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  • 1
    Electronic Resource
    Electronic Resource
    Morphological characterization of membrane systems in A- and B-cells of the Chinese hamster (1974)
    Springer
    Diabetologia 10 (1974), S. 529-539 
    Details
    ISSN: 1432-0428
    Keywords: Chinese hamster ; Cricetulus griseus ; endocrine pancreas ; islet of Langerhans ; A-cells ; B-cells ; D-cells ; spontaneous diabetes ; nuclear pores ; plasma membrane ; membrane-associated particles ; glycogen ; ultrastructure ; electron microscopy ; freeze-etching
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The nuclear and plasma membranes of islet cells from non-glycosuric and diabetic Chinese hamsters were examined by freeze-etching. The B-cells of diabetic animals presented a slight increase in the number of nuclear pores and marked alterations in the number, size and distribution of membrane-associated particles in the plasma membrane. In A-cells, identified by the presence of characteristic bundles of coarse filaments in the perinuclear region, a definite increase in the number of nuclear pores was found in the most severely diabetic animals. These preliminary findings point to alterations in the membrane systems as possible determinants for the abnormalities of islet function in diabetes mellitus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01221983
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  • 2
    Electronic Resource
    Electronic Resource
    Dynamics of calcium-induced insulin release (1977)
    Springer
    Diabetologia 13 (1977), S. 531-536 
    Details
    ISSN: 1432-0428
    Keywords: Ca2+ ; insulin release ; Mg2+ ; verapamil ; somatostatin ; cytochalasin B ; glucose ; theophylline ; perfused pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Extracellular Ca2+, at concentrations exceeding 10 mmol/l, causes a dose-related stimulation of insulin release. The dynamics of Ca2+-induced insulin release are characterized by a quick onset, a progressive build-up and a later return towards basal secretory rate. The release of insulin evoked by Ca2+ is inhibited in the presence of either Mg2+ (10 mmol/l) or the organic Ca2+-antagonist verapamil (81 μmol/l), both of which are known to inhibit Ca2+ entry in the B-cell. Glucose and theophylline, which are thought to affect the net uptake or intracellular distribution of Ca2+ in the B-cell, both enhance Ca2+-induced insulin release. As little as 2.7 mmol/l glucose is sufficient to augment Ca2+-induced insulin secretion. Exposure of the pancreas to somatostatin significantly retards the secretory response to Ca2+. Cytochalasin B potentiates the insulin release evoked by Ca2+ (12 mmol/l) and lowers the threshold concentration of Ca2+ required to stimulate secretion. These data suggest that high extracellular Ca2+ concentrations may sufficiently increase the amount of Ca2+ accumulated in the B-cell to eventually trigger insulin release. Agents known to cause a remodelling of Ca2+ fluxes across membrane systems in the B-cell interfere with Ca2+-induced insulin release, a process also dependent on the integrity of the cytochalasin B-sensitive microfilamentous effector system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01234509
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  • 3
    Electronic Resource
    Electronic Resource
    Interactions of α-ketoisocaproate, glucose and arginine in the secretion of glucagon and insulin from the perfused rat pancreas (1979)
    Springer
    Diabetologia 17 (1979), S. 121-126 
    Details
    ISSN: 1432-0428
    Keywords: α-ketoisocaproate ; KIC ; arginine ; glucose ; glucagon release ; insulin release ; perfusion ; rat pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects ofα-ketoisocaproate (KIC, 10 mmol/l) on glucagon and insulin release were studied in the in vitro perfused rat pancreas. The experiments were performed at low glucose concentration (3.3 mmol/l) in the absence or presence of arginine (10 mmol/l). In all the experiments KIC induced a marked and not rapidly reversible inhibition of glucagon release. This inhibition was more pronounced in the absence (76 percent) than presence of arginine (61 percent). These inhibitory patterns closely duplicated those which were seen in parallel experiments which included a rise in the concentration of glucose (from 3.3 to 11.1 mmol/l). KIC was also a potent stimulator of insulin release. The results are compatible with the view that the intracellular metabolism of KIC and glucose plays an essential role in the regulation of glucagon release by exogenous substrates.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01222213
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  • 4
    Electronic Resource
    Electronic Resource
    Dynamics of O2 consumption in rat pancreatic islets (1980)
    Springer
    Diabetologia 18 (1980), S. 395-405 
    Details
    ISSN: 1432-0428
    Keywords: Islets ; insulin release ; glucose ; 2-oxo acids ; O2 consumption ; respiration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The O2 consumption of rat pancreatic islets was determined by monitoring pO2 in the perifusate from groups of 200–300 islets. Basal respiration was maintained for up to 2 h. The insulin secretagogues, glucose and 4-methyl-2-oxopentanoate, provoked an immediate (〈5 s) increase in islet respiration which attained a new steady-state within 10–40 min. The respiratory changes were immediately reversible upon removal of the substrate and were parallelled by changes in insulin release and substrate oxidation. The concentration dependence of glucose-induced respiratory changes was sigmoidal with a threshold at 3 mmol/l. The concentration dependence with 4-methyl-2-oxopentanoate was characterised by a hyperbolic relationship. The weak insulin secretagogues 3-methyl-2-oxobutyrate and d,1-3-methyl-2-oxopentanoate, although stimulating islet respiration were not more effective than 4-methyl-2-oxopentanoate at non-insulinotropic concentrations. Rotenone, antimycin and oligomycin inhibited both basal O2 consumption and the ability of glucose and 4-methyl-2-oxopentanoate to increase islet respiration. 2,4-Dinitrophenol increased islet O2 consumption. The omission of Ca2+ and Mg2+ from the perifusing media, or the addition of the ionophore A23187, had little effect on respiration. The omission of K+ inhibited glucose-induced changes but had a lesser effect in the absence of substrate or in the presence of 4-methyl-2-oxopentanoate. The omission of HCO3 - reduced both basal and secretagogue-induced changes in islet respiration. It is concluded that mitochondrial O2 consumption linked to oxidative phosphorylation is a major component in the respiratory response, and that some energy consuming process in the islets depends on the availability of HCO3 -. Mitochondrial reactions may generate a signal initiating the secretory process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00276821
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  • 5
    Electronic Resource
    Electronic Resource
    The role of calcium in glucagon release, interactions between glucose and calcium (1976)
    Springer
    Diabetologia 12 (1976), S. 531-538 
    Details
    ISSN: 1432-0428
    Keywords: Glucagon release ; insulin release ; pefused rat pancreas ; calcium ; glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The interrelationships between glucose and calcium in glucagon release were investigated using the dynamic system of the in vitro perfused rat pancreas. When calcium deprivation was induced in the presence of fixed concentrations of glucose prevailing throughout the experiments (3.3, 5.5, 8.3 and 16.6 mM), an enhancement of glucagon release invariably occurred, the shape and amplitude of such response differing in relation to the environmental glucose concentration. Such enhancement of glucagon release was readily reversible upon restoration of normal calcium levels. By contrast, during the period of calcium deprivation itself, glucagon release was little influenced by either raised (from 3.3 to 16.6 mM) or decreased (from 16.6 to 3.3 mM) glucose concentrations. These results clearly indicate that calcium plays, at least, a dual role — both inhibitory and permissivein glucagon secretion, but the intimate mechanisms by which calcium exerts such a dual action are at present unknown.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01219520
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  • 6
    Electronic Resource
    Electronic Resource
    Insulinotropic effects of hypoglycaemic and hyperglycaemic sulphonamides: The ionophoretic hypothesis (1980)
    Springer
    Diabetologia 19 (1980), S. 335-340 
    Details
    ISSN: 1432-0428
    Keywords: Hypoglycaemic sulphonylureas ; diazoxide ; calcium ; insulin release ; ionophores ; organic calcium antagonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hypoglycaemic sulphonamides stimulate net uptake of 45Ca++ and insulin release in isolated pancreatic islets. These effects are antagonized by organic calcium-antagonists (e.g. suloctidil). In an artificial system, hypoglycaemic sulphonamides, such as gliclazide, stimulate the translocation of calcium into or across a hydrophobic immiscible domain, a process enhanced by the antibiotic ionophore A 23187 and antagonized by suloctidil. In this artificial system, the A 23187-mediated process of calcium countertransport is stimulated by gliclazide and inhibited by diazoxide. It is postulated that the insulinotropic action of hypoglycaemic and hyperglycaemic sulphonamides is primarily attributable to the ionophoretic action of these drugs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00280516
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  • 7
    Electronic Resource
    Electronic Resource
    The stimulus-secretion coupling of glucose-induced insulin release (1980)
    Springer
    Diabetologia 19 (1980), S. 458-464 
    Details
    ISSN: 1432-0428
    Keywords: Isolated rat islets ; phosphate flush ; glucose ; α-ketoisocaproate ; leucine ; glutamine ; lactate ; quinine ; menadione ; antimycin A ; barium ; potassium ; bicarbonate ; calcium ; theophylline ; tolbutamide ; arginine ; anoxia ; cyclic AMP ; insulin release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Above a threshold of 3.0–4.2 mmol/l, D-glucose provoked a transient increase in 32P fractional outflow rate from rat pancreatic islets prelabelled with 32P-orthophosphate. Nutrients which stimulate insulin release in the absence of glucose, α-ketoisocaproate and L-leucine, also provoked a phosphate flush. No flush occurred in islets exposed to non-insulinotropic nutrients (L-glutamine and L-lactate) or non-nutrient secretagogues (arginine, tolbutamide, theophylline). A late increase in 32P fractional outflow rate was observed in Ca2+ deprived islets stimulated with BaCl2 and theophylline. The occurrence of a phosphate flush did not appear to be attributable to changes in insulin release, cyclic AMP content, membrane polarisation, K+ conductance, or reduced pyridine nucleotide content. The 32P response to glucose was slightly decreased in the absence of extracellular Ca2+ or HCO3 -, markedly impaired in the absence of K+, and virtually abolished in the presence of menadione (10 μmol/l). It is proposed that the occurrence of a phosphate flush is linked to the metabolism of nutrient secretagogues, possibly via an increase in O2 uptake and the production rate of NAD(P)H and ATP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00281826
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  • 8
    Electronic Resource
    Electronic Resource
    Role of glucose and insulin in the dynamic regulation of glucagon release by the perfused rat pancreas (1983)
    Springer
    Diabetologia 24 (1983), S. 191-195 
    Details
    ISSN: 1432-0428
    Keywords: Glucose ; rat ; glucagon release ; insulin release ; perfused rat pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of glucose upon the release of glucagon and insulin from the perfused rat pancreas in vitro was studied by varying both the concentration of glucose (from 3.3 to 4.6, 8.5, or 11.1 mmol/l) and the time of exposure to an elevated concentration of the sugar (5, 10 or 23 min). The results suggest that the amount of insulin released during the early period of stimulation could contribute to both the speed and extent of the inhibition in glucagon release. The rate of recovery from inhibition in the A cell, however, appeared to be independent of insulin and was related, in a dose-dependent and time-dependent manner, only to the glucose stimulus. It is suggested that a direct effect of glucose upon the A cell is involved in the physiological regulation of glucagon secretion. An indirect effect of glucose, as mediated via insulin release, may contribute to the rapidity and magnitude of inhibition in A cell secretory activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00250160
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  • 9
    Electronic Resource
    Electronic Resource
    The insulinotropic action of D-erythrose (1977)
    Springer
    Diabetologia 13 (1977), S. 125-130 
    Details
    ISSN: 1432-0428
    Keywords: Insulin secretion ; glucose ; erythrose ; calcium ; isolated islets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary D-erythrose (5.0 to 20.0 mM) stimulates insulin release. This insulinotropic action of erythrose displays several features in common with that of glucose. First, erythrose (20 mM) causes a shift to the left of the sigmoidal curve relating the secretory rate to the glucose concentration, but fails to enhance the maximal response to glucose. Second, the secretory response to erythrose occurs as an early peak followed by a phase of sustained release. Third, erythrose increases the output of lactate from the islets. Last, erythrose inhibits the efflux of45calcium and favours its accumulation in isolated islets. It is suggested that, whether in response to glucose or erythrose, an increase in glycolytic flux may represent the key process involved in the identification of the secretagogue, a subsequent remodelling of calcium fluxes being apparently responsible for the activation of the insulin-releasing system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00745139
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  • 10
    Electronic Resource
    Electronic Resource
    Possible role of a microtubular-microfilamentous system in glucagon secretion (1974)
    Springer
    Diabetologia 10 (1974), S. 215-224 
    Details
    ISSN: 1432-0428
    Keywords: Glucagon release ; insulin release ; pancreatic pieces ; microtubular-microfilamentous system ; cytochalasin B ; colchicine ; vinblastine ; deuterium oxide ; arginine ; glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of a microfilament-modifier (cytochalasin B), of mitotic spindle-inhibitors (colchicine and vinblastine) and of a microtubule-stabilizer (D2O) on glucagon secretion were studied in vitro, using pieces of pancreas from duct-ligated rats. Cytochalasin B (10 μg/ ml) potentiated arginine-induced glucagon release, but was without effect on unstimulated glucagon release. Colchicine (10−4M) and vinblastine (10−4M) similarly stimulated arginine-induced glucacon release; colchicine did not affect unstimulated glucagon release. Deuterium oxide (100%, v/v) reversibly inhibited arginine-induced glucagon secretion. If it is assumed that the above mentioned drugs specifically interact with microfilaments and microtubules in the A2 cells, our results would suggest that a microtubular-microfilamentous system indeed participates in the process of glucagon secretion. The intimate mechanism by which such a system may apparently play both a restrictive and effector role in glucagon release remains, however, to be elucidated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00423038
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