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  • Articles: DFG German National Licenses  (12)
  • cholecystokinin  (8)
  • pancreatic polypeptide  (4)
  • omeprazole  (3)
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  • Articles: DFG German National Licenses  (12)
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Years
  • 1
    ISSN: 1432-0428
    Keywords: Islet of Langerhans ; transplantation ; metabolism ; dog ; glucose-dependent insulinotropic polypeptide ; pancreatic polypeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Successful transplantation of isolated islets of Langerhans has been reported in large mammals, including man, but metabolic control has not been well-established. We studied the glucose and islet hormone response to fasting, i. v. glucose bolus infusion, i.v. arginine bolus infusion during a 35-mmol/l hyperglycaemic clamp, mixed meals, and i. v. insulin-induced hypoglycaemia up to 3 years after intrasplenic islet autotransplantation in six pancreatectomised dogs. The individual postprandial insulinogenic index (ratio of 2-h postprandial insulin to glucose levels) at 1 month post-transplant, predicted (r=0.99) the time to functional graft failure (6–175 weeks). Metabolic studies at 6 months post-transplant in four dogs demonstrated normal fasting glucose and hormone levels, except for reduced pancreatic polypeptide levels. Intravenous glucose and arginine-stimulated insulin were reduced to 15% of preoperative values. In contrast, postprandial normoin-sulinaemia was observed — albeit with moderate hyperglycaemia (approximately 10 mmol/l). Postprandial glucagon and glucose-dependent insulinotropic polypeptide (GIP) had increased. Comparison of the post-transplant insulin responses to a meal and to intravenous challenges demonstrated maximal stimulation of the graft by the meal. Post-transplant pancreatic polypeptide responses to a meal and i.v. arginine were severely reduced, and no pancreatic polypeptide response to i.v. insulin-induced hypoglycaemia was observed — indicating absence of cholinergic reinnervation. Thus, glucose regulation and both the insulin secretory capacity and life expectancy of islet grafts were best documented by meal testing. Tentatively, a postprandial hyperglycaemia-enhanced incretin effect of glucose-dependent insulinotropic polypeptide and other gut hormones may account for the difference in the insulin response to i. v. glucose and a meal. Aside from the reduced insulin secretory capacity, both a deranged pulsatile delivery of insulin, hyperglucagonaemia, and pancreatic polypeptide deficiency may have been conducive to glucose intolerance.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Gallbladder emptying ; hyperglycaemia ; cholecystokinin ; Type 1 (insulin-dependent) diabetes mellitus ; autonomic neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Patients with diabetes mellitus are at increased risk of developing gallstones. This has been attributed, among other factors, to alterations in gallbladder motility in the presence of autonomic neuropathy. Since high blood glucose concentrations impair gastric emptying in diabetic patients, we have investigated the effect of acute hyperglycaemia on gallbladder motility. Seven Type 1 (insulin-dependent) diabetic patients were studied twice during euglycaemia (blood glucose 5 mmol/l) and hyperglycaemia (blood glucose 15 mmol/l) using a clamp technique. In addition, seven healthy volunteers were studied during euglycaemia and hyperglycaemia. Gallbladder volumes, measured with ultrasonography, were studied before and during infusion of step-wise increasing doses of cholecystokinin-33, 0.25, 0.5 and 1.0 Ivy Dog Unit · kg−1 · h−1, each dose for 30 min. Mean basal gallbladder volumes were not significantly different in the four experiments. Administration of cholecystokinin resulted in significant (p〈0.05) dose-dependent reductions in gallbladder volume in all experiments. During euglycaemia the gallbladder contraction in diabetic patients was not significantly different from the control subjects. During hyperglycaemia the gallbladder contraction in the diabetic patients was significantly (p〈0.05) reduced compared to euglycaemia only during infusion of 0.25 Ivy Dog Unit · kg−1 · h−1 of cholecystokinin (19±6% vs 33±6%). Compared to euglycaemia, during hyperglycaemia the gallbladder contraction in the control subjects was significantly (p〈0.05) reduced during infusion of 0.25, 0.5 and 1.0 Ivy Dog Unit · kg−1 · h−1 of cholecystokinin (14±4% vs 31±3%; 42±6% vs 65±5%; 74±4% vs 90±3%, respectively). It is concluded that during euglycaemia the gallbladder contraction in response to cholecystokinin in Type 1 diabetic patients is not significantly different from control subjects. During hyperglycaemia the gallbladder contraction in response to 0.25 Ivy Dog Unit · kg−1 · h−1 cholecystokinin, leading to cholecystokinin levels as observed after ingestion of a light meal, is significantly reduced in Type 1 diabetic patients.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1420-9071
    Keywords: Rats ; nutrients ; cholecystokinin ; pancreatic secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Isocaloric and isovolemic amounts of protein (casein), fat (intralipid) and carbohydrate (saccharose) and an isovolemic control solution of water were administered intragastrically to conscious rats. The plasma CCK levels, determined by a sensitive and specific radioimmunoassay, showed an increment of 6.3±0.6, 2.7±0.5, 1.7±0.4 and −0.9±0.4 pM, respectively (basal value 2.5±0.3 pM). The threshold increment of plasma CCK to stimulate pancreatic enzyme secretion by exogenous CCK was found to be 1.5 pM. It is therefore concluded that casein is a potent stimulus for CCK secretion and pancreatic secretion, but that fat and even carbohydrate, although less potent, also produce a CCK increment above the threshold for pancreatic secretion.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1041
    Keywords: Nifedipine ; omeprazole ; absorption ; gastric pH ; pharmacokinetic ; drug interaction ; adverse effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effects of single dose (20 mg) and short-term (20 mg/day for 8 days) oral treatment with omeprazole on the pharmacokinetics and effects of oral nifedipine (10 mg capsule) and on gastric pH have been investigated in a randomized, double-blind, placebo-controlled cross-over study in 10 non-smoking healthy male subjects. The single dose of omeprazole had no significant effect on any pharmacokinetic parameter of nifedipine, nor on gastric pH, or blood pressure or heart rate. Short-term omeprazole treatment increased the AUC of nifedipine by 26% (95% confidence interval 9–46%), but all other pharmacokinetic parameters of nifedipine, including elimination half-life, Cmax, tmax, and recovery of the main urinary metabolite, were not significantly changed. The median gastric pH during the absorption phase of nifedipine was increased by short-term omeprazole (pH 4.2) compared to placebo treatment (pH 1.4). Blood pressure and heart rate did not differ between treatments. The interaction between nifedipine and omeprazole is not likely to be of major clinical relevance.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 38 (1990), S. 367-370 
    ISSN: 1432-1041
    Keywords: cholecystokinin ; loxiglumide ; CCK-receptor antagonist ; bombesin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Cholecystokinin (CCK)-receptor antagonists have been reported to inhibit the effects of the hormone on the gastrointestinal tract. Their effect on plasma CCK levels in man has not been described. The present study in 5 normal subjects demonstrated that i.v. infusion of the potent, specific CCK-receptor antagonist loxiglumide (CR 1505) significantly augmented plasma CCK levels during infusion of bombesin (402 pM per 30 min) and after administration of a meal (1390 pM per 300 min) when compared to the bombesin- (192 pM per 30 min) and meal- (886 pM per 300 min) stimulated CCK responses during infusion of saline. The basal plasma CCK during saline infusion (0.1 pM per 40 min) was not significantly influenced by CR 1505 (−1.8 pM per 40 min). Thus, both enteral (meal) and parenteral (bombesin) stimulation of CCK secretion are augmented by CCK-receptor blockade.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1041
    Keywords: omeprazole ; pepsinogen A ; pepsinogen C ; fasting serum gastrin ; pentagastrin ; gastric-acid ; healthy volunteers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary A study has been done in 10 male healthy volunteers of the effect of oral omeprazole 20 mg daily for 3 days on the serum concentrations of Pepsinogens A and C in relation to changes in fasting serum gastrin and basal and pentagastrin stimulated gastric acid output. The concentrations of Pepsinogens A and C showed concomitant and variable but significant increases, and the Pepsinogen A, C ratio did not change during the 3-day course of omeprazole. The increments were also significantly correlated with the increase in fasting serum gastrin and with the reduction in pentagastrin stimulated acid output. The correlations were mainly due to the marked inhibition of gastric acid secretion and the corresponding increases in serum gastrin and Pepsinogens A and C in two subjects, as in the other 8 subjects the changes were only modest. There appears to be a relationship, therefore, between the degree of inhibition of acid by omeprazole and the parallel increases in both serum pepsinogens and fasting gastrin.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1573-2568
    Keywords: hyperglycemia ; amino acids ; parenteral nutrition ; gallbladder motility ; cholecystokinin ; pancreatic polypeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was undertaken to investigate the effect of acute hyperglycemia on the gallbladder contraction induced by intravenous administration of high doses of amino acids (Vamin 18, 250 mg protein/kg/hr). Six healthy volunteers were studied in random order on two occasions during normoglycemia and hyperglycemia with blood glucose levels stabilized at 15 mmol/liter. Gallbladder volumes, measured with ultrasonography, were studied for 60 min before and for 120 min during intravenous infusion of amino acids (IVAA). Administration of IVAA resulted in a significant reduction (P〈0.05) in gallbladder volume from 32±5 cm3 to 17±2 cm3 during normolgycemia. During hyperglycemia no significant changes in gallbladder volume were observed in response to IVAA. No significant changes in plasma CCK concentration, the major hormonal stimulus for gallbladder contraction, occurred in response to IVAA. During hyperglycemia, pancreatic polypeptide (PP) secretion, as an indirect measure of vagal cholinergic tone, in response to IVAA was significantly (P〈0.05) reduced compared to normoglycemia. It is concluded that: (1) administration of high doses of IVAA results in significant gallbladder contraction, (2) high doses of IVAA do not stimulate CCK secretion, (3) acute hyperglycemia inhibits IVAA-induced gallbladder contraction, and (4) acute hyperglycemia inhibits basal and stimulated plasma PP secretion, suggesting impaired vagal-cholinergic tone during hyperglycemia.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1573-2568
    Keywords: prostaglandin E2 analog ; enprostil ; omeprazole ; gastrin ; pepsinogen A ; pepsinogen C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study was undertaken to determine whether the synthetic prostaglandin E2 analog enprostil is able to inhibit basal and postprandial hypergastrinemia induced by omeprazole. We also studied the effect of omeprazole, enprostil, and the combination of both drugs on serum pepsinogen A and C levels. Eight normal subjects received in random order five-day courses of 40 mg omeprazole once a day, 35 µg enprostil three times a day, the combination of both drugs, and placebo. Omeprazole induced significant increases in basal and postprandial serum gastrin and in pepsinogen A and C levels. These increments persisted on the day after stopping treatment. Coadministration of enprostil inhibited omeprazole-induced basal hypergastrinemia and postprandial integrated serum gastrin, but not basal serum pepsinogen A and C, while the inhibition on the day after the treatment courses only reached statistical significance for the postprandial integrated serum gastrin concentration. It is concluded that enprostil inhibits omeprazole-induced basal and postprandial hypergastrinemia, with a tendency to protracted inhibition after stopping the drugs, and that enprostil does not significantly influence omeprazole-induced increases in pepsinogen A and C level. Coadministration of enprostil may be helpful in preventing pronounced hypergastrinemia in the few patients who show large serum gastrin increases during treatment with omeprazole.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 41 (1996), S. 2404-2408 
    ISSN: 1573-2568
    Keywords: orlistat ; tetrahydrolipstatin ; lipase inhibitor ; gallbladder motility ; cholecystokinin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Orlistat (tetrahydrolipstatin) is a potent inhibitor of gastric and pancreatic lipase activity causing a diminution of free fatty acids in the intestinal lumen. The release of cholecystokinin (CCK) critically depends on the presence of free fatty acids in the small intestine. Postprandial CCK release and gallbladder contraction might be decreased by orlistat, potentially resulting in an increased risk of gallstone formation. In this double-blind, placebo-controlled, six-way crossover study, six healthy volunteers ingested in a randomized order three isocaloric test meals (250 ml) of identical osmolality with either orlistat (200 mg) or placebo: (a) a pure-fat meal (25 g triglycerides), (b) a mixed meal containing fat (8 g; 29% of caloric content), protein (10 g; 17%), and dextrose (32 g; 54%), and (c) a fat-free meal containing albumin (25 g; 46%) and dextrose (32 g; 54%). Gallbladder volumes were determined by ultrasonography, and plasma CCK, pancreatic polypeptide and gastrin levels by RIA. Gallbladder contraction (AUC, % × 90 min; difference of means ± 95% CI) in subjects receiving orlistat or placebo did not significantly differ after intake of the pure-fat meal (443 ± 1174), the mixed meal (313 ± 1170), or the fat-free-meal (−760 ± 1180). The release of CCK (AUC; pM × 90 min; difference of means ± 95% CI) was not different between orlistat and placebo after ingestion of the pure-fat meal (−18 ± 64), the mixed meal (−45 ± 62), and the fat-free meal (27 ± 63). Likewise, the release of pancreatic polypeptide and gastrin was similar after intake of the meals with either orlistat or placebo. A single dose of orlistat did not reduce gallbladder motility after ingestion of meals with differing fat contents. The safety of long-term treatment with orlistat with respect to gallstone formation remains to be determined.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1573-2568
    Keywords: acromegaly ; octreotide ; somatostatin ; gallbladder motility ; cholecystokinin ; pancreatic polypeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The increased risk of gallstone formation in acromegalics treated with the somatostatin analog octreotide has been related to an impaired gallbladder emptying. To determine the duration of these inhibitory effects, meal-stimulated gallbladder motility, plasma cholecystokinin (CCK), and pancreatic polypeptide (PP) were measured in five acromegalics treated for 6–32 months with 200–300 μg octreotide daily. Meal tests were performed 45 min, 8 hr and two weeks after the last 100-μg subcutaneous dose. Results were compared with those in normal subjects. Integrated postprandial gallbladder contraction (−125±194 cm3/120 min) and integrated PP secretion (−0.1±0.2 nmol/liter/120 min) were completely suppressed in the 45-min study, but significantly improved (P〈0.05) when measured 8 hr (1376±322 cm3/120 min and 3.0±1.0 nmol/liter/120 min) and two weeks (1437±263 cm3/120 min and 10.6±1.6 nmol/liter/120 min) after the last dose of octreotide. The integrated gallbladder contraction in acromegalics at 8 hr was comparable to that at two weeks and to that in normal subjects, but the integrated PP response at 8 hr was significantly smaller (P〈0.05 vs two weeks and vs normals). Integrated plasma CCK secretion at 45 min (0.13±0.06 nmol/liter/120 min) was not statistically significantly different from the response at 8 hr (0.15±0.02 nmol/liter/120 min) and from that in normal subjects, but it was significantly increased at two weeks after cessation of octreotide (P〈0.05 vs 45 min and 8 hr). In conclusion, during long-term octreotide treatment in acromegalics, initial abolishment of postprandial gallbladder emptying is completely reverted to normal values 8 hr after the last subcutaneous dose. No major differences in postprandial plasma CCK at 45 min and at 8 hr were observed when compared with normal subjects, whereas plasma PP responses were diminished.
    Type of Medium: Electronic Resource
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