Abstract:
:Although insulin secretion is usually regarded as a Ca2+-dependent mechanism, recent studies have suggested the existence of a Ca2+-independent pathway of regulation by glucose. Here, mouse islets were used to compare the contribution of Ca2+-dependent and -independent pathways. Glucose increased insulin release in a concentration-dependent manner both in a control medium, when it depolarizes beta cells and raises [Ca2+]i (triggering signal), and in the presence of 30 mM K+ and diazoxide, when it does not further raise [Ca2+]i but increases its efficacy on exocytosis. Both Ca2+-dependent responses were amplified by glucagon-like peptide-1+acetylcholine, and were strongly potentiated by forskolin+PMA. Under conditions of mild or stringent Ca2+ deprivation, glucose had no effect either alone or with GLP-1 and acetylcholine, and was poorly effective even during pharmacological activation of protein kinases A and C. Similar results were obtained with rat islets. It is concluded that physiological regulation of insulin release by glucose is essentially achieved through the two Ca2+-dependent pathways without significant contribution of a Ca2+-independent mechanism.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Sato Y,Nenquin M,Henquin JCdoi
10.1016/s0014-5793(97)01547-0subject
Has Abstractpub_date
1998-01-09 00:00:00pages
115-9issue
2eissn
0014-5793issn
1873-3468pii
S0014-5793(97)01547-0journal_volume
421pub_type
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