Sensitivity of vagal mucosal afferents to serotonin and its role in the mediation of non-CCK–stimulated pancreatic secretion. Im Buch gefunden... B - Glukosidase Leberzirrhose pHt Calciumbilirubinat Calciumcarbonat und -phosphat D. Rolle der Gallenblase bei Cholelithiasis Vagotomie Schwangerschaft CCK - Mangel Vagotomie Schwangerschaft Galle : Cholesterin / Gallensalz 1 ( s . 270Gastrointest. Mol Endocrinol. Dr. Scott R. Brazer is a Gastroenterologist in Durham, NC. Mangel AW, Snow ND, Misukonis MA, Basavappa S, Middleton JP, Fitz JG, Liddle RA. 33 1996 G287G290 Abstract | ISI | Google Scholar 82 Issue 2, p174 Presents a letter to the editor regarding the role of exaggerated sensitivity of the colon to cholecystokinin in the motility changes experienced by patients with irritable bowel syndrome. These observations strongly support the hypothesis that DBI is the physiologic CCK-releasing peptide responsible for the feedback regulation of pancreatic secretion and the postprandial release of CCK in the rat. From Middle English wringere, equivalent to wring +?-er.. Pronunciation. [26] Mangel AW, Koegel A. Antagonists of the type 3 serotonin . After a 30-minute basal period, rats received an intraduodenal perfusion of PBS (20 mL/10 min). Jan 2011; However, the dietary protein sensory mechanisms and the intracellular signal pathway in the ente. The supernatant was completely aspirated, and the radioactivity of the pellet was counted in a gamma counter. We hypothesized that DBI is the CCK-RP responsible for the feedback regulation of pancreatic secretion and the postprandial release of CCK. In the basal state, no significant motility differences were noted between these two groups. Hyper-polarization may limit the increase in cytosolic calcium, as with hyper-polarization gCa activity decreases. The two most important potassium channel types identified to date are a calcium-activated potassium channel (gKCa) and an ATP-sensitive potassium channel (GKATP) [1-4] (Figure 1). Distal colonic motor activity was measured in 12 control subjects and seven constipation-predominant irritable bowel syndrome patients to examine the effects of intravenous administration of cholecystokinin. Apart from DBI, there are a number of luminally secreted peptides that have been shown to stimulate CCK release when administered intraduodenally. (ANOVA, total degrees of freedom, 59; F = 2128.3; P < 0.01.) To demonstrate the specificity of the anti-DBI antiserum to inhibit CCK-mediated pancreatic secretion, we showed that intraduodenal infusion of 300 mM maltose (3 mL/h) evoked a 2-fold increase of pancreatic protein output, but did not stimulate plasma CCK levels (15). Liddle, RA, Green, GM, Conrad, CK, Williams, JA. Snow ND, Prpic V, Mangel AW, Sharara AI, McVey DC, Hurst LJ, Vigna SR, Liddle RA. Irritable bowel syndrome (IBS) is a common gastrointestinal disorder with symptoms of abdominal pain, discomfort, and altered bowel function. in: Li, Y, Owyang, C. Non-CCK dependent duodenal stimuli stimulate pancreatic enzyme secretion via gastroduodenal vagal afferent fibers: mediation via 5HT sensory pathways. Patients with CKD suffer from the metabolic sequelae of poor kidney function, hypertension, progressive worsening of glomerular filtration rate (GFR), and from . Yoshida, H, Tsunoda, Y, Owyang, C. Diazepam-binding inhibitor 33-50 elicits Ca. 1992 Oct;24(5):341-2. At the same time, another group purified a luminal CCK-releasing factor from rat intestinal secretions (11). This lowering of luminal DBI concentrations and plasma CCK levels may be mediated by the release of somatostatin stimulated by increased plasma CCK secretion during bile–pancreatic juice diversion, which in turn inhibits CCK-RP secretion (12). This antibody showed complete cross-reactivity with porcine DBI1-86 and DBI33-50 but has no cross-reactivity with secretin, CCK, vasoactive intestinal polypeptide (VIP), or somatostatin. Rodger A Liddle. However, the mech- anism by which glucose increases cholecystokinin (CCK) secre- tion is not known. A.W. It is concluded that CCK plays a crucial role in the mediation of the gastrointestinal phase, but not the cephalic phase, of pancreatic secretion. Dr. Allen W. Mangel is a gastroenterologist in Chapel Hill, North Carolina. Effects of peptides on gastric emptying. In previous studies, we used the donor-recipient rat model to demonstrate that peptone and oleic acid stimulate pancreatic protein secretion and CCK release in a manner that parallels the changes in luminal CCK-RP levels (9, 14). Exaggeration of the cholecystokinin-induced motor response in the cat gastrointestinal tract. Pancreatic secretion was collected every 15 minutes as described previously. The Journal of Nutrition, Vol. Conventional pharmacological treatments to manage IBS-related visceral pain is unsatisfactory. A second agent which stimulates the release of CCK is bombesin which binds to a GRP-preferring receptor, and both activates gCa and stimulates the release of intracellularily sequestered calcium [11]. Recordings of single-channel currents from inside-out membrane patches showed activation of calcium channels by BAY K 8644 (1 microM), with a primary channel conductance of 26.0 +/- 1.2 pS. Am J Physiol 1996,270:G287-90. The activity of the former channel is increased following increases in cytosolic calcium, while GKATP is decreased following increases in cytosolic ATP levels (Figure 1). Pancreatic secretion was collected every 15 minutes. 5. Plasma CCK levels increased from 6.4 pM after the casein infusion to 8.2 pM after the DBI33-50 infusion (P < 0.05). Im Buch gefunden – Seite 350Jordinson M, Calam J (1996) Cholecystokinin release by lectins: evidence for involvement of N-acetyl galactosamine (GalNAc) ... Mangel AW, Gettys TW, Liddle RA (1996) 3-adrenergic regulation of cholecystokinin secretion in STC-1 cells. Im Buch gefunden – Seite 110Chronische Pankreatitis Duodenum Ansteigen des intrapankreatischen Obstruktion des Ganges Gangdrucks Reduzierte Sekretion Ansteigende Stimulation (CCK, ACH) Proteasenmangel Abb. 1. Hypothetisches Modell zur Pathogenese der Schmerzen bei ... Chernick, SS, Lepkovsky, S, Chaikoff, IL. To further evaluate if proteins such as casein in the intestine could prevent the inactivation of DBI33-50 by proteases, we investigated the action of DBI33-50 in the presence of casein in a rat model without bile–pancreatic juice diversion. Figure 6 shows that diversion of bile–pancreatic juice from the duodenum resulted in a rapid and sustained increase in protein output. Am J Physiol Gastrointest Liver Physiol 264: G1031-G1036, 1993 [Google Scholar] Modulation of colonic motility by substance P, cholecystokinin and neuropeptide Y. Mangel AW(1), Fitz JG, Taylor IL. *P < 0.01 by Student’s t test. This antibody showed complete cross-reactivity with DBI33-50 and DBI1-86 but demonstrated no cross-reactivity with secretin, CCK, VIP, or somatostatin. Author information: (1)Department of Medicine, Duke University Medical Center, Durham, NC 27710. 54 paper (Whatman International Ltd., Maidstone, England) to remove any large particles and intestinal debris. The final antibody titer was 1:40,000. This study was designed to determine neurochemical properties of the coeliac-superior mesenteric ganglion (CSMG) neurons supplying the prepyloric area of the porcine stomach in physiological state and following experimentally induced hyperacidity. To increase the antibody titer, intramuscular injections of the same antigen dose emulsified in Freund’s incomplete adjuvant were administered every 2 weeks for 3 months. 1998 Oct;275(4):G689-95. Im Buch gefunden – Seite 76might apply to access to endogenous CCK released into the mesenteric circulation . An example is the demonstration that in the rat , intraportal ... were involved in this effect ( Moran and McHugh 1982 ; Mangel and Koegel 1984 ) . Im Buch gefunden – Seite 50Mangel , A.W. and A. Koegel . Effects of peptides on gastric emptying . Am . Jr. Physiol . 246 : 6342-6345 , 1984 . 153. Mansbach , R.S. and D.N. Lorenz , Cholecystokinin ( CCK - 8 ) elicits prandial sleep in rats . Physiol . & Behav . Im Buch gefunden – Seite 1654... Sichelzellanämie VIPome Z.n. Querschnittslähmung Z.n. Gastrektomie / Vagotomie Leberzirrhose Myotone Dystrophie Zöliakie und totale parenterale Ernährung ( CCK - Mangel ) Medikamente : • Anitcholinergika • Opioide • Calciumblocker ... Cholecystokinin (CCK) plays important regulatory and modulatory roles in the gastrointestinal tract including involvement in: satiety; relaxation of the lower esophageal sphincter (LES); gastric emptying; gallbladder contractility; pancreatic enzyme secretion; and intestinal motility. We investigated the electrophysiological events underlying glucose-induced GLP-1 release in the GLP-1-secreting cell line, GLUTag. The standard binding curve of this antibody is shown in Figure 4. Associated with activation of gCa is a subsequent increase in cytosolic calcium [2, 4, 7, 9-11]. 4.2.2 Cholecystokinin. These increases gradually returned to basal levels after a 5-hour diversion as a result of a reduction in luminal CCK-RP (12). Dr. William Chey, MD is a gastroenterologist in Rochester, New York. Im Buch gefunden – Seite 242Ähnlichkeiten zwischen Erscheinungen von GH-Mangel und Alter (nach Laron 2008): ▷ Verdünnung der Haut (wrinkling) ... αMSH = α-melanozytenstimulierendes Hormon, CCK = Cholecystokinin, GLP = Glucagon-like Peptid, PYY = Peptid YY, ... To test the role of DBI in pancreatic secretion and responses to feeding, we used pancreaticobiliary and intestinal cannula to divert bile–pancreatic juice from anesthetized rats. Distal colonic motor activity was measured in 12 control subjects and seven constipation-predominant irritable bowel syndrome patients to examine the effects of intravenous administration of cholecystokinin. To demonstrate that DBI is responsible for the release of endogenous CCK, we used 2 experimental techniques that are known to elevate plasma CCK levels: diversion of bile–pancreatic juice secretion and intraduodenal peptone infusion. Results were expressed as the mean ± SE. This peptide has a partial sequence homology to epidermal growth factor and has been shown to stimulate CCK release (30) and pancreatic enzyme secretion (31) when administered into the rat proximal intestine by an atropine-insensitive mechanism (31). Furthermore, luminal nutrients, such as peptone-stimulated luminal DBI secretion. The subsequent increase in calcium stimulates the release of CCK and increases gKCa activity. To demonstrate that DBI mediates the postprandial rise in plasma CCK levels, we showed that intraduodenal administration of 5% peptone induced dramatic increases in pancreatic secretion and plasma CCK, effects that could be blocked by intraduodenal administration of anti-DBI antiserum. The volume was measured, and an aliquot was taken and diluted with distilled water for protein determination. The filtrate was ultrafiltered with an Amicon membrane (YM1; Amicon, Beverly, Massachusetts, USA), and the residue, which contained DBI (mol wt > 1000), was dissolved in water and lyophilized. . Buchan, AMJ, et al. Values are means ± SE for 6 rats in each group. Biochem Biophys Res Comm 1994;201:14831489. Moreover, CCK suppresses food intake by inhibiting gastric emptying (Moran & McHugh, 1982). Lateia Scott. 100th Anniversary of Insulin's Discovery (Jan 2021), Hypoxia-inducible factors in disease pathophysiology and therapeutics (Oct 2020), Immunotherapy in Hematological Cancers (Apr 2020), American Society for Clinical Investigation. A similar feedback control system has been shown to operate in chickens (3), pigs (4), and in humans (5). Am. Liver Physiol. The study was performed in 2 groups of rats: (a) those who received an intraduodenal injection of DBI33-50 (10 μg) at 1 hour after casein infusion and (b) those pretreated with the CCK antagonist L364,718 (0.5 mg/kg), given intravenously as a bolus, 10 minutes before casein infusion. Objective To investigate the analgesic effect (measured with Neonatal Infant Pain Scale (NIPS)) of breastfeeding (BF) in addition to skin-to-skin contact (SSC) versus other methods of non-pharmacological analgesia during blood sampling through heel lance in healthy term neonates. | For plasma CCK levels and luminal DBI immunoreactivities in the intestinal washings, data were compared by paired Student’s t test, and significance was accepted at the 5% level. I dag er sødekartofler stadig en favorit blandt atleter, som . Am J Physiol 1994;267:G859865. In summary, we have demonstrated the following: (a) intraduodenal administration of DBI33-50 dose-dependently increased pancreatic secretion and plasma CCK levels; (b) DBI immunoreactivities in the intestinal lumen paralleled changes in plasma CCK levels during diversion of bile–pancreatic juice and during intraduodenal peptone stimulation; and (c) intraduodenal administration of anti-DBI antisera abolished pancreatic secretion and release of CCK during bile–pancreatic juice diversion and peptone stimulation. However, the luminal concentration of DBI is low because of trypsin inactivation. Im Buch gefunden – Seite 371Ein primärer Mangel an Cholecystokinin liegt der hypotonen Dyskinesie offenbar nicht zu Grunde, da im Portalblut dieser Hypotoniker das Hormon in normalerMenge gefunden wurde. Die Gallenflüssigkeit reagiert neutral oder leicht alkalisch ... 16 Mangel A. W., Scott L., Liddle R. A. Depolarization-stimulated cholecystokinin secretion is mediated by L-type calcium channels in STC-1 cells. After a 5-hour diversion of bile–pancreatic juice, infusion of peptone resulted in a 5-fold increase in luminal DBI immunoreactivity. PubMed After the incubation, each sample was incubated with 100 μL of 125I-Tyr-DBI33-50 (0.012 μCi per tube) for 24 hours at 4°C. Join now to see all; Grant Support. | The titer of the antiserum was 1:40,000, and the IC50 was 7 pg. D ietary fatty acids (FAs) trigger release of a number of peptides, including cholecystokinin (CCK) and secretin, by enteroendocrine cells (EECs) (1, 2).CCK is secreted by I cells (3, 4) and secretin by S cells (5 - 7), localized primarily to the duodenum and jejunum.Both peptides influence fat absorption and participate in nutrient sensing and regulation of energy balance (1, 8, 9). Our studies demonstrated that under this experimental condition, intraduodenal infusion of DBI33-50 induced a significant increase in plasma CCK levels. Shown in Figure 3 is a model summarizing our current knowledge of the electrophysiologic basis of CCK secretion. Miyasaka, K, Guan, D, Liddle, RA, Green, GM. Anesthetized rats were prepared with pancreaticobiliary cannula. However, dietary protein in the intestine competes for trypsin and prevents protease-induced feedback inhibition of CCK release. The manner by which food affects the secretion of CCK is largely unknown. Am J Physiol. The goat anti-rabbit 1 gG serum (100 μL) and normal rabbit serum (100 μL) were then added and incubated for 90 minutes at 24°C. 1996 Oct;271(4 Pt 1):G650-4. These observations support the hypothesis that DBI is a CCK-RP and indicate that the pancreatic secretion responses observed after administration of DBI are mediated by the release of endogenous CCK. DBI-like immunoreactivity in the perfusates collected was measured to determine the luminal DBI concentrations under basal conditions. 11. However, a previous study has clearly shown that bile induced a negative feedback regulation of CCK release and inhibited postprandial CCK secretion (20). MeSH Im Buch gefunden – Seite 129Hyperparathyreoidismus , Hypophosphatämie , Hypomagnesiämie ) ; Blutungsneigung ( Vitamin - K - Mangel , TPZ ... exokrine Pankreasinsuffizienz durch reduzierte Cholecystokinin - Freisetzung aus der geschädigten Dünndarmmukosa Klinische ... Activation of gCa increases cytosolic calcium levels (infinity), which also may trigger a calcium-mediated calcium release ± [5]. Am J Physiol 1994;267 . Scott L, Prpic.V, Capel WD, Basavappa.S, Mangel AW, Gettys TW, Liddle RA. Values are means ± SE for 6 rats in each group. In the present study we evaluated the effects of agents anticipated to change NO levels on the secretion of cholecystokinin (CCK) from STC-1 . Careers. 131, Issue. Effect of rabbit anti-DBI33-50 antiserum on pancreatic secretion and plasma CCK stimulated by duodenal infusion of peptone. 47. doi: 10.1152/ajpgi.1995.268.1.G90. Our previous studies have confirmed that the increased levels of protein in the bile–pancreatic juice after CCK-8 stimulation were mainly from the pancreatic source. Five hours after diversion of bile–pancreatic juice, the pancreatic protein output was stable, averaging 120 ± 5 mg/h. Described below is a model outlining the ion channel basis of CCK secretion. Effects of DBI33-50 on plasma CCK levels and pancreatic secretion. Digestion, 43(4):196-203, 01 Jan 1989 Cited by: 2 articles | PMID: 2612742 Experimental evidence suggests that intact protein, such as casein, acts by competing for proteolytic enzymes that would otherwise inactivate the CCK-RP. The exact nature of the dual phosphorylation events responsible for calcium channel activation remains to be elucidated. CCK stimulation did not affect biliary protein levels. Im Buch gefunden – Seite 29Dozios & Kelly27 Secretin NT ✓ Human Chey et al28 Valenzuela & Difillippi31 CCK NT Human Chey et al28 Valenzuela ... VIP NT Rat Mangel & Koegal 35 Substance P NT Rat Mangel & Koebal35 Neurotensin NT Rat Mangel & Koebal35 NT ... 1 Introduction. We want to continue our hand-wringing and feel hostile toward anyone who acts as if there's . , , . Distribution and characterization of endogenous benzodiazepine receptor ligand (endozepine)–like peptides in the rat gastrointestinal tract. Im Buch gefunden – Seite 75Liddle , R.A. ( 1994 ) Cholecystokinin . ... Raven Press , Ltd. , New York , N.Y. Ljungberg , S. ( 1969 ) Biological assay of cholecystokinin in guinea pig gallbladder in ... Mangel , A.W. ( 1984 ) Potentiation of colonic contractility 75. Purification and characterization of a luminal cholecystokinin-releasing factor from rat intestinal secretion. V Prpic. Im Buch gefunden – Seite 10654364 CHOLINERGICALLY - MEDIATED EXAGGERATION OF THE COLONIC MOTOR RESPONSE TO CHOLECYSTOKININ ( CCK ) . A.W. Mangel , S. Wiese , K.M. Sanders , R.A. Gillis and R.J. Gould . Georgetown University , Washington , D.C. 20007 , Merck ... Li, Y, Owyang, C. Pancreatic secretion evoked by cholecystokinin and non-cholecystokinin-dependent duodenal stimuli via vagal afferent fibers in the rat. 1. Cholinergically mediated exaggeration of the colonic motor response to cholecystokinin. American Journal of Physiology 267 G595 - G600. 2011 Apr;300(4):G538-46. Phenylalanine-stimulated secretion of cholecystokinin is calcium dependent. Thomas Quincy Garvey III, M.D. To demonstrate that nutrient stimulates DBI secretion, 5% peptone was perfused for 1 hour after a 5-hour diversion of bile–pancreatic juice when plasma CCK concentrations had returned to basal levels. Experiments were designed to evaluate the relative contributions of extracellular and intracellular calcium to the contractile process in gallbladder smooth muscle. The 18–amino acid peptide fragment (octadecaneuropeptide) is present in DBI molecules of all species (21) and has been shown to displace labeled DBI-like ligand from specific binding sites (21, 23). Manglende CCK kan også føre . CCK-releasing activity of rat intestinal secretion: effect of atropine and comparison with monitor peptide. Barium-induced secretion was inhibited by the L-type calcium-channel blocker, nicardipine. By contrast, the T-type calcium-channel blocker, nickel chloride (10(-7)-10(-8) M), failed to significantly inhibit barium-induced CCK secretion. 12. Am J Physiol 1995. Mangel AW , Scott L , Liddle RA . Am J Physiol. Tissue strips from nonpregnant and pregnant guinea pigs were stimulated in vitro with maximally effective concentrations of potassium (80 mM), acetylcholine (10−4 M), and cholecystokinin-octapeptide (80 nM), both in the presence . The intra-assay and interassay variations were 5 and 12%, respectively. Li, Y, Owyang, C. Pancreatic secretion evoked by cholecystokinin and non-cholecystokinin dependent duodenal stimuli via vagal afferent fibers in rat. | Phenylalanine-stimulated secretion of cholecystokinin is calcium dependent A. W. Mangel , V. Prpic , H. Wong , S. Basavappa , L. J. Hurst , L. Scott , R. L. Garman , J. S. Hayes , A. I. Sharara , N. D. Snow , and al. This increase in calcium is an important trigger for the secretion of CCK [2, 4, 5, 7-9, 11]. Wang Y, Chandra R, Samsa LA, Gooch B, Fee BE, Cook JM, Vigna SR, Grant AO, Liddle RA. et 1995-01-01 00:00:00 METHODS is an important gastrointestinal hormone that plays a role in the regulation of pancreatic . Anti-ulcer potential of rohitukine was assessed in . These data are consistent with our previous observation that peptone in the duodenum acts by stimulating the luminal secretion of CCK-RP, which in turn stimulates CCK release (9, 14). Am J Physiol Gastrointest Liver Physiol 267:G859-G865. | Experimental evidence suggests that CCK secretion may be mediated by a trypsin-sensitive CCK-RP that is secreted into the intestinal lumen. Radioimmunoassay standard curve of 125I-DBI33-50. Noun. Derudover er der stigende bevis for, at afvigelser i ekspression af cholecystokinin eller dets receptor i den menneskelige . Im Buch gefunden – Seite 203Ähnlich NT ist CCK in hohem Maße im Mittelhirn mit Dopamin und in Neuronen des Hypothalamus, zudem mit dem ... Da CCK zudem neuroprotektive Eigenschaften hat und synaptische Kontakte fördert, wurde vermutet, dass ein Mangel an CCK ein ... 13. Biochem Biophys Res Comm 1994;204:855860. Effect of rabbit anti-DBI33-50 antiserum on pancreatic secretion and plasma CCK stimulated by diversion of BPJ. Dr. Scott Brazer, MD is a gastroenterologist in Durham, North Carolina. Amino acids stimulate cholecystokinin release through the Ca2+-sensing receptor. L364,718 was a gift from Victor Lotti, Merck Sharp and Dohme, West Point, Pennsylvania, USA. Google Scholar. doi: 10.1111/j.1472-8206.1989.tb00472.x. This occurs in up to 25% of patients on general wards1-3 and 63% of patients on intensive care units.4 5 Diarrhoea not only limits the efficacy of enteral feeding, but also adds to potential complications, distresses both . Exposure to the amino acid L-phenylalanine increased release of CCK by 135%, 180%, and 251% of control levels after 15-min treatments with 5, 20, and 50 mM phenylalanine, respective … In separate studies, intraduodenal infusion of DBI33-50 induced a dose-dependent increase in pancreatic protein and plasma CCK release (Figure 2). Freshly prepared acini are suspended at a biovolume of up to 1 mm³ per ml culture medium. Previously, it has been shown that an increase in adenosine 3',5'-cyclic monophosphate (cAMP) levels stimulates intestinal secretion of cholecystokinin (CCK); however, the mechanisms for increasing intracellular cAMP levels are not known. To demonstrate that DBI is released during diversion of bile–pancreatic juice, we measured luminal DBI-immunoreactivity at different time points after the diversion. Mangel, AW, et al. Am J Physiol Gastrointest Liver Physiol. CHOLECYSTOKININ AND GASTRIC EMPTYING administration ofthe secondoftwosuccessive peptonemealsas outlined above(i.e. This was a randomized-order,double-blind, sequential study design in each subject . Im Buch gefunden – Seite 191Mangel- ) zustände: 3.11.5. GIP (Gastric Inhibitory Peptide) Produktionsort: Duodenum - Wie CCK-PZ Jejunum Wirkungsort Magen: Hemmung der HCl-Produktion (hochund Hauptwir- wirksamer Gastrinantagonist) kung: Pankreas: Insulinfreisetzung ... Trypsin cleaves the internal bonds at the lysine or arginine residues. In addition, the gCa opener Bay K 8644 activates gCa [8]. CCK is produced primarily by endocrine cells in the mucosa of the proximal small intestine, and it is secreted into the circulation in response to protein (16) and fats (14). Am. Am J [27] Moran TH, McHugh PR. Liver Physiol. Calcium-dependent regulation of cholecystokinin secretion and potassium currents in STC-1 cells. Furthermore, we have shown that the inhibitory action of bile is mediated by inhibiting the ability of CCK-RP (DBI) to release CCK (20). Am J Physiol Gastrointest Liver Physiol 268: G90- G94, 1995. Depolarization of the plasma membrane of intestinal CCK-secreting cells activates L-type calcium channels (gCa) (Figure 2) [1-11]. Values are means ± SE for 6 rats in each group. Effect of intraduodenal administration of DBI33-50 on pancreatic protein secretion and plasma CCK levels with a background intraduodenal infusion of 12% casein. Amino acid sequencing and mass spectral analysis revealed that this peptide is composed of 70–75 amino acids with no homology to DBI. Administration of anti-DBI antiserum (2.5 mL over 30 minutes), but not preimmune rabbit serum, completely abolished protein secretion and CCK release in response to the diversion of bile–pancreatic juice. Mangel AW, Liddle RA. The intestinal perfusates collected from the rats were filtered with Whatman No. Following decrease in activity of g, Shown in Figure 3 is a model summarizing our current knowledge of the electrophysiologic basis of CCK secretion. In vitro studies showed that the recoveries of porcine DBI33-50 and DBI1-86 from intestinal washings were 84 ± 12% and 87 ± 7%, respectively. Corring, T. Mecanisme de la secretion pancreatique exocrine chez le porc: regulation par retroinhibition. Under basal conditions the resting potential is primarily determined by activity of potassium and chloride channels ¿ [1, 2, 4]. Our studies, however, do not rule out the participation of this peptide in the mediation of the feedback regulation of pancreatic secretion or the postprandial release of CCK. J. Physiol. CCK is the major stimulatory hormone of pancreatic exocrine secretions, secreted from enteroendocrine I-cells of the intestine. These channels are sensitive to gCa blockers such as nifedipine, nicardipine and diltiazem, but insensitive to the T-type calcium channel blocker nickel [8, 11]. With membrane depolarization, gCa are activated Ø [5, 8]. The resulting increase of active CCK-RP in the intestine induces the release of CCK and stimulates pancreatic secretion. Proteins but not amino acids, carbohydrates, or fats stimulate cholecystokinin secretion in the rat. Address correspondence to: Chung Owyang, 1500 East Medical Center Drive, University of Michigan Health System, Ann Arbor, Michigan 48109-0362, USA. Under basal conditions, GKATP activity is the predominant potassium channel type activated, and following decreases in channel activity membrane depolarization occurs (Figure 2) [2, 4]. Would you like email updates of new search results? 2016 Jun;30(6):614-29. doi: 10.1210/me.2015-1306. Fundam Clin Pharmacol. Potassium channel activity plays a pivotal role in the generation of the resting potential of intestinal CCK-secreting cells [, Depolarization of the plasma membrane of intestinal CCK-secreting cells activates L-type calcium channels (g, Figure 1. Activation of gCa plays an integral role in CCK secretion stimulated by a variety of agents including: glucose, which modulates GKATP [2, 3, 12]; the amino acid phenylalanine [7]; bombesin, which binds to a GRP-like receptor [11]; and cAMP which increases gCa [10] in a process dependent upon calcium calmodulin-dependent protein kinase II (CaM KII) [9, 13]. To examine the role of calcium channels in depolarization-activated cholecystokinin (CCK) release, studies were performed in an intestinal CCK-secreting cell line, STC-1. In contrast, intravenous infusion of anti-DBI antibody did not affect these physiologic responses (data not shown). doi: 10.1152/ajpgi.1998.275.4.G689. Mangel AW, Snow ND, Misukonis MA, Basavappa S, Middleton JP, Fitz JG, Liddle RA. 2011. Im Buch gefunden – Seite 854Characterization of the release of cholecystokinin from a murine neuroendocrine tumor cell line , STC - 1 . Biochim Biophys Acta 1221 : 339–347 , 1994 . 14. Prpic V , Basavappa S , Liddle RA , Mangel AW . Regulation of cholecystokinin ... The corresponding influx of calcium serves to trigger secretion of CCK.
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