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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 51 (1995), S. 556-560 
    ISSN: 1420-9071
    Keywords: Camostate ; endocrine and exocrine pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract It is well known that oral administration of camostate induces hyperplasia and hypertrophy of the rat pancreas. It is not clear, however, whether pancreatic hormone and enzyme secretion are affected by camostate treatment. In rats, daily administration of 200 mg camostate/kg b. wt for 14 days significantly increased pancreatic weight and pancreatic content of DNA, protein, amylase, lipase, trypsin and chymotrypsin, as well as the amount of insulin, glucagon and somatostatin. In the intact animal, blood glucose levels and serum concentrations of insulin and glucagon in response to an oral glucose load were not impaired after camostate treatment. In the isolated perfused pancreas, however, insulin and glucagon secretions were reduced, whereas somatostatin release was not affected. The volume of pancreatic juice produced by the unstimulated isolated perfused organ, as well as protein and enzyme secretion, were increased after camostate treatment. Likewise, the isolated perfused pancreas from camostate-treated rats secreted a larger volume of pancreatic juice and more protein in response to cholecystokinin (CCK), while enzyme secretion was affected in a non-parallel manner: amylase release was markedly reduced, lipase release was unchanged, and release of trypsin and chymotrypsin was increased.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 64 (1986), S. 332-332 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 69 (1991), S. 150-150 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 64 (1986), S. 215-215 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 62 (1984), S. 854-854 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 63 (1985), S. 97-105 
    ISSN: 1432-1440
    Keywords: Bile acids and salts ; Colonic neoplasms ; Cocarcinogenesis ; Cell division ; Mutagenicity tests ; Cholecystectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Several lines of evidence suggest that bile acids may be implicated in the pathogenesis of colonic cancer. A high consumption of fat and animal protein and a low dietary intake of fiber have been shown to be related to the incidence of colonic cancer. From these epidemiologic observations the hypothesis was proposed that the correlation between diet and colon cancer might be explained by the involvement of bile acids. Populations at a high risk of developing cancer were shown to have an increased excretion both of total and bacterially modified bile acids in their feces. Animal studies demonstrated a cocarcinogenic effect of bile acids and experimental diets containing large amounts of fat did not only induce an increased bile acid excretion but also an enhanced tumor formation in the colon. Furthermore, microbial in vitro tests showed a comutagenic activity of secondary bile acids. However, case control studies comparing the fecal bile acid excretion pattern in colonic cancer patients and control subjects failed to show such a clear relationship, which might be explained by rather similar dietary habits within one population and individual differences in sensitivity to environmental factors contributing to the tumor development. Cholecystectomy, leading to an increased exposure of bile acids to the intestinal microflora, has been suggested as a predisposing factor for the development of colonic cancer, but the results of experimental and epidemiologic studies so far are rather inconsistent. More recent studies of epithelial cell kinetics showed that bile acids alter cell proliferative activity in the colonic mucosa by increasing the number of DNA synthesizing cells and expanding the proliferative compartment up to the middle third of the crypt. This enhanced cell proliferation seems to be related to the bile acid induced tumor formation due to an increased opportunity of malignant transformation. Bile acids may be implicated in the causation of human colonic cancer by stimulating the growth of a small-size benign adenoma to a large size with a correspondingly high risk of malignancy.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 61 (1983), S. 118-118 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 64 (1986), S. 134-134 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1433-8580
    Keywords: Methylxanthines ; Phosphodiesterase ; Cyclic AMP ; Intestinal hormones ; Endocrine pancreas ; Exocrine pancreatic function ; Adrenergic alpha-receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The intravenous administration of secretin or cholecystokinin-pancreozymin alone led to a short rapid rise in radio-immunologically measurable insulin, and to a stimulation of the hydrokinetic as well as the ecbolic, exocrine pancreatic function. During the administration of 1-(5-oxohexyl-)-3.7-dimethylxanthine (BL 191) no significant change in the endocrine and exocrine pancreatic secretion was registered, compared to the secretin injection alone, whereas BL 191 was able to inhibit the insulin and enzyme secretion after the administration of cholecystokinin-pancreozymin. The influence neither of secretin nor cholecystokinin-pancreozymin on the endocrine as well as the exocrine pancreas seems to be mediated directly by cyclic 3′-5′ adenosine monophosphate (cAMP), and the decrease of endocrine and exocrine pancreatic secretion, induced by cholecystokinin-pancreozymin during administration of BL 191, is probably due to an inhibition of the alpha-receptor system. Additional experiments are required for further elucidation of these conclusions.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Release of sulfidopeptide (SP)-leukotrienes (LT)in vitro from normal human colonic mucosa and from mucosal tissue obtained from patients with Crohn's disease (CD) and ulcerative colitis (UC) was investigated. It was found that inflamed mucosal tissue released significantly more SP-LT than normal colonic mucosa both under control conditions and after addition of calcium ionophore A23187. These results indicate the presence of endogenous stimuli as well as an increased responsiveness to an exogenous stimulus of LT formation in the inflamed mucosa. Sulfasalazine (SASP), a drug used in inflammatory bowel diseases, and its active metabolite 5-aminosalicylic acid (5-ASA) were found to inhibit colonic mucosal SP-LT formation, while only 5-ASA inhibited simultaneously synthesis of another arachidonic acid-derived inflammatory mediator, prostaglandin (PG) E2. The results suggest that SP-LT might be important mediators of inflammation in CD and UC.
    Type of Medium: Electronic Resource
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