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1

Regulation of gastrointestinal mucosal growth during aging

100%

Majumdar A. P. N.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

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nr 4

143-154

The increase in the aging population has led to a growing interest in achieving a better understanding of the aging process and of diseases that are predominantly expressed during advancing age. Since the structural and, in turn, the functional integrity of the mucosa of the gastrointestinal tract (GI) are maintained by constant renewal of cells, a detailed knowledge of the events that initiate and regulate mucosal proliferative processes is essential for a better understanding of the normal aging process as well as age-associated dysfunctions, including malignancy that represent disorders of tissue growth. In Fischer-344 rats, aging is associated with increased mucosal proliferative activity in much of the GI tract. On the other hand, the functional properties are either decreased or remain unchanged during advancing age. Basal gastric acid and pepsin output decline during aging, as is gastrin secretion. In contrast, antral gastrin levels increase during this period, as is mucosal histidine decarboxylase activity. The age-related decline in gastrin secretion could partly be attributed to a higher ratio of somatostatin (D) to gastrin (G) cells in the antral mucosa. The age-related rise in GI mucosal proliferative activity could not be attributed to the trophic action of either gastrin or bombesin, since they caused no significant change in mucosal proliferation in aged rats. On the other hand, EGF and TGF-alphalpha appear to be involved in regulating mucosal proliferation during aging. Aging is associated with increased activation of EGF-receptor (EGFR), the common receptor for EGF and TGF-alpha. This could be due to (a) increased levels of membrane-bound precursor form(s) of TGF-alpha resulting in increased activation EGFR signaling processes through an autocrine/paracrine mechanism, (b) heightened sensitivity of mucosal EGFR to EGF and TGF-alpha such that comparatively lower levels of these peptides are required to activate EGFR in aged than in young animals and/or (c) loss of EGFR regulatory factor(s) such as ERRP (EGFR Related Protein), a "negative regulator" of EGFR.

2

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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

|

nr 3

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.

3

Experimental studies as an inspiration for clinical investigation

100%

Malecka-Panas E., Talar-Wojnarowska R., Kotynia J., Majumdar A. P. N.

Journal of Physiology and Pharmacology. Supplement

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2004

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tom 55

|

nr 2

139-150

This study represents an attempt of showing own author's example of using basic research data as an inspiration for the clinical studies. The project evaluates the role of gastrin in colorectal carcinogenesis as well as the differences of its action in proximal and distal colon. Colonocytes were isolated from Fischer-344 rats and incubated for 2 minutes with gastrin (10-8M). This treatment resulted with 60-70% rise in tyrosine kinase (Tyr-k) and 150-200% - in phospholipase C activity as regards to basal levels. In vivo infusion of gastrin for 5 days to Fischer-344 rats resulted with 90-150% increase in distal but not proximal colonic mucosal proliferative activity as well as tyrosine phosphorylation of several colonic mucosal proteins. In clinical study, the mean fasting gastrin level in the control group was significantly lower (p<0.01) than in patients with colorectal cancer before surgery. Mean plasma gastrin level in patients with distal tumor yielded 105,31 ± 12,5 µ U/l and was significantly higher than in patients with the proximal tumor site (42, 2 ± 3,1 µU/l) (p<0,001). We conclude, that Tyr-k is involved in the mechanism of the trophic action of gastrin, particularly in distal colon. The differences in gastrin concentration in patients with distal and proximal tumors may probably contribute to the distinct pathogenesis and biological properties of those cancers.

4

Gastric acid inhibitory profile of ebrotidine, a novel H2-receptor antagonist in humans

100%

Maczka M., Kwiecien N., Obtulowicz W., Konturek S. J., Kaminski K., Oleksy J., Gabryelewicz A., Torres J.

Journal of Physiology and Pharmacology

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1992

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tom 43

|

nr 2

This study was designed to assess the gastric secretory effects of ebrotidine, a novel H₂ receptor antagonist, in humans. Three groups (A, В and C) of male subjects with normal gastric mucosa were used. Group A (6 subjects) was used to determine the dose-dependency of gastric inhibitory effect of ebrotidine on basal and pentagastrin- induced maximal acid output. Group В (8 subjects) was employed to examine the duration of the inhibitory effect of ebrotidine on basal and pentagastrin-induced acid secretion. In group C (6 subjects), the 24 h pH-metry was assessed using intraluminal pH-electrode placed in the gastric corpus and connected to a portable recording unit. Single oral dose of ebrotidine (200, 400 or 800 mg) caused a dose- dependent reduction in basal and pentagastrin-induced acid secretion that at a dose of 800 mg amounted to about 89% and 93%, respectively. This inhibition was still observed after 6h and averaged 72% and 50%, respectively. After 12 and 24 h upon the drug intake, both basal and pentagastrin-induced acid secretion returned to the control values. Single oral dose of ebrotidine (800 mg) caused a significant reduction in circadian acidity and resulted in a marked and significant reduction of intragastric acidity for about 6 h upon the administration. This inhibition was accompanied by a transient increase in basal and postprandial gastrin levels. We conclude that ebrotidine is highly effective inhibitor of basal, pentagastrin-induced and circadian gastric acid secretion in humans.

5

Transcriptional upregulation of gastrin in response to peroxisome proliferator-activated receptor gamma agonist triggers cell survival pathways

100%

Ptak-Belowska A., Pawlik M. W., Krzysiek-Maczka G., Brzozowski T., Pawlik W. W.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 4

Peroxisome proliferator-activated receptor (PPAR ) are members of the largest nuclear hormone receptor family of transcription factors (1). PPAR gamma (PPAR) plays an important role in adipogenesis, control of sensitivity to insulin, inflammation and atherosclerosis but recent studies also suggest that PPAR is involved in cell cycle withdrawal. PPAR can promote cell differentiation, exert an antiproliferative action and inhibit angiogenesis (2, 3). However, there are studies showing that activation of PPAR promotes the development of colon cancer (4). These data are in sharp contrast with studies that attribute anticancer effects to PPAR in gastrointestinal malignancies. Probably, the action of PPAR on cell cycle and proliferation depends on the cell type and presence of other stimuli that predispose cells to cancer development. Amidated and non-amidated gastrins may play an important role in the proliferation and carcinogenesis of GI cancers. It is known that gastrin peptides activate phosphorylation of Protein Kinase B (PKB/Akt) and anti-apoptotic signalling but there is little known about the link between gastrins and PPAR receptors in relation to apoptosis.

6

Sensory nerves and calcitonin gene related peptide in the effect of ischemic preconditioning on acute and chronic gastric lesions induced by ischemia-reperfusion

100%

Pawlik M., Ptak A., Pajdo R., Konturek P. C., Brzozowski T., Konturek S. J.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 4,1

Ischemic preconditioning is considered as the most powerful gastroprotective intervention against mucosal lesions and ulcerations but the mechanism of this phenomenon has been little examined. In this study we tested the effects of inactivation of sensory nerves in new rat model combining acute gastric erosions with subsequent ulcers induced by ischemia-reperfusion (I/R). I/R lesions were produced in rats by clamping the celiac artery for 0.5 h followed by 3 h ofreperfusion in rats with intact or inactivated sensory nerves by pretreatment with capsaicin for two weeks before the I/R. The animals were killed at 0 and 3 h and 3 days after I/R and the area of gastric lesions was determined planimetrically, the gastric blood flow (GBF) by H2-gas clearance technique and the plasma levels of gastrin by RIA. Gastric mucosal content of calcitonin gene related peptide (CGRP) was assessed by RIA. Following I/R, gastric erosive lesions occurred after 3 h and these erosive lesions then progressed into gastric ulcers within 3 days in all rats. Sensory-inactivation with capsaicin caused several fold increase in the area of early (at 3 h) acute lesions and later (at 3 d) gastric ulcers induced by I/R. This enhancement of acute and then chronic gastric lesions was accompanied by a significant fall in GBF, an elevation of plasma gastrin and a decrease in mucosal expression of CGRP. Ischemic preconditioning markedly reduced acute lesions and chronic ulcerations induced by I/R and attenuated the changes in plasma gastrin and mucosal CGRP contents but these effects were significantly more pronounced in rats with intact sensory nerves but less in capsaicin-inactivated animals. We conclude that: 1) The I/R resulted in the formation of early acute gastric lesions followed 3 days later by chronic gastric ulcers and this gastric injury was accompanied by an impairment of gastric microcirculation, hypergastrinemia and suppression the gastric mucosal CGRP; 2) Gastric ischemic-preconditioning significantly attenuated both acute mucosal damage and chronic ulcers induced by I/R and this was accompanied by a rise in gastric blood flow; 3) The inactivation of sensory nerves with capsaicin enhanced the formation of I/R-induced acute and chronic gastric lesions and strongly attenuated the gastroprotection afforded by I/R possibly due to the decline in mucosal blood flow and the fall in expression of integrity peptides such as CGRP and 4) The excessive release of gastrin may limit the extent of mucosal lesions observed during progression of gastric erosions into ulcers induced by I/R.

7

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

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1991

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tom 42

|

nr 2

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.

8

Role of proton pump inhibitors in preventing hypergastrinemia-associated carcinogenesis and in antagonizing the trophic effect of gastrin

84%

Man Y.-M., Park J.-M., Kangwan N., Jeong M., Lee S., Cho J. Y., Ko W. J., Hahm K. B.

Journal of Physiology and Pharmacology

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2015

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tom 66

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nr 2

9

Involvement of Helicobacter pylori infection in neuro-hormonal control of food intake

84%

Konturek P. C., Czesnikiewicz-Guzik M., Bielanski W., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

|

nr 5

67-81

Ghrelin and leptin are endogenous peptides that have been implicated in the control of food intake, energy homeostasis and body weight gain. Although the stomach is the major source of circulating ghrelin and partly contributes also to plasma leptin, controversy exists over the influence of gastric Helicobacter pylori (Hp) infection on the ghrelin and leptin release. To resolve this controversy, plasma immunoreactive ghrelin and leptin levels were determined in Hp-positive and Hp negative children (N=60) and in adults (N=120) and daily concentrations of these hormones were measured at 2 h intervals before and after meals. Serum levels of ghrelin and leptin as well as gastrin were measured by RIA. Hp status was assessed using 13C-urea breath test (UBT) and serology. Children with negative UBT showed significantly higher basal serum levels of ghrelin and lower concentrations of leptin than those with positive UBT. Adults without Hp infection also showed significantly higher fasting serum levels of ghrelin and lower levels of leptin than those in Hp infected subjects. In adults, especially without Hp infection, plasma levels of ghrelin showed a marked rise before the meal and sudden decrease following the food intake, while plasma leptin did not showed significant meal-related alterations, but in general its level was significantly higher in Hp positive than Hp negative subjects. Serum gastrin concentrations were significantly elevated in both Hp positive children and adults and these levels were significantly lower in Hp negative subjects. We conclude that Hp infection in children and adults causes a marked reduction in plasma levels of ghrelin, while increasing plasma levels of leptin and gastrin. These alterations in plasma levels of gastric originated appetite-controlling hormones in Hp infected children and adults may contribute to the alterations of the appetite and dyspeptic symptoms observed in these subjects.

10

Gastric secretion - from Pavlov's NERVISM to Popielski's histamine as direct secretagogue of oxyntic glands

84%

Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

|

nr 3

43-68

Gastric acid and pepsin secretions result from the interplay of neurohormonal factors with stimulatory and inhibitory actions on oxyntic glands. At the turn of XIX century, the notion of nervism or entire neural control of digestive functions, developed by Pavlov prevailed. However, in the second part of XX century, hormonal control has been thought to play a major role in the mechanism of gastric secretion, especially gastrin, which was isolated and synthesized in 1964 by Gregory. Polish traces in gastroenterological history started with the discovery of histamine, a non-nervous and non-gastrin compound in oxyntic mucosa by L. Popielski in 1916, who found that this amine is the most potent and direct stimulant of gastric acid secretion. This histamine concept was supported by leading American gastroenterologists such as A.C. Ivy, championed later by C.F. Code, and clinically applied for testing gastric secretion by K. Kowalewski. Recently, it received a strong support from pharmacological research when J. Black designed H2-receptors antagonists, which were first discovered by M.I. Grossman and S.J. Konturek to inhibit not only histamine-, but also meal- and vagally-induced gastric acid secretion, thus reinforcing the notion of the crucial significance of histamine in the control of gastric secretion as the final common chemostimulator. In conclusion, Polish traces appear to be substantial in gastric history due: 1) to discovery by Popielski that histamine is a major, direct stimulus of gastric secretion; 2) to clinical application of this agent by Kowalewski in testing maximal gastric secretory activity; and 3) to clinical use of histamine H2-antagonists in control of gastric acid secretion and treatment of peptic ulcers.

11

Gastrin mediated down regulation of ghrelin and its pathophysiological role in atrophic gastritis

84%

Rau T. T., Sonst A., Rogler A., Burnat G., Neumann H., Oeckl K., Neuhuber W., Dimmler A., Faller G., Brzozowski T., Hartmann A., Konturek P. C.

Journal of Physiology and Pharmacology

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2013

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tom 64

|

nr 6

12

Gastrin activates tyrosine kinase and phospholipase C in isolated rat colonocytes

84%

Malecka-Panas E., Tureaud J., Majumdar A. P. N.

Acta Biochimica Polonica

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1996

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tom 43

|

nr 3

Postreceptor regulation of the trophic action of gastrin is not fully elucidated. Tyrosine kinase (Tyr-kinase) has been associated with receptors of a number of growth factors and plays an important role in regulation of cellular growth within the gastrointestinal tract. The aim of this study was to determine, whether Tyr-kinase plays a role in mediating the growth promoting action of gastrin and whether phospholipase C (PLC) is involved in the signal transduction pathway. Colonocytes isolated from Fischer 344 rats were incubated for 2 min with gastrin (10-8 M) and assayed for Tyr-kinase and PLC activities. Incubations with gastrin resulted in 60%-70% rise in Tyr-kinase and 150%-200% rise in PLC activities over the corresponding basal levels. When processed separately, in proximal colon Tyr-kinase activation by gastrin was 15%-20%, while in distal colon 70%-80% as compared to the buffer control. Gastrin activation of both Tyr-kinase and PLC was abolished by Tyr-kinase inhibitor, tyrphostin-25 (3.2 nM) and was not affected by staurosporine (20 ng/ml). We conclude that Tyr-kinase is involved in the mechanism of trophic action of gastrin, and PLC activation appears to be the next step in the signal transduction pathway.

13

Locomotor activity and behavior of mutant mice deleted for gastrin gene expression

84%

Singh P., Cobb S., Rengifo-Cam W., Deng X., Willis W., Li Q.

Journal of Physiology and Pharmacology

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2004

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tom 55

|

nr 1,2

The current studies were initiated to investigate the role of brain-gut peptide, gastrin, on locomotor activity and anxiety-like behavior. Young, male mutant mice, lacking gastrin gene expression (GAS-KO mice), were used in the experiments. The locomotor activity of GAS-KO vs wild type (WT) mice was compared by open field test. The anxiety-like behavior was examined using elevated plus maze. The time and entries to the open arms of the elevated plus maze were used as an indicator for the anxiety-like behavior and the data were analyzed using Hindsight program. On the open field test, locomotor activity of GAS-KO mice was similar to that of the WT mice for the first 10 min of the test, but decreased significantly after that. Anxiety-like behavior was more evident in the GAS-KO vs WT mice in the elevated plus maze experiments. The number of entries to and time spent on the open arms of plus-maze were significantly reduced for the GAS-KO vs WT mice suggesting an increased anxiety-like behavior of GAS-KO mice. Our studies suggest that normal circulating levels of gastrins may play a direct or indirect role in the regulation of locomotor activity and anxiety-like behavior.

14

Involvement of cyclooxygenase (COX)-2 products in acceleration of ulcer healing by gastrin and hepatocyte growth factor

84%

Brzozowski T., Konturek P. C., Konturek S. J., Pajdo R., Schuppan D., Drozdowicz D., Ptak A., Pawlik M., Nakamura T., Hahn E. G.

Journal of Physiology and Pharmacology

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2000

|

tom 51

|

nr 4,1

15

Fundectomy evokes elevated gastrin and lowered ghrelin serum levels accompanied by decrease in geometrical and mechanical properties of femora in rats

84%

Puzio I., Kapica M., Filip R., Bienko M., Radzki R. P.

Bulletin of the Veterinary Institute in Puławy

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2005

|

tom 49

|

nr 1

16

An immunohistochemical study of endocrine cells in the stomach of hypertensive rats

84%

Kasacka I., Majewski M.

Journal of Physiology and Pharmacology

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2007

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tom 58

|

nr 3

Essential hypertension is a complex disease with both genetic and environmental determinants. The effect of spontaneous hypertension on the distribution and occurrence of somatostatin-, gastrin- and serotonin-immunoreactive cells in the fundus and pylorus of the rat stomach was examined by immunohistochemistry. The animals were killed by decapitation at 4 and 16 weeks of age (5 control rats and 5 hypertensive rats). Endocrine cells generally increase in number in hypertensive rats as compared to control rats. However, the detailed responses of endocrine cells to hypertension depend on the cell type, region of gastric mucosa and age of animals. The present results suggest that hypertension has an influence on the intrinsic regulatory system by endocrine cells control in the rat stomach.

17

Helicobacter pylori, gastrin and cyclooxygenases in gastric cancer

84%

Konturek P. C., Hartwich A., Zuchowicz M., Labza H., Pierzchalski P., Karczewska E., Bielanski W., Hahn E. G., Konturek S. J.

Journal of Physiology and Pharmacology

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2000

|

tom 51

|

nr 4,1

18

Ornithine decarboxylase in large bowel mucosa: regulation by gastrin, secretin and EGF

84%

Johnson L. R., Wang P., Haddox K.

Journal of Physiology and Pharmacology

|

1992

|

tom 43

|

nr 1

Rats were fasted 48 h and then injected once with either saline, pentagastrin, EGF, secretin or combinations of secretin and pentagastrin or EGF. Another group of rats was fasted and refed. Animals were killed 4 h later and ODC assayed in mucosa of the cecum, proximal colon, and distal colon. EGF significantly increased ODC activity in all 3 tissues. Secretin had no effect by itself on ODC or ODC stimulated by EGF. Pentagastrin significantly increased ODC of the cecum, and secretin completely inhibited the effect of pentagastrin. Refeeding fasted rats significantly induced activity in all three tissues. Immunocytochemistry using a highly specific polyclonal ODC antibody showed that ODC was confined to the crypt cells of the proximal colon. Antibody dilution techniques demonstrated that gastrin, EGF and refeeding increased the level of enzyme in these cells. Refeeding in addition caused the appearance of enzyme in surface epithelial cells. These results showed that colonic mucosal ODC is present in proliferative cells and is regulated by the same peptides known to regulate growth in this tissue. Colonic mucosal ODC also responds the same way as it does in the oxyntic gland and small bowel mucosa.

19

Effect of moderate incremental exercise, performed in fed and fasted state on cardio-respiratory variables and leptin and ghrelin concentrations in young healthy men

84%

Zoladz J. A., Konturek S. J., Duda K., Majerczak J., Sliwowski Z., Grandys M., Bielanski W.

Journal of Physiology and Pharmacology

|

2005

|

tom 56

|

nr 1

Background: Although hormonal responses to exercise performed in fed state are well documented, far less in known about the effect of a single exercise bout, performed after overnight fasting, on cardio-respiratory responses and hormones secretion. It has been reported that recently discovered hormones as leptin and ghrelin may affect cardiovascular responses at rest. However, their effect on the cardiovascular responses to exercise is unknown. Aims: This study was designed to determine the effect of overnight fasting on cardio- respiratory responses during moderate incremental exercise. We have hypothesised that fasting / exercise induced changes in plasma leptin / ghrelin concentrations may influence cardiovascular response. Material and Methods: Eight healthy non-smoking men (means ± SE.: age 23.0 ± 0.5 years; body mass 71.9 ± 1.5 kg; height 179.1 ± 0.8 cm; BMI 22.42 ± 0.49 kg . m-2 with VO2max of 3.71 ± 0.10 l . min-1) volunteered for this study. The subjects performed twice an incremental exercise test, with the increase of power output by 30 W every 3 minutes. Tests were performed in a random order: once in the feed state - cycling until exhaustion and second, about one week later, after overnight fasting - cycling until reaching 150 W. Results: In the present study we have compared the results obtained during incremental exercise performed only up to 150 W (59 ± 2 % of VO2max) both in fed and fasted state. Heart rate measured during exercise at each power output, performed in fasted state was by about 10 bt . min-1 (p = 0.02) lower then in fed subjects. Respiratory quotient and plasma lactate concentration in fasted state were also significantly (p<0.001) lower than in the fed state. Pre-exercise plasma leptin and ghrelin concentrations were not significantly different in fed and fasted state. Exercise induced increase in hGH was not accompanied by a significant changes in the studied gut hormones such as ghrelin, leptin, and insulin, except for plasma gastrin concentration, which was significantly (p = 0.008) lower in fasting subjects at the power output of 150 W. Plasma [IL-6] at rest before exercise performed in fasted state was significantly (p = 0.03) elevated in relation to the fed state. This was accompanied by significantly higher (p = 0.047) plasma noradrenaline concentration. Plasma IL-6 concentration at rest in fed subjects was negatively correlated with plasma ghrelin concentration (r = - 0.73, p < 0.05) and positively correlated with plasma insulin concentration (r = 0.78, p < 0.05). Significant negative correlation (r = - 0.90; p < 0.05) was found between plasma insulin and ghrelin concentration at rest in fed subjects. Conclusions: We have concluded that plasma leptin and ghrelin concentrations have no significant effect on the fasting-induced attenuation of heart rate during exercise. We have postulated that this effect is caused by increased plasma norepinephrine concentration, leading to the increase in systemic vascular resistance and baroreceptor mediated vagal stimulation. Moreover we believe, that the fasting-induced significant increase in plasma IL-6 concentration at rest, accompanied by higher plasma norepinephrine concentration and lower RQ, belongs to the physiological responses, maintaining energy homeostasis in the fasting state.

20

Role of Helicobacter pylori infection in gastro-duodenal secretion and in pathogenesis of peptic ulcer and gastritis

84%

Konturek P.Ch., Konturek S. J.

Journal of Physiology and Pharmacology

|

1994

|

tom 45

|

nr 3

Ograniczanie wyników

Regulation of gastrointestinal mucosal growth during aging

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

Experimental studies as an inspiration for clinical investigation

Gastric acid inhibitory profile of ebrotidine, a novel H2-receptor antagonist in humans

Transcriptional upregulation of gastrin in response to peroxisome proliferator-activated receptor gamma agonist triggers cell survival pathways

Sensory nerves and calcitonin gene related peptide in the effect of ischemic preconditioning on acute and chronic gastric lesions induced by ischemia-reperfusion

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

Role of proton pump inhibitors in preventing hypergastrinemia-associated carcinogenesis and in antagonizing the trophic effect of gastrin

Involvement of Helicobacter pylori infection in neuro-hormonal control of food intake

Gastric secretion - from Pavlov's NERVISM to Popielski's histamine as direct secretagogue of oxyntic glands

Gastrin mediated down regulation of ghrelin and its pathophysiological role in atrophic gastritis

Gastrin activates tyrosine kinase and phospholipase C in isolated rat colonocytes

Locomotor activity and behavior of mutant mice deleted for gastrin gene expression

Involvement of cyclooxygenase (COX)-2 products in acceleration of ulcer healing by gastrin and hepatocyte growth factor

Fundectomy evokes elevated gastrin and lowered ghrelin serum levels accompanied by decrease in geometrical and mechanical properties of femora in rats

An immunohistochemical study of endocrine cells in the stomach of hypertensive rats

Helicobacter pylori, gastrin and cyclooxygenases in gastric cancer

Ornithine decarboxylase in large bowel mucosa: regulation by gastrin, secretin and EGF

Effect of moderate incremental exercise, performed in fed and fasted state on cardio-respiratory variables and leptin and ghrelin concentrations in young healthy men

Role of Helicobacter pylori infection in gastro-duodenal secretion and in pathogenesis of peptic ulcer and gastritis