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  • 1
    Electronic Resource
    Electronic Resource
    β-Cell cytoplasmic Ca2+ balance as a determinant for glucose-stimulated insulin release (1985)
    Springer
    Diabetologia 28 (1985), S. 494-501 
    Details
    ISSN: 1432-0428
    Keywords: Glucose ; cytoplasmic Ca2+ balance ; β cells ; insulin release ; depolarization ; intracellular Ca2+ sequestration ; diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The introduction of new techniques and the access to clonal lines of insulin-secreting cells have enabled re-evaluation of glucose effects on Ca2+ movements in pancreatic β cells. It became evident that glucose, in addition to stimulating the entry of Ca2+ also promotes active sequestration of the ion in intracellular stores and its extrusion from the β cells. The balance between these processes will determine the activity of Ca2+ in the cytoplasm and consequently the rate of insulin release. With the demonstration that glucose can not only increase but also lower cytoplasmic Ca2+, it follows that exposure to the sugar under certain conditions results in a paradoxical inhibition of insulin release. In diabetic patients this may be manifest as prompt reduction of circulating concentrations of insulin and C-peptide after an intravenous injection of glucose. The concept of the dual action of glucose might aid in explaining a number of poorly understood phenomena, such as the induction of rhythmic oscillations of the membrane potential of β cells and the fact that their secretory response is improved by prolonged exposure to glucose and after priming with the sugar.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00281983
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  • 2
    Electronic Resource
    Electronic Resource
    Function of microdissected pancreatic islets cultured in a chemically defined medium. I. Insulin content and release (1975)
    Springer
    Diabetologia 11 (1975), S. 535-540 
    Details
    ISSN: 1432-0428
    Keywords: Microdissected pancreatic islets ; ob/ob-mouse islets ; tissue culture ; insulin release ; insulin content
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Microdissected pancreatic islets from non-inbredob/ob-mice, were cultured for 6 or 7 days in serum-free tissue culture medium 199. The insulin content of the islets decreased 60% during culture in 17 mM or 28 mM glucose and about 70% in the presence of 3.3 mM or 5.6 mM glucose. At the end of a culture period in high glucose, the sum of the insulin in the islet plus that in the culture medium was almost twice as high as the insulin content of fresh islets, indicating an active insulin biosynthesis. The maximal insulin response to glucose after culture in 17 mM or 28 mM glucose was about 40% of that in fresh islets; after culture in 3.3 mM glucose it was 10%. Half-maximal stimulation was observed at a glucose concentration of 5 mM for islets cultured with high glucose as compared to 9 mM for fresh islets. Like glucose, glibenclamide was a more effective insulin stimulator after culture with a high glucose concentration than with a low one. However, leucine-induced insulin release was not affected by the glucose concentration in the preceding culture medium. Whereas potentiation of glucose-stimulated release by arginine or dibutyryl-cAMP was independent of glucose concentration during the culture, theophylline released three times more insulin when the islets had been cultured with high glucose.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01222103
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  • 3
    Electronic Resource
    Electronic Resource
    Metabolism of cold-stored pancreatic islets (1978)
    Springer
    Diabetologia 15 (1978), S. 187-190 
    Details
    ISSN: 1432-0428
    Keywords: Pancreatic islets ; cold-storage ; culture ; glucose utilization ; oxygen consumption ; 86Rb+-uptake ; metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A previous study showed that the ability of glucose to stimulate insulin release was retained in islets stored at 8 °C for one week provided that glucose was present in a high concentration in the storage medium. The metabolic properties of islets stored in the cold have now been further explored in an attempt to clarify the protective effect of glucose. During storage in the cold the islet formation of 3H2O from (5-3H) glucose and oxygen consumption were only a few per cent of that of fresh islets whereas the uptake of 86Rb+ was 20–48%. Rewarming the cold-stored islets to 37 °C after one week of cold-storage restored the 86Rb+ uptake, the formation of 3H2O and 14CO2 from labelled glucose and oxygen consumption to 75, 80, 60 and 40% respectively of fresh islet levels. The results emphasize the usefulness of cold-storage for preservation of functionally intact isolated islets.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00421237
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of various modifiers of insulin release on the lanthanum-nondisplaceable45ca2+ uptake by isolated pancreatic islets (1977)
    Springer
    Diabetologia 13 (1977), S. 49-53 
    Details
    ISSN: 1432-0428
    Keywords: Calcium uptake ; islets of Langerhans ; insulin release ; ob/ob-mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The uptake of45Ca2+ by a lanthanum-nondisplaceable pool in pancreatic islets was studied. Raising the extracellular D-glucose concentration from 3 to 20 mM stimulated the45Ca2+ uptake in hand-dissected islets of ob/ob-mice as well as in collagenase-isolated islets of ob/ob or normal mice. The effect was dose-dependent in the range of 0–20 mM D-glucose and was seen throughout a wide range of extracellular calcium concentrations (16 μmol — 2.56 mmol of Ca2+ added per litre of medium). The45Ca2+ uptake was also enhanced by other known insulin secretagogues (D-mannose, L-leucine, tolbutamide) and was uninfluenced by compounds lacking insulinreleasing capacity (3-O-methyl-D-glucose, L-glucose, D-galactose, D-leucine). The stimulatory effect of D-glucose was blocked by inhibitors of glucoseinduced insulin release (D-mannoheptulose, diazoxide, L-adrenaline). The results support the view that the lanthanum-nondisplaceable calcium pool is related to the insulin-releasing mechanism, although the exact nature of this relationship is still unclear.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00996327
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  • 5
    Electronic Resource
    Electronic Resource
    Regulation of pancreatic β-cell glycogen through cyclic-3,5-AMP (1971)
    Springer
    Diabetologia 7 (1971), S. 139-142 
    Details
    ISSN: 1432-0428
    Keywords: Pancreatic β-cell ; glycogen ; cyclic-3,5-AMP ; obese-hyperglycaemic mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Le glycogène a été mesuré dans des îlots pancréatiques isolés de souris obèses-hyperglycémiques. Les enregistrements ont été faits sur des extraits bruts de tissus, à l'aide d'un dosage enzymatique hautement spécifique. La quantité de glycogène dépendait de la concentration extracellulaire de glucose. Le 3′,5′-AMP cyclique dibutyril ainsi que des composés (glucagon et théophylline) connus pour augmenter le taux insulaire de 3′,5′-AMP cyclique, diminuaient le contenu en glycogène. L'adrénaline, dont l'effet inhibiteur sur la synthèse du 3′,5′-AMP cyclique a été rapporté, augmentait le taux de glycogène des îlots en présence de 3,0 mg/ml de glucose. Les résultats suggèrent que le taux de 3′,5′-AMP cyclique est un régulateur important du métabolisme du glycogène dans les cellulesβ insulino-sécrétrices.
    Abstract: Zusammenfassung An isolierten Pankreasinseln von fettsüchtigen, hyperglykämischen Mäusen wurde der Glykogengehalt gemessen. Die Untersuchungen wurden an rohen Gewebsextrakten mit Hilfe einer hoch spezifischen enzymatischen Methode durchgeführt. Der Glykogengehalt hing von der extrazellulären Glukosekonzentration ab. Dibutyryl-zyklisches 3,5-AMP als auch Substanzen (wie Glukagon und Theophyllin), welche bekannt sind, den zyklischen 3,5-AMP-Spiegel der Inseln zu heben, verminderten den Glykogengehalt. Epinephrin, das die Synthese von zyklischem AMP hemmen soll, erhöhte den Glykogenspiegel der Inseln in Anwesenheit von 3,0 mg/ml Glukose. Die Ergebnisse deuten darauf hin, daß der zyklische 3,5-AMP-Spiegel ein wichtiger Regulator des Glykogen-Metabolismus in der Insulin produzierenden Zelle ist.
    Notes: Summary Glycogen was measured in isolated pancreatic islets from obese-hyperglycaemic mice. The recordings were made on crude tissue extracts using a highly specific enzymatic assay. The amount of glycogen depended on the extracellular glucose concentration. Dibutyryl cyclic-3,5-AMP as well as compounds (glucagon and theophylline) known to increase the islet level of cyclic-3,5-AMP reduced the content of glycogen. Epinephrine, which has been reported to inhibit the synthesis of cyclic-3,5-AMP, increased the level of islet glycogen in the presence of 3.0 mg/ml of glucose. The results suggest that the level of cyclic-3,5-AMP is an important regulator of glycogen metabolism in the insulin-producingβ-cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01212544
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  • 6
    Electronic Resource
    Electronic Resource
    Annual Meeting of the Scandinavian Society for the Study of Diabetes (1972)
    Springer
    Diabetologia 8 (1972), S. 362-370 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01218498
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  • 7
    Electronic Resource
    Electronic Resource
    The pancreatic β-cell recognition of insulin secretagogues (1973)
    Springer
    Diabetologia 9 (1973), S. 210-216 
    Details
    ISSN: 1432-0428
    Keywords: Glibenclamide ; insulin release ; pancreatic islets ; sulfonylurea ; tolbutamide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The study was aimed at testing the hypothesis that sulfonylureas do not readily penetrate the pancreaticβ-cells but more probably stimulate insulin release by a direct action on theβ-cell plasma membrane. Uptake of radioactively labelled tolbutamide and glibenclamide by microdissected pancreatic islets of obesehyperglycemic mice was compared with the uptake of 3-O-methyl-D-glucose, to which theβ-cells are permeable. In contrast to tolbutamide, glibenclamide was taken up in amounts exceeding the 3-O-methyl-D-glucose space of islets incubated in the absence of serum albumin. Uptake of the sulfonylureas was easily reversible. It was depressed by serum albumin, whereas glucose, leucine or diazoxide had no effects. Antimycin A,p-chloromercuriphenylsulfonic acid and chlorpromazine, all of which increase the uptake of extracellular space markers, strongly stimulated the islet uptake of tolbutamide and glibenclamide but had no effect on the uptake of glibenclamide by subcellular particles of homogenized islets. The results suggest that sulfonylureas bind reversibly to islet tissue but are normally restricted to the outside of theβ-cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01219785
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  • 8
    Electronic Resource
    Electronic Resource
    Glucose induces oscillatory Ca2+ signalling and insulin release in human pancreatic beta cells (1994)
    Springer
    Diabetologia 37 (1994), S. S11 
    Details
    ISSN: 1432-0428
    Keywords: Ca2+ signalling ; diabetes mellitus ; glucose insulin secretion ; islets of Langerhans ; oscillations pancreatic beta cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mechanisms of pulsatile insulin release in man were explored by studying the induction of oscillatory Ca2+ signals in individual beta cells and islets isolated from the human pancreas. Evidence was provided for a glucose-induced closure of ATP-regulated K+ channels, resulting in voltage-dependent entry of Ca2+. The observation of step-wise increases of capacitance in response to depolarizing pulses suggests that an enhanced influx of Ca2+ is an effective means of stimulating the secretory activity of the isolated human beta cell. Activation of muscarinic receptors (1–10 μmol/l carbachol) and of purinergic P2 receptors (0.01–1 μmol/l ATP) resulted in repetitive transients followed by sustained elevation of the cytoplasmic Ca2+ concentration ([Ca2+]i). Periodic mobilisation of intracellular calcium was seen also when injecting 100 μmol/l GTP-γ-S into beta cells hyperpolarized to −70 mV. Individual beta cells responded to glucose and tolbutamide with increases of [Ca2+]i, manifested either as large amplitude oscillations (frequency 0.1–0.5/min) or as a sustained elevation. Glucose regulation was based on sudden transitions between the basal and the two alternative states of raised [Ca2+]i at threshold concentrations of the sugar characteristic for the individual beta cells. The oscillatory characteristics of coupled cells were determined collectively rather than by particular pacemaker cells. In intact pancreatic islets the glucose induction of well-synchronized [Ca2+]i oscillations had its counterpart in 2–5 min pulses of insulin. Each of these pulses could be resolved into regularly occurring short insulin transients. It is concluded that glucose stimulation of insulin release in man is determined by the number of beta cells entering into a state with Ca2+-induced secretory pulses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400821
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  • 9
    Electronic Resource
    Electronic Resource
    Evidence for an inhibitor of insulin release in the pancreatic islets (1969)
    Springer
    Diabetologia 5 (1969), S. 22-24 
    Details
    ISSN: 1432-0428
    Keywords: Isolated pancreatic islets ; insulin releasein vitro ; inhibitor of insulin release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé La libérationin vitro d'insuline par les îlots isolés de souris fut significativement réduite en présence d'un extrait de protéine îlotique contenant plus de 100 fois le taux normal d'insuline dans le sérum. La nature de la substance répressive d'origine insulaire reste obscure. La possibilité que la circulation de sang à travers les îlots puisse avoir de l'importance pour la régulation locale de la libération d'insuline en réduisant les taux élevés de cette hormone à proximité immédiate des cellules bêta doit être considérée.
    Abstract: Zusammenfassung Die Freisetzung von Insulin aus isolierten Mäuseinselnin vitro wurde in Gegenwart eines Proteinextraktes aus Langerhans'schen Inseln, das mehr als das Hundertfache der normalen Insulinmenge im Serum enthielt, merklich gehemmt. Die Natur dieses Hemmfaktors bleibt unklar. Man sollte die Möglichkeit besonders berücksichtigen, daß die Durchblutung der Inseln für die lokale Regelung der Insulinfreisetzung über eine Reduktion der hohen Konzentration dieses Hormons in der unmittelbaren Umgebung derβ-Zellen von Bedeutung sein kann.
    Notes: Summary The release of insulinin vitro from isolated mouse islets was significantly inhibited in the presence of an islet protein extract equivalent to more than 100 times the normal serum level of insulin. The nature of the inhibitory islet substance remains unclear. The possibility that the blood circulation through the islets may be important for the local regulation of insulin release by reducing high levels of this hormone in the immediate surroundings of theβ cells should be considered.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01212214
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  • 10
    Electronic Resource
    Electronic Resource
    Transport of α-aminoisobutyric acid in mammalian pancreatic ß-cells (1971)
    Springer
    Diabetologia 7 (1971), S. 256-265 
    Details
    ISSN: 1432-0428
    Keywords: α-aminoisobutyric acid ; diazoxide ; dibut-yryl cyclic 3′5′-AMP ; glucose ; insulin release ; islets of Langerhans ; mannoheptulose ; membrane transport ; 3-0-methyl glucose ; neutral amino acids ; obese-hyperglycemic mice ; pancreaticβ-cell ; sodium ; sucrose space ; urea space
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Le transport de l'acide α-aminoisobutyrique (AIB) a été étudié dans des îlots pancréatiques microdisséqués de souris obèses-hyperglycémiques. Ces îlots sont caractérisés par une proportion inhabituellement élevée de celluleβ insulino-sécrétrices. Les principales observations suivantes ont été faites: 1. Les cellules des îlots montraient une captation concentrante d'AIB, aboutissant à des rapports de distribution bien plus élevés que l'unité. La captation était diminuée par l'anoxie et par la suppression de sodium du milieu. 2. La L-alanine et la L-méthionine, mais non la L-leucine, réduisaient l'accumulation d'AIB dans les îlots qui avaient été préincubés en l'absence d'acide aminé exogène. Après charge préalable avec la L-alanine il y avait une captation accrue d'AIB. 3. Le D-glucose, le D-galactose, le diazoxide, le 3′,5′-AMP cyclique dibutyril et le D-mannoheptulose avaient des effets mineurs ou non significatifs sur la captation d'AIB. 4. La libération d'AIB des cellules insulaires était stimulée par l'AIB exogène ou par la L-alanine. Les auteurs concluent que les cellulesβ pancréatiques contiennent un mécanisme pour le transport des acides aminés neutres semblable au système A de beaucoup d'autres cellules. L'effet stimulant du glucose sur la biosynthèse de l'insuline ne semble pas être assuré par l'intermédiaire de ce système. Le co-transport d'acide aminé et de sodium ne suffit probablement pas à provoquer une décharge d'insuline à partir de cellulesβ mûres.
    Abstract: Zusammenfassung Der Transport von α-Aminoisobuttersäure (ABS) wurde in mikrosezierten Pankreasinseln von fettsüchtigen hyperglykämischen Mäusen untersucht. Diese Inseln sind durch eine ungewöhnlich hohe Menge von Insulin sezernierendenβ-Zellen charakterisiert. Es wurden folgende wesentliche Beobachtungen gemacht: 1. Die Inselzellen führten eine konzentrierende Aufnahme von ABS durch. Die Aufnahme wurde durch Anoxämie und durch Fehlen von Natrium im Milieu verringert. 2. L-Alanin und 1-Methionin, aber nicht 1-Leuzin verringerten die Speicherung von ABS in den Inseln, die ohne exogene Aminosäuren vorinkubiert worden waren. Nach einer vorherigen Anreicherung mit 1-Alanin wurde ABS verstärkt aufgenommen. 3. D-Glukose, D-Galaktose, Diazoxid, dibutyryl zyklisches 3,5-AMP und D-Manno-heptulose hatten einen geringeren Effekt auf die ABS-Aufnahme. 4. Der Efflux von ABS aus den Inselzellen wurde durch exogenes ABS oder 1-Alanin stimuliert. Es wurde daraus geschlossen, daß dieβ-Zellen des Pankreas einen Mechanismus für den Transport von neutralen Aminosäuren, ähnlich dem A-System mancher anderer Zellen enthalten. Der stimulierende Effekt von Glukose auf die Insulin-Biosynthese scheint nicht durch diesen vermittelt zu sein. Der Ko-Transport von Aminosäuren und Natrium ist wahrscheinlich nicht ausreichend, um Insulin aus der reifenβ-Zelle zu entladen.
    Notes: Summary Transport of α-aminoisobutyric acid (AIB) was studied in microdissected pancreatic islets of obesehyperglycaemic mice. These islets are characterized by an unusually high proportion of insulin-secretingβ-cells. The following main observations were made. 1. The islet cells exhibited a concentrative uptake of AIB, yielding distribution ratios much higher than unity. The uptake was depressed by anoxia and by the omission of sodium from the medium. 2. L-Alanine and L-methionine, but not L-leucine, reduced the accumulation of AIB in islets which had been preincubated in the absence of exogenous amino acid. After preloading with L-alanine there was an enhanced uptake of AIB. 3. D-Glucose, D-galactose, diazoxide, dibutyryl cyclic 3′,5′-AMP, and D-mannoheptulose had minor or insignificant effects on the uptake of AIB. 4. Efflux of AIB from the islet cells was stimulated by exogenous AIB or L-alanine. It is concluded that the pancreaticβ-cells contain a mechanism for transport of neutral amino acids similar to the A-system of many other cells. The stimulating effect of glucose on insulin biosynthesis does not seem to be mediated by this system. Co-transport of amino acid and sodium is probably not enough to elicit a discharge of insulin from matureβ-cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01211878
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