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  • Electronic Resource  (3)
  • nitric oxide  (2)
  • Growth hormone  (1)
  • 1
    ISSN: 1432-0428
    Keywords: Islet of Langerhans ; insulin secretion ; nitric oxide ; cyclic guanosine monophosphate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The involvement of nitric oxide as an intracellular messenger in the control of insulin secretion from pancreatic Beta cells was studied in rat islets of Langerhans by measuring: (i) nitric oxide generation in response to physiological insulin secretagogues; (ii) the effects of inhibitors of nitric oxide synthesis on insulin secretory responses to physiological secretagogues, and on insulin synthesis; (iii) changes in islet cyclic guanosine monophosphate in response to secretagogues; (iv) the effects of exogenous cyclic guanosine monophosphate and dibutyryl cyclic guanosine monophosphate on insulin secretion from electrically permeabilised islets and from intact islets, respectively. These studies produced no evidence that nitric oxide generation is required for the initiation of insulin secretion by common secretagogues. However, the results of our experiments suggest that the generation of nitric oxide may be involved in long-term, glucose-dependent increases in cyclic guanosine monophosphate content of islet cells, although the physiological relevance of these changes requires further investigation.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 37 (1994), S. S30 
    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
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 190 (1978), S. 163-171 
    ISSN: 1432-0878
    Keywords: Growth hormone ; Somatotrophs ; Microtubules ; Colchicine, vinblastine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Pulse-chase experiments utilising(3H)leucine have been used to study the effects of colchicine and vinblastine on intracellular transport and secretion of newly synthesised growth hormone from rat anterior pituitary fragments. Growth hormone was isolated from medium and fragments by polyacrylamide gel electrophoresis. When colchicine or vinblastine, which disrupt microtubules, were added immediately after pulse labelling, inhibition of the subsequent secretion of newly synthesised growth hormone was detected throughout the succeeding 5 h. Similar inhibition was seen if the drugs were added after a 1 h delay. However, if colchicine or vinblastine were added only after a 2 h chase incubation, then no significant effect on subsequent release of labelled growth hormone was seen. The results suggest that these agents may inhibit the transport of newly formed growth hormone storage granules from the Golgi complex to the cytoplasmic pool. Microtubules do not appear to be involved in the mechanism of the final secretion of newly synthesised hormone by exocytosis.
    Type of Medium: Electronic Resource
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