When thyroids were perfused with measured concentrations of CGRP within the range of 0.6-600 nM, the secretion rate of calcitonin (CT) was stimulated while the release of T3, T4, and somatostatin remained unchanged. Specific binding of 125I-CGRP to pig thyroid plasma membranes was demonstrated, and binding was inhibited by unlabelled CGRP but not by CT or by other peptides unrelated structurally to CGRP. The findings indicate that the pig thyroid gland contains plasma membrane binding sites for CGRP and that CGRP is capable of stimulating the secretion of CT.

Animals↗

PubMed1991

Intracolonic infusion of bile salt stimulates release of peptide YY and inhibits cholecystokinin-stimulated pancreatic exocrine secretion in conscious dogs.

The purpose of this study was to examine the effect of transanal (intracolonic) infusion of bile acid on release of peptide YY (PYY) and cholecystokinin (CCK)-stimulated pancreatic exocrine secretion in seven conscious dogs. CCK-8 (50 ng/kg/h) was given intravenously for 120 min and either taurocholic acid (TA, 1 or 2 mmol/h) or saline was infused transanally (150 ml/h) during the 0-60-min period of CCK infusion. Transanal infusion of TA (1 or 2 mmol/h) significantly inhibited output of CCK-8-stimulated pancreatic protein, compared to transanal infusion of saline during the first 60 min. On the average, the magnitude of inhibition was approximately 45%. Plasma concentrations of PYY increased significantly in response to intracolonic infusion of TA or saline. Transanal infusion of TA (1 or 2 mmol/h) significantly increased plasma levels of PYY when compared with transanal infusion of saline during the first 60 min. The magnitude of the increase of plasma PYY levels was approximately 50 pg/ml (p less than 0.05). Plasma levels of pancreatic polypeptide were not altered significantly by transanal infusion of TA. Our results suggest that release of endogenous PYY by TA in the colon plays a role in the inhibition of CCK-stimulated pancreatic exocrine secretion. Bile salts in the hindgut may participate in the physiologic regulation of pancreatic exocrine secretion by stimulation of release of ilealcolonic PYY.

Animals↗

PubMed1991

Inhibitory action of islet amyloid polypeptide and calcitonin gene-related peptide on release of insulin from the isolated perfused rat pancreas.

Islet (or insulinoma) amyloid polypeptide (IAPP) is a 37-residue peptide recently purified from amyloid deposits in the pancreas of patients with type 2 diabetes and from amyloid deposits of a human insulinoma. IAPP immunoreactivity has been identified in islet B cells of diabetic and nondiabetic humans. IAPP is structurally similar to calcitonin gene-related peptide (CGRP). The purpose of this study was to examine the effects of IAPP and CGRP on glucose- and carbachol-stimulated release of insulin and pancreatic polypeptide (PP) from the isolated perfused rat pancreas. IAPP and CGRP, at 10(-7) M, failed to inhibit glucose-stimulated (16.7 mM) release of insulin. At the same concentration, however, IAPP significantly (p less than 0.05) inhibited carbachol-stimulated (10(-7) M) release of insulin by 30%, and CGRP significantly inhibited carbachol-stimulated release of insulin by 33% when compared with the control group. IAPP also significantly decreased carbachol-stimulated release release of PP. IAPP and CGRP, at 10(-8) M, did not inhibit carbachol-stimulated release of insulin and PP. These results suggest that IAPP and CGRP may have roles in the regulation of secretion of insulin. IAPP may inhibit secretion of insulin, at least in part, by blocking cholinergic mechanisms.

Amyloid↗

PubMed1991

Regulation of pancreastatin release from a human pancreatic carcinoid cell line in vitro.

The objective of these experiments was to investigate the influence of activation of three second messenger systems (protein kinase-C, adenylate cyclase-cAMP, and calcium mobilization) on the secretion of pancreastatin (PST) and chromogranin-A (CGA) by a human pancreatic carcinoid cell line (BON) in tissue culture. Stimulation of protein kinase-C by a phorbol ester (0.025-7.5 microM) caused a significant dose-related release of PST (186 +/- 22-4271 +/- 228% over controls). Treatment of BON cells with graded doses of 8-bromo-cAMP (0.14-3.0 mM) and isobutylmethylxanthine (IBMX; 0.01-1.0 mM) also stimulated a dose-related release of PST (107 +/- 22-284 +/- 28 and 16 +/- 12-1076 +/- 100% over controls, respectively). Incubation of BON cells with ionomycin (0.134-13.4 microM) increased the release of PST (102 +/- 15-554 +/- 21% over controls) in a dose-related manner. A combination of IBMX and ionomycin resulted in an additive effect, whereas treatment with a phorbol ester plus IBMX resulted in a synergistic effect on PST release. Pretreatment of BON cells with monensin, an agent that prevents processing of precursors to smaller peptides, significantly decreased PST, but not CGA, secretion in response to phorbol ester or ionomycin. These findings indicate that protein kinase-C, cAMP, and Ca2+ mobilization participate in CGA and PST secretion. Although the observation that secretions of PST and CGA in response to theophylline are quantitatively associated, the absence of a quantitative relationship in the release patterns of PST and CGA in response to phorbol ester and ionomycin do not support a simple precursor-product relationship between CGA and PST. The monensin experiments are consistent with the notion that PST is derived from CGA in BON cells.

1-Methyl-3-isobutylxanthine↗

PubMed1991

Peptide-YY, a new partner in the negative feedback control of pancreatic secretion.

Peptide YY (PYY), a newly discovered ileocolonic peptide, is released by nutrients in the proximal and distal intestine and inhibits pancreatic secretion. However, it is not clear whether PYY can be released in the absence of nutrients in the intestine or whether a physiological role exists for endogenous PYY in negative feedback regulation of pancreatic secretion by pancreatic proteases. In the present study we measured plasma PYY concentrations and determined the effects of anti-PYY serum during stimulation of pancreatic secretion by pancreatic juice diversion (PJD). The effect of SMS 201-995 (SMS; an analog of somatostatin), another inhibitor of pancreatic secretion, on regulation of PYY release induced by PJD was also investigated. Male Wistar rats equipped with pancreatic, biliary, duodenal, and jugular venous cannulas were studied 4-6 days postoperatively. After 90 min of basal collection, pancreatic juice was diverted for 4 h with or without infusion of SMS (2 micrograms/kg.h), given either iv or intraduodenally (ID). Plasma PYY concentrations were significantly increased from a basal level of 177 +/- 15 pg/ml to a peak level of 328 +/- 43 pg/ml 2 h after PJD. These increases in PYY concentration paralleled those in pancreatic protein and fluid outputs. Both iv and ID infusion of SMS during the first 2 h of PJD markedly decreased the plasma PYY concentration to 134 +/- 27 pg/ml and 156 +/- 19 pg/ml, respectively; the total incremental PYY release during 4 h of PJD was inhibited by 100% and 84% by iv and ID SMS, respectively. One milliliter of anti-PYY serum given iv significantly augmented the increment in protein and fluid output during PJD. These results suggest that endogenous PYY released by PJD may play a physiological role in negative feedback regulation of pancreatic secretion in rats.

Animals↗