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  • 1
    Electronic Resource
    Electronic Resource
    Effect of cholera toxin on insulin release in monolayer cultures of the endocrine pancreas (1974)
    Springer
    Diabetologia 10 (1974), S. 783-787 
    Details
    ISSN: 1432-0428
    Keywords: Insulin release ; cholera toxin ; cyclic AMP ; monolayer culture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of cholera toxin on insulin release by monolayer cultures of endocrine pancreas has been studied. The toxin has a marked stimulatory effect upon insulin release at concentrations as low as 10−10M. The toxin had a small effect at low glucose concentrations, but was strongly stimulatory at high glucose concentrations and in the presence of arginine. Its effect could be detected within 30 min of application and only two minutes' exposure to the toxin was required for it to subsequently stimulate release. In comparative studies on insulin release the toxin was equal to, or slightly more potent than, 1.5 μM glucagon and significantly more potent than cyclic AMP (10 mM) or theophylline (5 mM).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01219541
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  • 2
    Electronic Resource
    Electronic Resource
    Calcium induced glucagon release in monolayer culture of the endocrine pancreas. Studies with ionophore A23187 (1976)
    Springer
    Diabetologia 12 (1976), S. 287-294 
    Details
    ISSN: 1432-0428
    Keywords: Glucagon release ; monolayer culture ; ionophore A23187 ; calcium ; endocrine pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possible role of Ca2+ in glucagon release has been investigated by the use of ionophore A23187. This ionophore permits Ca2+ entry down a suitable concentration gradient by complexing and releasing Ca2+, thereby acting as a carrier in plasma membranes. Cultured cells obtained by enzymatic digestion of pancreases from newborn rats were studied on the third day of culture. As expected the effects of the ionophore were dependent upon the presence of Ca2+ in the medium. However, either stimulation or inhibition of glucagon release resulted when different concentrations of ionophore and Ca2+ were used. With 1.0 mM Ca2+ in the medium, glucagon release was stimulated in the presence of 0.01 and 0.1 μg/ml ionophore, but inhibited in the presence of 3.0 and 10.0 μg/ml. With 0.1 μg/ml ionophore, glucagon release was stimulated by 0.3 and 1.0 mM Ca2+ but not by 2.5 mM Ca2+. With 10 μg/ml ionophore glucagon release was stimulated by 0.03, 0.1 and 0.3 mM Ca2+, whereas at 1.0 mM, glucagon release was depressed. These findings suggest that by increasing Ca2+, glucagon is released from the A-cells, whereas too large an increase in Ca2+ is inhibitory. The effect to stimulate release was not completely specific for Ca2+ in that while the ionophore did not stimulate release in the presence of either Mg2+ or Sr2+ in the absence of Ca2+, it did stimulate release when Ba2+ was tested. Furthermore Ba2+ at 0.3 mM was stimulatory even in the absence of ionophore. Glucagon release in the absence of ionophore was also enhanced by addition of 30 mM Ca2+ or by omission of Ca2+ from the medium. It is concluded that Ca2+, which plays an essential role in the stimulus-secretion coupling in several different cell types, may be involved in the stimulation of glucagon release from the A-cells of the pancreas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00420970
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  • 3
    Electronic Resource
    Electronic Resource
    Studies in vivo and in vitro on chemically-induced primary islet cell tumours and non-tumour endocrine pancreatic tissue (1983)
    Springer
    Diabetologia 24 (1983), S. 30-37 
    Details
    ISSN: 1432-0428
    Keywords: Islet cell tumour ; intravenous glucose tolerance ; primary monolayer culture ; isolated islets ; insulin release ; immunoreactive insulin ; immunoreactive glucagon ; immunoreactive somatostatin ; streptozotocin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rat islet cell tumours induced by injection of streptozotocin and nicotinamide have been studied in vivo and after the establishment of monolayer cultures of tumour cells. During an intravenous glucose tolerance test, tumour-bearing rats had increased release of immunoreactive insulin, with a high proportion of proinsulin, as well as accelerated glucose disposal relative to control rats. The tumours were rich in immunoreactive insulin and somatostatin, poor in glucagon. Non-tumour pancreatic tissue or isolated islets contained 10% or less of the corresponding normal amounts of insulin whereas the islet content of somatostatin was unchanged and that of glucagon increased. This is best interpreted as a selective suppression of non-tumour B cells, further supported by the observation that the initially reduced insulin release and content of non-tumour islets were partially restored after 2 days in tissue culture. In monolayer culture, tumour cells maintained insulin production and acute responsiveness to glucose for prolonged periods. There was no sign of cell proliferation. It is concluded that primary, chemically-induced insulin-producing pancreatic islet cell tumours retain several features characteristic of normal B cells and continue to influence glucose homeostasis in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00275944
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  • 4
    Electronic Resource
    Electronic Resource
    Stimulatory and inhibitory effects of cyclic AMP on pancreatic glucagon release from monolayer cultures and the controlling role of calcium (1976)
    Springer
    Diabetologia 12 (1976), S. 269-277 
    Details
    ISSN: 1432-0428
    Keywords: Monolayer culture ; glucagon release ; cyclic AMP ; Ca++ ; cholera toxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary When glucagon release from monolayer cultures of newborn rat pancreas was measured over four hours in media containing 2.5 mM Ca++, a significant cyclic AMP-related inhibition of release was observed. This was noted whether intracellular cyclic AMP levels were raised by the addition of exogenous cyclic AMP or dibutyryl cyclic AMP, by phosphodiesterase inhibition with theophylline, or by the stimulation of adenylate cyclase with cholera toxin. The inhibition was concentration dependent for cyclic AMP and could not be reproduced by the addition of AMP, ADP or ATP. Adenosine also inhibited glucagon release while ATP was stimulatory. From time course studies it appeared that the inhibitory effects of cyclic AMP and cholera toxin were progressive after two hours of incubation. With cholera toxin an early stimulation of glucagon release was observed. The effects of cyclic AMP and cholera toxin on argininestimulated glucagon release were to stimulate further the glucagon release during the first hour of the incubation. Thus, the effects of raising intracellular cyclic AMP levels were biphasic in that both an early stimulation and a late inhibition of glucagon release were observed. In examining the nature of these responses a remarkable controlling role for Ca++ was uncovered: at Ca++ concentrations of 0.3 mM and lower no effect of cyclic AMP on glucagon release was found. With 1 mM Ca++ in the medium cyclic AMP stimulated glucagon release early (30 min) and thereafter had no further effect. In the presence of 2.5 mM Ca++ cyclic AMP did not stimulate early but did cause the delayed inhibition of release. It is concluded that the effect of cyclic AMP on glucagon release can be either stimulatory or inhibitory depending upon the Ca++ concentration of the medium and the duration of exposure to raised cyclic AMP levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00422095
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  • 5
    Electronic Resource
    Electronic Resource
    Effect of a new hypoglycaemic agent (HB 699) on the in vivo secretion of pancreatic hormones in the dog (1981)
    Springer
    Diabetologia 20 (1981), S. 501-505 
    Details
    ISSN: 1432-0428
    Keywords: Acyl-amino-alcyl benzoic acid derivative ; hypoglycaemic agent ; insulin release ; pancreatic polypeptide ; glucagon ; somatostatin ; tolbutamide ; unanaesthetized dogs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of HB 699, a non-sulphonyl urea acyl-amino-alcyl benzoic acid derivative, were studied in unanaesthetized dogs. Changes in blood glucose and plasma insulin, glucagon, pancreatic polypeptide and somatostatin were measured after a single intravenous injection. HB 699 caused hypoglycaemia and stimulated insulin secretion in a dosedependent manner. The effects of HB 699 (40 mg/ kg) on pancreatic hormone secretion were compared to those of tolbutamide given at a dose (12 mg/kg) which induced a similar maximal hypoglycaemia. Both drugs caused a similar increase in insulin release (180±32% for tolbutamide and 240±41% for HB 699) lasting for approximately 1 hour. Despite hypoglycaemia, plasma glucagon concentrations were unaltered by either substance. HB 699 caused a marked increase in the secretion of pancreatic polypeptide (220±60% at 30 min) for up to 2 hours, whereas tolbutamide caused no significant change in plasma pancreatic polypeptide levels. In contrast, while tolbutamide caused a significant (45±12%) but short-lived increase in plasma somatostatin concentrations, HB 699 had no significant effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00253415
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  • 6
    Electronic Resource
    Electronic Resource
    Cytosolic free Ca2+ in insulin secreting cells and its regulation by isolated organelles (1984)
    Springer
    Cellular and molecular life sciences 40 (1984), S. 1052-1060 
    Details
    ISSN: 1420-9071
    Keywords: Pancreatic B-cell ; insulin secretion ; cytosolic free Ca2+
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The role of Ca2+ in secretagogue-induced insulin release is documented not only by the measurements of45Ca fluxes in pancreatic islets, but also, by direct monitoring of cytosolic free Ca2+, [Ca2+]i. As demonstrated, using the fluorescent indicator quin 2, glyceraldehyde, carbamylcholine and alanine raise [Ca2+]i in the insulin secreting cell line RINm5F, whereas glucose has a similar effect in pancreatic islet cells. The regulation of cellular Ca2+ homeostasis by organelles from a rat insulinoma, was investigated with a Ca2+ selective electrode. The results suggest that both the endoplasmic reticulum and the mitochondria participate in this regulation, albeit at different Ca2+ concentrations. By contrast, the secretory granules do not appear to be involved in the short-term regulation of [Ca2+]i. Evidence is presented that inositol 1,4,5-trisphosphate, which is shown to mobilize Ca2+ from the endoplasmic reticulum, is acting as an intracellular mediator in the stimulation of insulin release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01971451
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  • 7
    Electronic Resource
    Electronic Resource
    Islet cell metabolism is reflected by the MTT (tetrazolium) colorimetric assay (1992)
    Springer
    Diabetologia 35 (1992), S. 482-485 
    Details
    ISSN: 1432-0428
    Keywords: Tetrazolium salt ; glucose metabolism ; insulin secretion ; insulin-secreting cell lines ; islets of Langerhans
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin secretion depends critically on glucose metabolism. We investigated whether a rapid viability test could be established for assessing glucose metabolism in insulin secreting cells. The MTT (C,N-diphenyl-N′-4,5-dimethyl thiazol 2 yl tetrazolium bromide) colorimetric assay (reduction of tetrazolium salt to formazan) was applied to rat islets and rat insulinoma cell lines. It was found that the rate of formazan production correlated with glucose oxidation and glucose utilization at glucose concentrations which also stimulated insulin secretion. In differentiated insulinoma INS-1 cells, salt reduction paralleled the insulin release, at glucose concentrations of up to 8.3 mmol/l. The glucose-induced formazan production in INS-1 cells and islets was abolished by exposure to the Beta-cell cytotoxic agents, streptozotocin or alloxan. The MTT assay thus provides a convenient tool for the rapid assessment of Beta-cell metabolism and viability.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02342448
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  • 8
    Electronic Resource
    Electronic Resource
    Functional and morphological abnormalities of mitochondria harbouring the tRNALeu(UUR) mutation in mitochondrial DNA derived from patients with maternally inherited diabetes and deafness (MIDD) and progressive kidney disease (1999)
    Springer
    Diabetologia 42 (1999), S. 485-492 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Mitochondrial DNA ; diabetes mellitus ; deafness ; haplotype ; mutation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. An A to G transition at nucleotide position 3243 in the mitochondrial tRNA Leu(UUR) gene has been identified in patients with maternally inherited diabetes and deafness, as well as in patients with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes, chronic progressive external ophpthalmoplegia, cardiomyopathy and progressive kidney disease. Variations in the mitochondrial DNA haplotype as well as differences in the degree and distribution of heteroplasmy in a certain tissue are factors that may contribute to the variety in phenotypical expression of the 3243 tRNA Leu(UUR) mutation. We have done morphological and functional experiments on mitochondria carrying the 3243 mutation derived from patients with either maternally inherited diabetes and deafness or progressive kidney disease to prove the pathogenicity of the 3243 mutation and to examine whether the mtDNA haplotype modulates the pathobiochemistry of this mutation. Methods. We constructed clonal cell lines that contain predominantly mutated or exclusively wild-type mtDNA with a distinct mtDNA haplotype by the methodology of mitochondria-mediated transformation. Cells lacking mitochondrial DNA (ϱ°) were used as recipients and donor mitochondria were derived from fibroblasts of a patient with either maternally inherited diabetes and deafness or progressive kidney disease. The fibroblasts from these clinically distinct patients carry different mitochondrial DNA haplotypes with the 3243 mutation in heteroplasmic form. Results. Heteroplasmy in the clonal cybrid cells ranged from 0 to 100 %, reflecting the heterogeneity of the mitochondrial donor cell. Cybrid cells containing predominantly mutant mitochondrial DNA showed lactic acidosis, poor respiration and marked defects in mitochondrial morphology and respiratory chain complex I and IV activities. No differences were observed in the extent of the mitochondrial dysfunction between the mutant cells derived from the two donors. Conclusion/interpretation. These results provide evidence for a pathogenic effect of the tRNA Leu(UUR) mutation in maternally inherited diabetes and deafness and progressive kidney disease, and show no evidence of a contribution of the mitochondrial DNA haplotype as a modulating the biochemical expression of the mutation. [Diabetologia (1999) 42: 485–492]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051183
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  • 9
    Electronic Resource
    Electronic Resource
    Eighth annual meeting of the European Association for the Study of Diabetes (1973)
    Springer
    Diabetologia 9 (1973), S. 57-96 
    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/BF01226005
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  • 10
    Electronic Resource
    Electronic Resource
    Beta-cell mitochondria in the regulation of insulin secretion: a new culprit in Type II diabetes (2000)
    Springer
    Diabetologia 43 (2000), S. 265-277 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Beta-cell dysfunction, mitochondrial metabolism, mitochondrial DNA, exocytosis, ATP, cytosolic Ca2+, mitochondrial Ca2+, ϱ0 cells, HNF-1α, MODY.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Insulin is stored in secretory granules in the beta-cell and is secreted by exocytosis. This process is precisely controlled to achieve blood glucose homeostasis. Many forms of diabetes mellitus display impaired glucose-induced insulin secretion. This has been shown to be the primary cause of the disease in the various forms of maturity-onset diabetes of the young (MODY) and has also been implicated in adult-onset Type II (non-insulin-dependent) diabetes mellitus. Glucose generates ATP and other metabolic coupling factors in the beta-cell mitochondria. By plasma membrane depolarisation ATP promotes Ca2+ influx, which raises cytosolic Ca2+ and triggers insulin exocytosis. Through hyperpolarisation of the mitochondrial membrane glucose also increases the Ca2+ concentration in the mitochondrial matrix activating Ca2+-sensitive dehydrogenases in the tricarboxylic acid cycle. The resulting generation of glutamate participates in Ca2+-stimulated exocytosis. Mitochondrial DNA (mtDNA) encodes some of the polypeptides of the respiratory chain enzyme complexes. Mutations in mtDNA lead to maternally inherited diabetes mellitus characterised by impaired insulin secretion. The impact of altered mtDNA on insulin secretion has been shown in mtDNA-deficient beta-cell lines which have lost glucose-stimulated insulin secretion but retain a Ca2+-induced insulin secretion. A cellular model of MODY3 expressing dominant-negative hepatocyte nuclear factor-1α (HNF-1α) also displayed deletion of glucose-induced but not Ca2+-induced insulin secretion. Reduced mitochondrial metabolism explains this secretory pattern. Thus, genetically manipulated beta-cell lines are essential tools in the investigation of the molecular basis of beta-cell dysfunction in diabetes and should explain the role of other transcription factors in the disease. [Diabetologia (2000) 43: 265–277]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050044
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