Abstract
It has been previously demonstrated that DBI is present in endocrine pancreas and it is able to inhibit insulin release in isolated rat islets. Its mechanism of action has been investigated, demonstrating the possible involvement of cAMP and ATP-dependent K(+) channels. DB1(33-50), a post-translational product of DBI, is also able to inhibit insulin release, but its action has not been characterized. In the present study, we have investigated the presence of DBI mRNA in pancreas, islets and cultured ß cells. The possible mechanism of action of DBI(33-50) and the involvement of BZ/GABA(A) receptors has been studied.
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