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  • 1
    ISSN: 1432-1440
    Keywords: Somatostatin ; Insulin ; C-peptide ; Diabetes ; Pituitary function ; Gastric acid secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A case of somatostatinoma syndrome in a 30-year-old woman is presented. Basal levels of growth hormone and of pancreatic and gastric hormones were reduced and the response of growth hormone, insulin and C-peptide to stimuli such as arginine, glucose, glibenclamide and calcium was virtually abolished. Similarly, gastric acid secretion, pancreatic exocrine function and intestinal absorption were significantly reduced. On the other hand, basal and stimulated levels of adrenocorticotropic hormone (ACTH), luteinizing hormone (LH), follicle-stimulating hormone (FSH) and thyroid-stimulating hormone (TSH) were within the normal range. Plasma somatostatin-like immunoreactivity was increased to 600 2,000 pg/ml (normal: 88–140 pg/ml). Immunocytochemical studies demonstrated the presence of somatostatin immunoreactive material in the primary tumour in the head of the pancreas and in the liver metastases. In spite of two courses of chemotherapy with streptozotocin and 5-fluorouracil the patient died due to liver failure 5 months after the first admission to hospital.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1433-8580
    Keywords: Oscillations ; Insulin ; Glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present study was designed to determine the effect of low dose continuous and oscillatory intraportal insulin infusions upon subsequent glucose-induced insulin release. In overnight-fasted and anesthetized rats with indwelling catheters in the jugular vein, carotic artery, and mesenteric vein insulin was infused intraportally for 3 h via the mesenteric vein catheter at a continuous rate of 45 µU/kg·min, or the same amount of insulin was administered at alternating high (72 µU/kg·min) and low infusion rates (18 µU/kg·min), respectively, in 2-, 4-, 8-, and 16-min cycles (oscillatory infusions). Another group received a continuous infusion of saline. Glucose (0.4 g/kg) was given i.v. 30 min after the end of the insulin or saline infusion. During the 3-h infusion of insulin or saline the peripheral glucose level remained unchanged in all groups. In response to the i.v. glucose load peripheral arterial plasma insulin levels were significantly elevated after preceding oscillatory infusions compared to the continuous insulin infusion. As compared to the group receiving saline the glucose-induced insulin response after continuous insulin infusion was significantly reduced. The plasma glucose responses were not different except for inexplicably elevated glucose levels in the 4-min cycle group. No difference was observed for plasma glucagon levels in all groups. The present data demonstrate an augmented responsiveness of theβ-cell to glucose after a preceding oscillatory infusion of insulin and an impaired responsiveness to glucose after continuous insulin infusion. This indicates that an oscillatory insulin release might be of importance for an adequate regulation ofβ-cell function.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Glucose ; duct ligation ; IMI ; secretin ; pancreozymin ; K-value
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé L'influence de la sécrétine et de la pancréozymine intravenieuses sur la sécrétion d'insuline a été étudiée chez des rats ayant une insuffisance pancréatique exocrine. La sécrétine et la pancréozymine ont causé une sécrétion d'insuline significative chez des rats normaux. L'effet de ces hormones a été différent chez les animaux ayant une insuffisance pancréatique exocrine; alors que la pancréozymine causait une sécrétion d'insuline chez ces animaux, la sécrétine n'en causait aucune. Le glucose intravenieux, quant à lui, produisait une augmentation d'insuline du sang même chez les rats ayant une insuffisance pancréatique exocrine. Il semble que seule l'action de la sécrétine sur la sécrétion d'insuline soit liée au pancréas exocrine intact. Par contre la pancréozymine stimule la sécrétion d'insuline même dans le cas d'une insuffisance pancréatique exocrine. Ces résultats in vivo sont indentiques à ceux obtenus avec les ilôts isolés du pancréas des rats.
    Abstract: Zusammenfassung Bei Ratten mit exokriner Pankreasinsuffizienz, erzeugt durch vollständige Ligatur sämtlicher Pankreasausführungsgänge mit anschließender fettiger Degeneration, wurde der Einfluß von Sekretin und Pankreozymin i.v. auf das immunologisch meßbare Insulin geprüft. Bei normalen Ratten führten Sekretin und Pankreozymin zu einer signifikanten Insulinausschüttung. Bei Tieren mit Pankreasinsuffizienz war ein unterschiedlicher Effekt beider Hormone nachzuweisen. Während Pankreozymin auch bei pancreasinsuffizierten Tieren einen deutlichen Anstieg der Insulinsekretion bewirkt, fehlt nach Sekretin die reaktive Insulinsecretion. I.v. Glucose bewirkte hingegen auch bei den pankreasinsuffizienten Ratten einen Insulinanstieg in Plasma. Offensichtlich ist lediglich die insulinstimulierende Wirkung von Sekretin an ein intaktes exokrines Pankreas gebunden, während Pankreozymin auch bei Pankreasinsuffizienz das Inselsystem zur Insulinabgabe veranlaßt. Diese Befunde in vivo sind übereinstimmend mit den Versuchen an isolierten Inseln der Ratten.
    Notes: Summary A comparison was made of the effects of the intestinal hormones secretin and pancreozymin on insulin secretion in non-diabetic rats with experimentically induced exocrine pancreatic insufficiency and in control animals. The rats with exocrine pancreatic insufficiency exhibited normal disappearence of glucose and secretion of insulin. In rats with exocrine pancreatic insufficiency secretin did not lead to any increase in insulin secretion in contrast to its effect in the controls. In rats with exocrine pancreatic insufficiency pancreozymin evoked secretion of insulin to the same extent as in the normal animals. — From these results it is inferred that the effect of secretion upon the β-cells of the rat is dependent upon the presence of intact exocrine pancreatic tissue. However, pancreozymin and glucose exert their effects upon the β-cells directly without the involvement of the exocrine portion of the pancreas. All of these findings made under conditions in vivo are in perfect accord with studies made on isolated islets of rats subjected to the same stimuli in the preparation in vitro.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: C-peptide ; insulin secretion ; effect of insulin ; alloxan-diabetic rats ; C-peptide effect in vivo ; somatostatin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of synthetic rat C-peptide 1 and C-peptide 2 on plasma insulin and blood glucose concentrations in the rat were studied. Infusion of rat C-peptide (500μg·h-1· kg-1) diminished glucose induced increase of plasma insulin by 56% (15.2±0.9 versus 6.6± 0.6 ng/ml, p〈0.01, mean±SEM). Somatostatin infused at a rate of 50 μg·h-1·kg-1 body weight inhibited glucose-induced insulin secretion by 33%. In the presence of a mixture of both C-peptides or somatostatin, blood glucose after intravenous glucose was higher than in the control experiments. In alloxan-diabetic rats, C-peptide (160 μg/kg) significantly increased and prolonged the hypoglycaemic effect of exogenous insulin. It is suggested that C-peptide may not be a biologically inert substance.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 56 (1978), S. 111-120 
    ISSN: 1432-1440
    Keywords: C-peptide ; Diabetes mellitus ; Glibenclamide, therapeutic use ; Insulin secretion ; C-Peptid ; Diabetes mellitus ; Glibenclamid, therapeutische Anwendung ; Insulinsekretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Erwachsene Diabetiker wurden je nach Therapie vor und nach einem Behandlungsversuch mit Diät und Glibenclamid in 4 Gruppen eingeteilt: I: vorher Insulin — nachher Insulin, II: Tabletten — Insulin, III: Insulin — Tabletten und IV: Tabletten — Tabletten. Bei 6 Stoffwechselgesunden und 10 Patienten aus jeder Diabetikergruppe wurde die Sekretionskapazität der Beta-Zellen nach i.v. Belastung mit Glibenclamid-Glukose mittels C-Peptid Messungen untersucht. Bei den Diabetikern aller Gruppen kam eine Sekretionsstarre in einem verminderten und verzögerten Anstieg von immunologisch meßbarem C-Peptid (IMCP) zum Ausdruck. Bei tablettenbedürftigen Patienten hielt die Sekretion allerdings länger an als bei Stoffwechselgesunden. Im Mittel waren der Zuwachs von IMCP und die integrierten Stimulationsflächen bei tablettenbedürftigen Patienten (III+IV) viel größer als bei insulinbedürftigen (I+II). Eine Varianzanalyse wurde für die insulinbedürftigen Fälle einerseits und die tablettenbedürftigen Patienten andererseits durchgeführt. Die Gruppen I und II unterscheiden sich überzufällig bezüglich der Gruppenmittelwerte für IMCP, während der zeitliche Verlauf der IMCP Mittelwerte der beiden Gruppen nur zufällig von der Parallelität abweicht. In den Gruppen III und IV unterscheiden sich weder die Gruppenmittelwerte überzufällig, noch konnte eine Abweichung der jeweiligen zeitlichen Verläufe von der Parallelität nachgewiesen werden. Der zeitliche Verlauf konnte für Insulinbedürftige durch ein Regressionspolynom 2. Grades, für Tablettenbedürftige durch ein Regressionspolynom 4. Grades dargestellt werden. Die Kurven unterscheiden sich erheblich in Ausmaß und Steilheit ihres Anstiegs. Die Therapievorhersage nach i.v. Belastung mit Glibenclamid-Glukose, die bisher auf Kriterien des Blutglukoseverlaufs beruhte, ist bei Kenntnis des IMCP Verlaufs leichter und zuverlässiger möglich. Als natürlicher Verlauf des Diabetes mellitus im Erwachsenenalter ist die Entwicklung der Restsekretion der Beta-Zellen vom Stadium der Gruppen III und IV über Gruppe II zum Stadium der Gruppe I wahrscheinlich.
    Notes: Summary Adult diabetics were divided into 4 groups according to therapy before and after a therapeutic trial with diet and glibenclamide: I: insulin before — insulin afterwards, II: tablets — insulin, III: insulin — tablets and IV: tablets — tablets. The secretion capacity of the beta-cells, determined by C-peptide was examined in 6 healthy subjects and in 10 diabetics of each group following an i.v. glibenclamide-glucose load. A decreased insulinogenic reserve showing itself in a reduced and delayed rise of immunomeasurable C-peptide (IMCP) was found in all diabetics. However, the secretion of IMCP lasted longer in the diabetics requiring tablets than in the healthy subjects. The average values for the increment of IMCP and the integrated stimulation areas were much more considerable in the patients treated with tablets (III+IV) than in the insulin-dependent patients (I+II). An analysis of variance was performed for the diabetics depending on insulin, on the one hand, and the patients depending on tablets on the other. Between groups I and II the group average values for IMCP are significantly different while differences in the time course of the IMCP mean values of both groups are accidental. Neither the group average values of IMCP nor the time course of the IMCP mean values show significant differences between groups III and IV. The time course of IMCP was described by a regression polynomial of 2nd degree in insulin-dependent diabetics and a polynomial of 4th degree in diabetics depending on tablets; the corresponding curves differ considerably as to extent and steepness of their rise. Prediction of suitable diabetes therapy from an i.v. glibenclamide-glucose load based on blood glucose evaluation up to now is easier and more reliable since C-peptide levels are known. A development of the residual beta-cell function from the stage in groups III and IV via group II to the stage in group I is likely to be the natural course of adult diabetes.
    Type of Medium: Electronic Resource
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