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  • 1990-1994  (2)
  • Key words Gallbladder emptying, hyperglycaemia, cholecystokinin, Type 1 (insulin-dependent) diabetes mellitus, autonomic neuropathy.  (1)
  • intestinal transit  (1)
  • Childhood
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  • 1
    ISSN: 1432-0428
    Keywords: Key words 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. [Diabetologia (1994) 37: 75–81]
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-2568
    Keywords: hyperglycemia ; gallbladder ; intestinal transit ; pancreatic polypeptide ; cholecystokinin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the present study was to investigate the effect of acute hyperglycemia on (1) the intestinal phase of gallbladder contraction induced by the intraduodenal administration of emulsified fat, and (2) the small intestinal transit time measured by the lactulose breath hydrogen test. Six healthy volunteers were studied in random order during normoglycemia and hyperglycemia (blood glucose levels 15 mmol/liter). Gallbladder volumes were measured with ultrasonography. Administration of 1 and 2 g/hr of fat resulted in significant reductions in gallbladder volumes from 24±2 cm3 to 11±1 cm3 (P〈0.05) and 8±1 cm3 (P〈0.05), respectively during normoglycemia, and from 24±2 cm3 to 21±2 cm3 (P〈0.05) and 16±2 cm3, respectively (P〈0.05) during hyperglycemia. Compared to normoglycemia, the gallbladder contraction was significantly (P〈0.05) reduced during hyperglycemia. No significant differences in CCK secretion were observed between experiments. Small intestinal transit time during hyperglycemia (101±12 min) was significantly (P〈0.05) prolonged compared to normoglycemia (57±12 min). During hyperglycemia, basal PP levels and PP secretion in response to intraduodenal fat were significantly (P〈0.05) reduced compared to normoglycemia. It is concluded that (1) low doses of intraduodenal emulsified fat result in significant gallbladder contraction and CCK secretion, (2) acute hyperglycemia inhibits intraduodenal fat induced gallbladder contraction, (3) acute hyperglycemia does not affect the intraduodenal fat induced CCK secretion, (4) small intestinal transit is significantly prolonged during acute hyperglycemia, and (5) 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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