Hyperglycemia modulates gallbladder motility and small intestinal transit time in man
| Autor: | J.B.M.J. Jansen, S. Y. De Boer, Ad A.M. Masclee, W. F. Lam, C. B. H. W. Lamers, J. Schipper |
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| Rok vydání: | 1993 |
| Předmět: |
Adult
Male medicine.medical_specialty endocrine system diseases Duodenum Physiology Pancreatic Polypeptide Gastroenterology Lactulose Internal medicine medicine Humans Pancreatic polypeptide Gastrointestinal Transit Cecum Ultrasonography Cholecystokinin Glucose tolerance test medicine.diagnostic_test business.industry Gallbladder nutritional and metabolic diseases Vagus Nerve Hepatology Small intestine medicine.anatomical_structure Endocrinology Basal (medicine) Hyperglycemia Acute Disease business medicine.drug |
| Zdroj: | Digestive Diseases and Sciences. 38:2228-2235 |
| ISSN: | 1573-2568 0163-2116 |
| DOI: | 10.1007/bf01299901 |
| Popis: | 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 (P0.05) and 8 +/- 1 cm3 (P0.05), respectively during normoglycemia, and from 24 +/- 2 cm3 to 21 +/- 2 cm3 (P0.05) and 16 +/- 2 cm3, respectively (P0.05) during hyperglycemia. Compared to normoglycemia, the gallbladder contraction was significantly (P0.05) reduced during hyperglycemia. No significant differences in CCK secretion were observed between experiments. Small intestinal transit time during hyperglycemia (101 +/- 12 min) was significantly (P0.05) prolonged compared to normoglycemia (57 +/- 12 min). During hyperglycemia, basal PP levels and PP secretion in response to intraduodenal fat were significantly (P0.05) 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. |
| Databáze: | OpenAIRE |
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