cholecystokinin and Diabetic-Neuropathies

cholecystokinin has been researched along with Diabetic-Neuropathies* in 7 studies

Reviews

1 review(s) available for cholecystokinin and Diabetic-Neuropathies

ArticleYear
Physiologic considerations in radionuclide imaging of the extrahepatic biliary tract.
    American journal of physiologic imaging, 1988, Volume: 3, Issue:2

    Scintigraphy of the biliary system using 99mTc-labeled radiopharmaceuticals enables the clinician to assess kinetics of bile flow through the gallbladder, common bile duct, and sphincter of Oddi. We review some aspects of biliary tract physiology and imaging which may be of interest to the physicians ordering and performing these studies.

    Topics: Cholecystokinin; Diabetic Neuropathies; Gallbladder; Gallbladder Diseases; Humans; Radionuclide Imaging; Technetium

1988

Other Studies

6 other study(ies) available for cholecystokinin and Diabetic-Neuropathies

ArticleYear
Gastroparesis is associated with oxytocin deficiency, oesophageal dysmotility with hyperCCKemia, and autonomic neuropathy with hypergastrinemia.
    BMC gastroenterology, 2009, Feb-25, Volume: 9

    Gastrointestinal (GI) dysmotility and autonomic neuropathy are common problems among diabetics with largely unknown aetiology. Many peptides are involved in the autonomic nervous system regulating the GI tract. The aim of this study was to examine if concentrations of oxytocin, cholecystokinin (CCK), gastrin and vasopressin in plasma differ between diabetics with normal function and dysfunction in GI motility.. Nineteen patients with symptoms from the GI tract who had been examined with gastric emptying scintigraphy, oesophageal manometry, and deep-breathing test were included. They further received a fat-rich meal, after which blood samples were collected and plasma frozen until analysed for hormonal concentrations.. There was an increase in postprandial oxytocin plasma concentration in the group with normal gastric emptying (p = 0.015) whereas subjects with delayed gastric emptying had no increased oxytocin secretion (p = 0.114). Both CCK and gastrin levels increased after the meal, with no differences between subjects with normal respective delayed gastric emptying. The concentration of vasopressin did not increase after the meal. In patients with oesophageal dysmotility the basal level of CCK tended to be higher (p = 0.051) and those with autonomic neuropathy had a higher area under the curve (AUC) of gastrin compared to normal subjects (p = 0.007).. Reduced postprandial secretion of oxytocin was found in patients with delayed gastric emptying, CCK secretion was increased in patients with oesophageal dysmotility, and gastrin secretion was increased in patients with autonomic neuropathy. The findings suggest that disturbed peptide secretion may be part of the pathophysiology of digestive complications in diabetics.

    Topics: Autonomic Nervous System Diseases; Case-Control Studies; Cholecystokinin; Diabetic Neuropathies; Esophageal Motility Disorders; Female; Gastric Emptying; Gastrins; Gastroparesis; Humans; Male; Oxytocin; Vasopressins

2009
Cholecystokinin and pancreatic polypeptide release in diabetic patients with and without autonomic neuropathy.
    Digestive diseases and sciences, 1995, Volume: 40, Issue:2

    The present study was undertaken to investigate postprandial responses of cholecystokinin (CCK) and pancreatic polypeptide (PP) and their interrelationship in patients with diabetes mellitus (DM) with and without autonomic neuropathy (AN). Twenty-two patients with DM (seven with AN and 15 without AN) and 14 age-matched healthy controls were studied. AN was diagnosed according to several tests of cardiovascular autonomic function. CCK and PP plasma levels were measured by specific radioimmunoassays before and at several time points after the oral administration of a test meal. Basal CCK plasma levels in DM patients were normal, whereas basal PP plasma levels were increased (139 +/- 18 vs 72 +/- 7 pg/ml; P < 0.01). Integrated postprandial CCK response was increased in DM patients (208 +/- 27 vs 110 +/- 14 pmol/liter/2 hr; P < 0.05), mainly due to the patients with AN. Postprandial PP response was increased in DM patients without AN (37,273 +/- 5241 vs 13,418 +/- 3299 pg/ml/2 hr; P < 0.001) but not in those with AN (8887 +/- 3461 pg/ml/2 hr). Moreover, PP response was closely (P < 0.002) correlated with the degree of AN. A direct and linear correlation between postprandial CCK and PP responses was found in healthy controls (r = 0.78; P < 0.005) but not in DM patients. We conclude that the CCK response to a meal is increased in diabetic patients with AN, whereas the PP response is increased only with an intact autonomic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Adult; Aged; Autonomic Nervous System Diseases; Cholecystokinin; Diabetes Mellitus; Diabetic Neuropathies; Eating; Female; Humans; Male; Middle Aged; Pancreatic Polypeptide; Radioimmunoassay; Statistics, Nonparametric; Time Factors

1995
Gallbladder dysfunction in diabetes mellitus.
    Digestive diseases and sciences, 1993, Volume: 38, Issue:3

    To further elucidate the mechanism of impaired gallbladder emptying in diabetics with and without neuropathy, gallbladder function was assessed by ultrasonography following a medium-chain triglyceride (lipomul, 1.5 mg/kg) infusion into the duodenum and compared to that during intravenous infusion of cholecystokinin in diabetic women. Results were compared with five healthy control women. Mean (+/- SD) maximal percent gallbladder volume in diabetics following lipomul was reduced to 49 +/- 8% and after intravenous cholecystokinin to 47 +/- 9%, which was less than those in controls, 21 +/- 9% and 24 +/- 6%, respectively, but not significantly different. Further analysis of gallbladder emptying to lipomul differentiated two subgroups of diabetics: one subgroup (N = 5) had emptying comparable to controls (responders), while the other (N = 5) had very modest emptying (nonresponders). Two of the patients in the latter group had normal gallbladder emptying during exogenous cholecystokinin and their response would be compatible with visceral neuropathy. Blood levels of cholecystokinin, measured by bioassay, following lipomul and exogenous cholecystokinin were similar in controls and diabetics. Presence of diabetic neuropathy did not correlate with impaired gallbladder emptying. Follow up at 6 and 12 months of the three nonresponder diabetics revealed that no gallstones had developed and that two of them became responders to exogenous cholecystokinin.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Adult; Autonomic Nervous System Diseases; Cholecystokinin; Cholelithiasis; Corn Oil; Diabetes Mellitus; Diabetic Neuropathies; Female; Follow-Up Studies; Gallbladder; Gallbladder Emptying; Humans

1993
Cholecystokinin, gallbladder function, and diabetes mellitus.
    The American journal of gastroenterology, 1991, Volume: 86, Issue:1

    Topics: Autonomic Nervous System Diseases; Cholecystokinin; Diabetic Neuropathies; Gallbladder; Humans

1991
Gallbladder function and plasma cholecystokinin levels in diabetes mellitus.
    The American journal of gastroenterology, 1990, Volume: 85, Issue:8

    Contractile motility of the gallbladder and plasma cholecystokinin (CCK) responses to egg yolk administration were studied in 28 diabetic patients and 12 normal subjects. The patients were divided into three groups: group A (n = 10) had no diabetic neuropathy, group B (n = 8) had diabetic neuropathy with little autonomic neuropathy, and group C (n = 10) had advanced diabetic autonomic neuropathy. In groups A and B, contraction of the gallbladder after egg yolk administration was not significantly different from that of normal subjects. However, in group C, gallbladder contraction was impaired (p less than 0.01-0.05), compared with that in normal subjects. After the administration of egg yolk, plasma CCK levels increased from 12.4 +/- 4.5 to 25.3 +/- 12.0 pg/ml in normal subjects. In group A, plasma CCK levels increased from 17.9 +/- 8.5 to 39.3 +/- 14.2 pg/ml, and in group B, from 15.2 +/- 5.1 to 38.3 +/- 9.9 pg/ml. In group C, however, plasma CCK levels increased from 33.1 +/- 13.9 to 72.4 +/- 31.9 pg/ml, and fasting CCK levels and responses to egg yolk were significantly higher than those in normal subjects and in groups A and B (p less than 0.01-0.05). In conclusion, this study showed that in a group of diabetic patients with autonomic neuropathy, gallbladder contraction was impaired despite the exaggerated CCK response to egg yolk.

    Topics: Adult; Autonomic Nervous System Diseases; Cholecystokinin; Diabetes Complications; Diabetes Mellitus; Diabetic Neuropathies; Egg Yolk; Fasting; Female; Gallbladder; Humans; Male; Middle Aged

1990
Impaired exocrine pancreatic function in diabetics with diarrhea and peripheral neuropathy.
    Digestive diseases and sciences, 1988, Volume: 33, Issue:6

    Exocrine pancreatic insufficiency has been observed in some diabetics with peripheral neuropathy and diarrhea. Several mechanisms may be responsible for this insufficiency: (1) pancreatic atrophy, (2) disruption of the cholinergic enteropancreatic reflexes, or (3) elevated serum levels of peptides such as glucagon and pancreatic polypeptide which are known to inhibit pancreatic exocrine secretion. To clarify the mechanism(s) involved in this exocrine pancreatic impairment, we studied 10 diabetics with diarrhea and peripheral neuropathy. Their results were compared to those of eight normal volunteers. Each subject underwent a standardized pancreatic function study which assessed nonstimulated secretion, the response to intrajejunal infusion of a mixture of amino acids, and the output following intravenous administration of secretin and cholecystokinin (CCK). In separate studies, the effect of a background infusion of bethanechol and secretin on the pancreatic response to CCK was assessed in six patients and six normal controls. Compared to normals, all diabetics exhibited a significant reduction in both enzyme and bicarbonate secretion to all stimuli. This reduction was not corrected by administering bethanechol. Plasma glucagon and pancreatic polypeptide levels in diabetics were not significantly higher than those in controls. We conclude that diabetics with diarrhea and peripheral neuropathy exhibit impairment of their exocrine pancreatic secretion and possible mechanisms for this are discussed.

    Topics: Adult; Amino Acids; Bethanechol; Bethanechol Compounds; Cholecystokinin; Chronic Disease; Diabetes Mellitus, Type 2; Diabetic Neuropathies; Diarrhea; Dose-Response Relationship, Drug; Humans; Intubation, Gastrointestinal; Male; Middle Aged; Pancreas; Secretin

1988