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  • DBA2 mice  (1)
  • Inhibitory peptides  (1)
  • Islets of Langerhans  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Protein phosphorylation in the regulation of insulin secretion: the use of site-directed inhibitory peptides in electrically permeabilised islets of Langerhans (1995)
    Springer
    Acta diabetologica 32 (1995), S. 32-37 
    Details
    ISSN: 1432-5233
    Keywords: Islet of Langerhans ; Insulin secretion ; Protein phosphorylation ; Protein kinase C ; Protein kinase A ; Inhibitory peptides
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have used electrically permeabilised rat islets of Langerhans to investigate the role of protein phosphorylation in the regulation of insulin secretion using pseudosubstrate inhibitory peptides for cyclic AMP-dependent protein kinase (PKA) and for protein kinase C (PKC). The protein kinase inhibitor (PKI) peptide, PKI(6–22), completely inhibited the effects of cyclic AMP on islet PKA activity in vitro, on endogenous protein phosphorylation and on insulin secretion. This peptide had no significant effect on islet PKC activity in vitro, on CA2+-induced protein phosphorylation and on secretory responses to Ca2+ or to the PKC activator, 4β-phorbol myristate acetate (PMA). The PKC pseudosubstrate inhibitory peptide, PKC(19–36), caused a marked inhibition of islet PKC activity in vitro and inhibite PMA-induced insulin secretion without affecting secretory responses to cyclic AMP and Ca2+. These results demonstrate that PKA-and PKC-induced protein phosphorylation is obligatory for cyclic AMP-and PMA-stimulated insulin secretion, respectively, and suggest that there is little “crosstalk” between the response elements of the secretory pathways to the different, second messengers, at least after the generation of the messengers within the β-cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00581042
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Regulation of insulin secretion: the role of second messengers (1994)
    Springer
    Diabetologia 37 (1994), S. S30 
    Details
    ISSN: 1432-0428
    Keywords: Islets of Langerhans ; insulin secretion ; protein kinase A ; cyclic AMP ; calcium-calmodulin ; protein kinase C ; arachidonic acid ; nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This review summarises briefly studies performed in the last 5–6 years concerning the role of second messengers in the regulation of insulin secretion, using intact and electrically permeabilized rat islets of Langerhans. It is concluded that cyclic AMP (through protein kinase A), calcium (through calcium-calmodulin dependent protein kinases) and diacylglycerol (through protein kinase C) may be important second messengers in modulating the effects of specific secretagogues on insulin release. However, recent studies strongly suggest that neither protein kinase A nor protein kinase C are directly involved in the regulation of insulin secretion by glucose. The possible involvement of other second messengers, nitric oxide and arachidonic acid, in the regulation of secretion is also briefly reviewed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400823
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Biochemical and ultrastructural changes in A and B cells of the islets of Langerhans of mice infected with EMC virus (1979)
    Springer
    Diabetologia 17 (1979), S. 51-57 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes ; EMC virus ; DBA2 mice ; islets of Langerhans ; ultrastructure ; insulin ; glucagon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Infection of DBA2 mice with the M strain of EMC virus was used to study the effects of virusinduced diabetes on the A and B cells of the islets of Langerhans. A transient hypoglycaemia was seen in 48% of mice 2–3 days after infection and probably resulted from increased serum insulin concentrations together with inhibition of glucagon secretion at that time. Islets from hypoglycaemic mice showed no significant alterations from control level in basal or fluoride-stimulated adenylate cyclase activity. Overall, 70% of infected mice became hyperglycaemic with a maximum incidence 6 days after infection. Hyperglycaemia was accompanied by a dramatic reduction in the total pancreatic insulin content and in insulin secretory responses to glucose and theophylline, while A-cell structure and function appeared relatively unaffected in diabetic animals. Basal adenylate cyclase activity was increased in hyperglycaemic mice at 7 days after infection, while fluoride-stimulated adenylate cyclase activity was normal throughout the course of infection. Ultrastructural alterations were observed in a small proportion of B cells from two days after infection and included abnormalities of mitochondrial structure and increased electron opacity of the cytoplasm of affected cells, which subsequently led to complete necrosis. The results suggest that EMC virus specifically affects the B cells of the islets and that disturbances of A cell function may be secondary to B cell damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01222978
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    Paper (German National Licenses)
    Fulltext
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