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Forskolin stimulates adenylate cyclase and idodine metabolism in thyroid
Author(s) -
van Sande J.,
Cochaux P.,
Dumont J.E.
Publication year - 1982
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(82)81321-5
Subject(s) - adenylate kinase , cyclase , forskolin , endocrinology , thyroid , medicine , chemistry , metabolism , biochemistry , biology , enzyme , receptor
Forskolin is a potent activator of the cyclic AMP‐generating system in many tissues. In dog thyroid slices, the enhancement of cyclic AMP level was rapid, sustained in the presence of forskolin, but easily reversible after its withdrawal. Contrary to TSH, forskolin induced little apparent desensitization. Forskolin potentiated the effects of TSH, PGE 1 and cholera toxin. However, the forskolin‐induced cyclic AMP accumulation was still sensitive to inhibitors of dog thyroid adenylate cyclase such as iodide, norepinephrine and adenosine. As fluoride, but contrary to TSH and PGE 1 , forskolin stimulated adenylate cyclase in a medium where Mg 2+ was replaced by Mn 2+ . This suggests that in thyroid, as in other tissues, forskolin acts beyond the receptor level but, as it potentiates hormone action and does not impair modulation by inhibitors, it may interact with the nucleotide‐binding regulatory proteins. Forskolin mimicked the effect of TSH on iodide organification and secretion.