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  • 1
    Electronic Resource
    Electronic Resource
    Role of pylorus in mediating cholecystokinin-stimulated satiety in the Zucker rat (1986)
    Springer
    Digestive diseases and sciences 31 (1986), S. 502-505 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Obese Zucker rats are less responsive than their lean littermates to the effects of cholecystokinin-octapeptide on satiety and pancreatic growth and exocrine function. We hypothesized that the hyperphagia observed in obese Zucker rats may be caused by a decreased pyloric contractile response to cholecystokinin, resulting in an increased rate of gastric emptying, decreased postprandial gastric distention, and thus decreased satiety. Pyloric muscle strips from six obese Zucker rats and six lean littermates were mounted in separate tissue baths and isometric contraction was measured in response to acetylcholine and cholecystokinin-octapeptide. The dose-response curves for acetylcholine-and cholecystokinin-octapeptide-stimulated pyloric muscle contraction were similar for both the obese and the lean rats. (For cholecystokinin, D50 obese=4.0±0.6 nM, D50 lean=3.4±0.2 nM;P=0.16). We conclude that the decreased satiety response to cholecystokinin-octapeptide observed in obese Zucker rats is not secondary to a decreased pyloric responsiveness to cholecystokinin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01320315
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  • 2
    Electronic Resource
    Electronic Resource
    Evidence for an intestinal mechanism of pancreatic polypeptide release (1981)
    Springer
    Digestive diseases and sciences 26 (1981), S. 587-590 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The purpose of this study was to define the existence of an intestinal phase of pancreatic polypeptide (PP) release and to assess whether it was mediated by a cholinergic-sensitive mechanism. Four conscious dogs with 20-cm upper intestinal Thiry-Vella loops and chronic gastric fistulas were used. The Thiry-Vella (T-V) loops were perfused with 10% liver extract or 0.154 M NaCl at a rate of 1 ml/min for 120 min. In a separate experiment, 240 ml of 10% liver extract was infused over a 5-min period into the stomach via the gastric fistula. Basal PP levels were 29±4 fmol/ml. The gastric infusion of liver extract caused a significant increase of plasma PP levels to a peak of 215±29 fmol/ml (P〈0.05). The perfusion of the T-V loop with liver extract significantly increased plasma PP levels over basal to a peak of 73±14 fmol/ml (P〈0.05). This value was significantly less than that released by gastric infusion of liver extract (P〈0.05). Perfusion of the loop with NaCl did not significantly alter basal plasma PP levels (P〉0.05). PP release by perfusion of the T-V loop with liver extract was abolished by atropine intravenous bolus (0.2 mg/kg). Although the combination of bethanechol (100 μg/kg/hr intravenous) and liver extract consistently increased the plasma levels of PP, the values did not attain statistical significance when compared to liver extract alone (P〉0.05). The data presented are thus consistent with the hypothesis that there is an enteric phase of pancreatic polypeptide release and that this enteropancreatic reflex is mediated by a cholinergic-sensitive mechanism which might be hormonal or neural.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01367669
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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