Wyniki wyszukiwania - Biblioteka Nauki

1

The effect of antagonist of receptors for gastrin, cholecystokinin and bombesin on growth of gastroduodenal mucosa and pancreas

100%

Dembinski A. , Warzecha Z. , Konturek S. J. , Banas M. , Cai R.-Z. , Schally A. V.

Journal of Physiology and Pharmacology

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1991

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tom 42

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nr 3

EN

The effects of gastrin, cholecystokinin (CCK) and bombesin on the DNA synthesis, as a biochemical indicator of trophic action in the gastroduodenal mucosa and the pancreas, have been examined in rats fasted for 48 h and in rats refed for 16 h with or without administration of specific receptor antagonists for bombesin, gastrin and CCK. Bombesin and gastrin administered three times daily for 48 h in fasted rats significantly increased the rate of DNA synthesis as measured by the incorporation of [³H] thymidine into DNA in each tissue tested. CCK significantly increased DNA synthesis in the duodenal mucosa and pancreatic tissue, but not in the gastric mucosa. The stimulation of DNA synthesis induced by bombesin in the gastroduodenal mucosa and pancreas was abolished by bombesin/GRP receptor antagonist, RC-3095. RC-3095 did not affect DNA synthesis stimulated by gastrin and CCK in these tissues. L-365,260, a receptor antagonist for gastrin suppressed the DNA synthesis induced by gastrin but not by CCK or bombesin in the gastrointestinal mucosa and pancreas. L-364,718, a specific antagonist for CCK receptors was effective only against CCK stimulated duodenal mucosa and pancreatic growth. Refeeding of 48 h fasting rats strongly enhanced the DNA synthesis in all tissues tested, and this effect was significantly reduced in the gastroduodenal mucosa by blocking only gastrin receptors (with L-365, 260) and that in the duodenal mucosa and the pancreas by antagonizing of CCK receptors (with L-364, 718). Antagonism of bombesin receptors (with RC-3095) did not significantly affect the stimulation of DNA synthesis induced by refeeding in all tissues tested. This study indicates that the stimulation of DNA synthesis can be achieved by exogenous gastrin, CCK and bombesin acting through separate receptors, but that only gastrin and CCK play the major role in the postprandial stimulation of the growth of gastroduodenal mucosa and pancreatic tissue.

2

Somatostatin-like immunoreactivity in the amygdala of the pig

100%

Rowniak M. , Robak A. , Bogus-Nowakowska K. , Kolenkiewicz M. , Bossowska A. , Wojtkiewicz J. , Skobowiat C. , Majewski M.

Folia Histochemica et Cytobiologica

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2008

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tom 46

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nr 2

229-238

3

Gastrin-CCC-like immunoreactivities in the CNS of man

100%

Dorn A. , Rinne A.

Folia Histochemica et Cytobiologica

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1984

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tom 22

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nr 3-4

4

Centrally acting cholecystokinin induces depressor circulatory effects in haemorrhage-shocked rats

100%

Jasikowska K. , Zając M. A. , Jochem J.

Annales Academiae Medicae Silesiensis

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2021

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nr 75

18-23

EN

INTRODUCTION: Cholecystokinin (CCK) is a peptide gastrointestinal hormone involved in the stimulation of lipid and protein digestion as well as a neurotransmitter/neuromodulator in the central nervous system. After intravenous administration, it induces a resuscitating effect in rats subjected to haemorrhagic shock. Since CCK is able to directly and indirectly affect the cardiovascular centre function, the aim of the study was to examine the action of the sulphated octapeptide form of CCK (CCK-8) given intracerebroventricularly (icv) in the sympathoinhibitory phase of haemorrhagic shock. MATERIAL AND METHODS: Studies were carried out in male Wistar rats anaesthetized with ketamine/xylazine (100 mg/kg + 10 mg/kg, intramuscularly) and subjected to irreversible haemorrhagic shock (0% survival at 2 h) with a mean arterial pressure (MAP) of 20–25 mmHg. At 5th min of critical hypotension, the rats were injected icv with CCK-8 (5, 15 nmol) or saline (5 μl). RESULTS: Haemorrhage led to a decrease in pulse pressure (PP), heart rate (HR) as well as increases in renal (RVR) and mesenteric vascular resistance (MVR). In the control group injected with saline, there were no significant increases in the measured cardiovascular parameters, and the survival time was 32.5 ± 5.1 min. CCK-8 induced dose-dependent decreases in MAP, PP and HR accompanied by increases in RVR and MVR, and also shortened the survival time in comparison to the control animals. CONCLUSIONS: Centrally acting CCK-8 induces depressive circulatory effects in haemorrhage-shocked rats.

PL

WSTĘP: Cholecystokinina (CCK) należy do hormonów peptydowych układu pokarmowego regulujących trawienie lipidów i białek, a ponadto jest ośrodkowym neurotransmiterem/neuromodulatorem. Po podaniu dożylnym wywołuje efekt resuscytacyjny u szczurów we wstrząsie krwotocznym. Ze względu na fakt, iż CCK może wpływać bezpośrednio i pośrednio na czynność ośrodka sercowo-naczyniowego, celem pracy było zbadanie działania pochodnej siarczanowej oktapeptydu CCK (CCK-8) podawanej do komory bocznej mózgu (intracerebroventricularly – icv) w fazie hamowania czynności układu współczulnego we wstrząsie krwotocznym. MATERIAŁ I METODY: Badania przeprowadzono u samców szczurów szczepu Wistar w znieczuleniu ogólnym (ketamina [100 mg/kg]/ksylazyna [10 mg/kg]), u których wywołano nieodwracalny wstrząs krwotoczny (0% przeżycia 2 h) ze średnim ciśnieniem tętniczym (mean arterial pressure – MAP) 20–25 mmHg. W 5 min krytycznej hipotensji szczurom podawano icv CCK-8 (5, 15 nmol) lub 0,9% roztwór NaCl (5 μl). WYNIKI: Krwotok prowadził do obniżenia ciśnienia tętna (pulse pressure – PP), częstości rytmu serca (heart rate – HR) oraz wzrostu nerkowego (renal vascular resistance – RVR) i krezkowego oporu naczyniowego (mesenteric vascular resistance – MVR). W grupie kontrolnej nie stwierdzono wzrostu badanych parametrów układu krążenia, a średni czas przeżycia wynosił 32,5 ± 5,1 min. CCK-8 wywoływała zależne od dawki spadki MAP, PP i HR ze wzrostem RVR i MVR, a także skracała czas przeżycia w porównaniu ze zwierzętami kontrolnymi. WNIOSKI: Ośrodkowo działająca CCK-8 wywołuje działanie depresyjne na układ krążenia u szczurów we wstrząsie krwotocznym.

5

The ghrelin pentapeptide inhibits the secretion of pancreatic juice in rats

100%

Kapica M. , Laubitz D. , Puzio I. , Jankowska A. , Zabielski R.

Journal of Physiology and Pharmacology

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2006

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tom 57

|

nr 4

EN

Ghrelin, a 28 amino acids polypeptide was recognized as an endogenous ligand for the growth hormone secretagogue receptor. It turned out that the entire sequence of ghrelin is not necessary for performing the above-mentioned functions. It was suggested that 5 residues (Gly-Ser-Ser(n-octanoyl)-Phe, pentaghrelin) constituted functionally active part of the full-length polypeptide. Ghrelin-28 was found to inhibit pancreatic enzyme output in rats, though the effect of pentaghrelin was not studied so far. The study aimed to determine the involvement of pentaghrelin in pancreatic juice secretion in anaesthetized rats. Male Wistar rats (220 ± 20 g body weight, b. wt.) were anesthetized, the external jugular vein and common biliary-pancreatic duct were cannulated. Pentaghrelin boluses (iv, 1.2, 12, and 50 nmol kg-1 b. wt.) were injected every 30 min with or without CCK-8 infusion, duodenal mucosal CCK1 receptor blockade with tarazepide, vagotomy and capsaicin pretreatment. Pentaghrelin boluses reduced the volume of pancreatic-biliary juice, protein and trypsin outputs both under basal and CCK-8-stimulated conditions in a dose-dependent manner. However, exogenous pentaghrelin failed to affect the pancreatic secretion in rats subjected to vagotomy, capsaicin deactivation of afferents or pretreatment with Tarazepide. In conclusion, pentaghrelin may control exocrine pancreas secretion by affecting duodenal neurohormonal mechanism(s) involving CCK and vagal nerves in rats.

6

The influence of cholecystokinin on gastric myoelectrical activity in duodenal ulcer following Helicobacter pylori eradication - an electrogastrographic study

100%

Budzynski A. , Dobrzynski A. , Lorens K. , Konturek P. C. , Thor P. , Konturek S. J.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 2

EN

Cholecystokinin (CCK) plays an important role in the regulation of postprandial gastric motor activity which was found to be abnormal in duodenal ulcer patients. This study was designed to compare the influence of CCK on gastric myoelectrical function in duodenal ulcer patients and healthy controls. Fifteen patients with active duodenal ulcer and Helicobacter pylori (H. pylori) infection and 15 healthy controls were included into this study. Electrogastrography (EGG) was performed before and 4 weeks after the eradication of H. pylori in ulcer patients and in healthy controls. We compared EGG parameters in the fasting and postprandial period and during intravenous infusion of caerulein, an analog of CCK with or without addition of loxiglumide, a specific CCK-1 receptor antagonist. The amplitude of fasting EGG in duodenal ulcer patients was similar to that in control subjects and was not affected by H. pylori eradication. In contrast, the amplitude of postprandial EGG was markedly increased in duodenal ulcer patients when compared to that in healthy controls and it was significantly reduced following the eradication of H. pylori. The blockade of CCK-1 receptors with loxiglumide in healthy controls or H. pylori eradicated ulcer patients significantly enhanced postprandial EGG amplitude almost to the level observed in the infected duodenal ulcer patients, but failed to affect this amplitude in ulcer patients. Exogenous caerulein, an analog of CCK, failed to affect EGG amplitude in duodenal ulcer patients with H. pylori infection, but it reduced significantly EGG amplitude in these patients after H. pylori eradication and in control subjects. This inhibitory effect of caerulein in H. pylori negative ulcer patients and healthy controls was abolished by the addition of loxiglumide. Ulcer patients showed significant dysrhythmia with tachygastria up to 20% of the recording time both under basal conditions and postprandially and H. pylori eradication was followed by a significant decrease in tachygastria to about 5%, the value being similar to that in healthy controls. We conclude that the amplitude and frequency of gastric myoelectrical activity are enhanced in duodenal ulcer patients and impaired in response to CCK but these changes can be normalized by successful H. pylori eradication.

7

The effect of concomitant stimulation with cholecystokinin and epidermal growth factor on extracellular signal-regulated kinase (ERK) activity in pancreatic acinar cells

100%

Daniluk J. , Dabrowski A.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 3

EN

The transmission of extracellular proliferation and differentiation signals into their intracellular targets is mediated by a signaling cascade culminating in mitogen-activated protein kinase (MAPK) also known as ERK. In pancreatic acinar cells both cholecystokinin (CCK) and epidermal growth factor (EGF) are known to stimulate ERK. Regulatory interactions among individual receptor-coupled signaling cascades are critically important for establishing cellular responses in the face of multiple stimuli. The aim of our study was to evaluate the effect of concomitant stimulation of G protein-coupled receptors (GPCR) and EGF receptors on ERK activity in isolated pancreatic acinar cells. ERK activity was determined by means of Western-blotting, with the use of the antibody which recognizes active, tyrosine-phosphorylated kinase (pY-ERK). pY-ERK level was strongly elevated by 10 nM CCK-8, 100 µM carbachol (CAR), or 100 nM EGF. The addition of EGF to 60 min-lasting incubations of acini with CCK-8 or CAR caused abrupt decrease of pY-ERK level to 56 and 59% of control, respectively. Similar phenomenon was observed when short stimulation with CCK-8 or CAR was superimposed on the effect of EGF. After the addition of EGF to acini incubated previously with phorbol ester TPA, strong decrease in pY-ERK level was also observed. In conclusion, in pancreatic acinar cells, concomitant stimulation with CCK or CAR and EGF has strong inhibitory effect on ERK cascade. This inhibitory cross-talk may be mediated, at least partially, by protein kinase C (PKC). These mutual inhibitory interactions demonstrate novel mechanism for integration of multiple signals generated by activation of G-protein-coupled and growth factor receptors in pancreatic acinar cells.

8

The effects of cowpea [Vigna unguiculata] feeding on basel, exogenous cholecystokinin [CCK33] and secretin stimulated pancreatic secretions of the anaesthetized rat

100%

Erlwanger K. H. , Umapathy E. , Musara C. , Kandiwa E. , Kruszewska D. , Mattsson I. , Pierzynowski S. G.

Journal of Animal and Feed Sciences

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2001

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tom 10

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nr 3

9

On the tissue-specific processing of procholecystokinin in the brain and gut - a short review

84%

Rehfeld J. F. , Bundgaard J. R. , Friis-Hansen L. , Goetze J. P.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

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nr 4

73-79

EN

Cholecystokinin (CCK) is a major peptide hormone in the gut and a major peptide transmitter in the brain. Its synthesis requires endoproteolytic cleavage of proCCK at several mono- and dibasic sites by prohormone convertases (PCs). Of these, PC1 and PC2 are expressed in cerebral neurons and intestinal endocrine cells. Characteristically, however, the processing of proCCK varies markedly between the brain and the gut. In neurons, CCK-8 is always the predominating form, whereas the endocrine gut cells (I-cells) contain a mixture of small and larger CCK-peptides of which CCK-33 or CCK-22 often predominate. The role of PC1 and PC2 in the processing of proCCK have now been examined by measuring the concentrations of prohormone, processing intermediates and amidated end-products in jejunal and cerebral extracts of PC1 and PC2 deficient mice and corresponding wild type controls. The PC1 null mice revealed a pattern opposite to that of the PC2 null mice, in whom only the cerebral processing of proCCK was affected. Thus PC1 knockouts reveal a severe block in the processing of intestinal proCCK. Accordingly, the intestinal concentration of proCCK was many fold increased, and also the concentrations of different processing intermediates were raised; but the concentration of bioactive, a-amidated and O-sulfated CCK was reduced to a few percent of normal. The only bioactive CCK peptide in the gut of PC1 deficient mice was CCK-22, and it was present only in trace amounts. The cerebral processing of proCCK was, however, not at all affected by the lack of PC1 - in sharp contrast to the effect of PC2. The results show that the tissue-specific processing of proCCK to a large extent can be explained by prohormone convertases, as PC1 plays a decisive role in the maturation of hormonal CCK in the gut, whereas PC2 governs the processing of brain proCCK.

10

Role of cholecystokinin in postprandial and vagally stimulated duodenal and gallbladder motility in dogs

84%

Thor P. , Laskiewicz J. , Maczka M. , Konturek S. J.

Journal of Physiology and Pharmacology

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1991

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tom 42

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nr 4

EN

This study was designed to determine the role of cholecystokinin (CCK) in postprandial motility pattern of the duodenum and gallbladder (GB) in conscious dogs provided with chronic duodenal electrodes for recording of myoelectric activity and GB fistulas for measurement of intraluminal pressure and volume of GB and to calculate the GB motility index (MI) and GB emptying rate. During naturally occuring activity front (phase III MMC) in the duodenum there was significant increase in the MI of GB accompanied by about 20-30% reduction in the GB volume. These changes in duodenal and GB motility pattern could be duplicated by i. v. motilin. Feeding abolished the appearence of spontaneous activity front in the duodenum and greatly increased motility of GB while reducing its volume. Administration of CCK receptor antagonists in fed dogs failed to affect the motility changes induced by meal in the duodenum but abolished these of the GB. Vagal cholinergic stimulation with insulin, 2DG or urecholine caused similar effects to that induced by food i. e. increased duodenal spike activity, abolished phase III of the MMC, decreased GB volume and increased GB motility. Pretreatment with CCK antagonists did not affect significantly duodenal spike activity or GB motility but significantly increased the GB volume. Atropine 125 µg/kg) blocked almost completely spontaneous activity front in the duodenum and accompanying alterations in the motiliti and volume of GB. We conclude that CCK contributes to the MMC related alterations in the GB motor activity and is essential in cholinergic stimulation induced of the GB emtying but not in vagally induced duodenal and GB motility.

11

Luminal sensing in the gut: an overview

84%

Dockray G. J.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

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nr 4

9-17

EN

The wall of the gut responds to an impressive array of signals originating in the lumen, including nutrient and non-nutrient chemicals, mechanical factors, and micro-organisms. The idea that the gut wall exhibits luminal chemo-sensitivity is implied in the original discovery of secretin by Bayliss and Starling, and has become an integral part of models of neurohumoral control of gastrointestinal function. Entero-endocrine cells are specialised for luminal nutrient sensing but sub-epithelial nerve fibres may also respond to luminal chemicals that freely diffuse across the epithelium eg short chain fatty acids. The molecular recognition mechanisms include G-protein coupled receptors (GPCRs) eg the extracellular Ca2+ sensing receptor which also responds to aromatic amino acids. There are also GPCRs sensing fatty acids, as well as bitter or noxious compounds. In addition, though, gating of ion channels including events secondary to energy availability eg ATP, may be involved in sensing some luminal chemicals. There is likely to be integration of luminal signals at several levels including at the level of entero-endocrine cells and at sub-epithelial nerve fibers. For example, the intestinal hormone CCK acts on primary afferent nerve fibers of the vagal trunk. The same fibers also express leptin receptors that are thought to respond to leptin released from gastric chief cells, orexin receptors (activation of which inhibits CCK) and possibly ghrelin receptors. Multiple signalling mechanisms allow specific responses to be matched to meals of differing content.

12

Intervention of GI neuropeptides in pancreatic growth and regeneration: comparison with cholecystokinin

84%

Morisset J.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

|

nr 4

127-141

EN

The pancreatic gland has an enormous potential for growth and regeneration, mainly in rodents. These processes remain mostly under the control of the GI hormone cholecystokinin (CCK). The human pancreas however does not show proliferative properties after partial pancreatectomy, but research in this field has been scarce. Recent studies indicate that CCK might not be the expected trophic agent since its two receptors CCKA and CCKB were not found on human exocrine pancreas. Therefore, if human pancreas grows and regenerates, it has to be under the influence of some unknown trophic factors. Neuropeptides receiving much attention lately as regulators of pancreatic functions could be among the searched trophic agents. This presentation focusses on neuropeptides growth potential: GRP-Bombesin, GABA, PP, PYY, Neurotensin, SP, VIP, PACAP, CGRP and galanin. Some neuropeptides have moderate effects on pancreatic enzymes and electrolytes secretion: SP, VIP, PACAP. However, their trophic effects remain unexplored except for GRP-bombesin and PACAP. PACAP preferentially exhibits its mitogenic and proliferative effects on the pancreatic acinar cells AR4-2J via tyrosine kinase, phospholipase D and ornithine decarboxylase activation but not through adenylate cyclase. The growth promoting action of GRP-bombesin is well documented on rodent's pancreas. However, recent studies indicate that this neuropeptide is potentially trophic for larger mammals' pancreas. Indeed, investigators recently documented that bombesin induced pancreatic regeneration in the pig after partial pancreatectomy through mitogen-activated protein kinases activation as do CCK-8 and caerulein on rat pancreas. Have we found the magic pancreatic trophic factor in large mammals? Further investigations will tell.

13

Leptin is able to stimulate pancreatic enzyme secretion via activation of duodeno-pancreatic reflex and CCK release

84%

Nawrot-Porabka K. , Jaworek J. , Leja-Szpak A. , Palonek M. , Szklarczyk J. , Konturek S. J. , Pawlik W. W.

Journal of Physiology and Pharmacology. Supplement

|

2004

|

tom 55

|

nr 2

47-57

EN

Leptin, 16- kDa protein produced and secreted from white adipocytes is known to regulate food intake and energy expenditure. Leptin receptors have been detected in the pancreas and it has been shown that systemic application of this protein diminished postprandial pancreatic secretion. Leptin is also produced in the stomach and released into the gastrointestinal lumen but the implication of luminal leptin in the regulation of pancreatic enzyme secretion has not been elucidated. The aim of our study was to evaluate the effects of intraduodenal (i.d.) leptin administration on pancreatic enzyme secretion and to assess the involvent of afferent nerves and CCK in above effects. The secretory studies were carried out on anaesthetized Wistar rats with acute pancreatic fistulae. Leptin was administered to the animals at doses of 0.1 1.0 or 10.0 µg/kg i.d. Tarazepide (2.5 mg/kg i.d.), a CCK1 receptor antagonist, was given to the rats prior to the application of leptin. Rats with capsaicin deactivated sensory nerves were used in part of the study. Samples of pancreatic juice were taken at 15 min intervals to measure the volume flow and protein and amylase concentrations. CCK plasma level was measured by radioimmunoassay (RIA) following administration of leptin to the rats. Intraduodenal administration of leptin (1.0 or 10.0 µg/kg) to the fasted rats significantly and dose-dependently increased pancreatic protein and amylase outputs. Pancreatic secretory responses to leptin were totally abolished by prior capsaicin deactivation of sensory nerves or by pretreatment of the rats with tarazepide. Under basal conditions plasma CCK level averaged about 15.46 ± 1,4 pg/ml. Exogenous leptin, given i.d. at doses of 0.1 1.0 or 10.0 µg/kg i.d. to the rats with intact or capsaicin-deactivated sensory nerves resulted in dose-dependent rise of plasma CCK level, reaching the highest value at the dose of 10.0 µg/kg i.d. We conclude that leptin given i.d. stimulates pancreatic enzyme secretion and this effect could be related to the stimulation of CCK release and activation of duodeno-pancreatic reflexes.

14

Alteration of peptidergic gut-brain signaling under conditions of obesity

84%

Kuhne S. G. , Stengel A.

Journal of Physiology and Pharmacology

|

2019

|

tom 70

|

nr 5

15

Luminal CCK and its neuronal action on exocrine pancreatic secretion

84%

Zabielski R.

Journal of Physiology and Pharmacology. Supplement

|

2003

|

tom 54

|

nr 4

81-94

EN

Gut regulatory peptides are produced by mucosal endocrine cells and released both into the circulation as well as into the gut lumen. Following stimulation the distribution between the circulation and gut lumen changes in favor of the gut lumen. In the blood plasma, the biological half-life of gut regulatory peptides is counted in single minutes due to high aminopeptidase activity and liver extraction. In the gut lumen, however, regulatory peptides retain their biological activity much longer, especially in newborn and young animals. A series of studies was performed in neonatal calves and pigs to explore the role of luminal cholecystokinin (CCK) on the regulation of exocrine pancreatic secretion. In anaesthetized neonatal calves, CCK was secreted into the duodenal lumen, and electrical vagal stimulation increased CCK release into the duodenal lumen but not into the circulating blood. In conscious calves, luminal CCK-8 stimulated pancreatic protein secretion by a neurohormonal mechanism dependent on a duodenal mucosal CCK1 receptor and vagal nerve activity. Immunocytochemistry pointed to an association of mucosal CCK1 and CCK2 receptors with neuronal components in the small intestine of neonatal calves. Experiments in calves and pigs with CCK-8 infusions into the duodenal branches of the right gastroepiploic artery confirmed the results of luminal CCK-8 and questioned the physiological relevance of a direct mechanism of CCK on the pancreatic acini.

16

Exocrine pancreas; molecular basis for intracellular signaling, damage and protection - Polish experience

84%

Dabrowski A.

Journal of Physiology and Pharmacology. Supplement

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2003

|

tom 54

|

nr 3

167-181

EN

Polish experience in molecular pancreatology mostly involves experimental work on intracellular signal transduction mechanisms in pancreatic acinar cells. It was found that stimulation with cholecystokinin (CCK) or exposure of pancreatic acini to reactive oxygen species induces three separate signaling cascades leading to activation of ERKs, JNK/SAPKs and p38 MAPK. In pancreatic acini, ERK cascade is also activated by epidermal growth factor (EGF). However, CCK and EGF activate this cascade by different mechanisms. EGF activates the cascade in a classical Ras-dependent manner, while CCK-induced activation of the ERK cascade is Ras-independent. Furthermore, stimulation with CCK leads to a rapid activation of PKC, which in turn may directly activate Raf family of kinases. Freshly isolated pancreatic acini contain pancreatic stellate cells which respond to EGF by activation of ERK cascade. It is possible that stimulation with CCK and EGF induces a cross-talk between acinar and stellate cells. Isolated pancreatic acinar cells irradiated with UV-B die predominantly by apoptosis while necrosis predominates among the cells subjected to supraphysiological concentrations of CCK. In pancreatic acini subjected to stressful stimuli the regulation of apoptosis may involve interaction between ERK and p38 MAPK signaling pathways. Acute pancreatitis in rats and in humans is associated with a marked increase in the plasma level of leptin which is caused by increased production of this peptide in the inflamed pancreas. It is possible that exogenous leptin protects the pancreas against development of acute pancreatitis by the activation of nitric oxide pathway.

17

Spinal transient receptor potential ankyrin 1 channel induces mechanical hypersensitivity, increases cutaneous blood flow, and mediates the pronociceptive action of dynorphin A

84%

Wei H. , Saarnilehto M. , Falck L. , Viisanen H. , Lasierra M. , Koivisto A. , Pertovaara A.

Journal of Physiology and Pharmacology

|

2013

|

tom 64

|

nr 3

18

The effects of antagonists of receptors for gastrin, cholecystokinin and bombesin on growth of gastroduodenal mucosa and pancreas

84%

Dembinski A. , Warzecha Z. , Konturek S. J. , Zhi Cai R. , Schally A. V.

Journal of Physiology and Pharmacology

|

1991

|

tom 42

|

nr 2

EN

The effects of gastrin, cholecystojdnin (CCK) and bombesin on the DNA synthesis, as a biochemical indicator of trophic action in the gastroduodenal mucosa and the pancreas have been examined in rats fasted for 48 h and in rats refed for 16 h with or without administration of specific receptor antagonists for bombesin, gastrin and CCK. Bombesin and gastrin administered three times daily for 48 h in fasted rats significantly increased the rate of DNA synthesis as measured by the incorporation of [³H] thymidine into DNA in each tissue tested. CCK significantly increased DNA synthesis in the duodenal mucosa and pancreatic tissue, but not in the gastric mucosa. The stimulation of DNA synthesis induced by bombesin in the gastroduodenal mucosa and pancreas was abolished by bombesin/GRP receptor antagonist, RC-3095. RC-3095 did not affect DNA synthesis stimulated by gastrin and CCK in these tissues. L-365,260, a receptor antagonist for gastrin suppressed the DNA synthesis induced by gastrin but not by CCK or bombesin in the gastrointestinal mucosa and pancreas. L-364, 718 a specific antagonist for CCK receptors was effective only against CCK stimulated duodenal mucosa and pancreatic growth. Refeeding of 48 h fasting rats strongly enhanced the DNA synthesis in all tissues tested, and this effect was significantly reduced in the gastroduodenal mucosa by blocking only gastrin receptors (with L-365, 260) and that in the duodenal mucosa and the pancreas by antagonizing of CCK receptors (with L-364, 718). Antagonism of bombesin receptors (with RC-3095) did not significantly affect the stimulation of DNA synthesis induced by refeeding in all tissues tested. This study indicates that the stimulation of DNA synthesis can be achieved by exogenous gastrin, CCK and bombesin acting through separate receptor but that only gastrin and CCK play the major role in the postprandial stimulation of the growth of gastroduodenal mucosa and pancreatic tissue.

19

Influence of vagal nerve stimulation on food intake and body weight - results of experimental studies

84%

Sobocki J. , Krolczyk G. , Herman R. M. , Matyja A. , Thor P. J.

Journal of Physiology and Pharmacology. Supplement

|

2005

|

tom 56

|

nr 6

27-33

EN

The paper reviews recent advances in vagal nerve stimulation for the control of food intake and body weight. The vagal nerves are the predominant pathway in the "brain-gut axis" responsible for short term regulation of food intake. Stimulation of afferent vagal traffic attenuates food intake by vagal projections to nucleus tractus solitarius, arcuate nucleus and its convergence’s to thalamic center of satiety. A few studies have been published in this field so far. All of them are consistent and show significant decrease in body mass during vagal stimulation. Due to promising results of experimental studies, clinical trials are expected in the near future.

20

Central action of cholecystokinine antagonists in the intestinal stress induced by duodenal distension in sheep

84%

Kania B. F. , Matczuk J. , Majcher A. , Cieciera M. , Wronska-Fortuna D.

Journal of Physiology and Pharmacology. Supplement

|

2001

|

tom 52

|

nr 2