The sum activity of peripheral 5′-deiodinases – theoretically what the peripheral deiodinases produce.
GD is reduced in nonthyroidal illness syndrome (NTIS) and increased in states of hyperdeiodination, and it correlated in two large trials with TSH concentrations, thus mirroring intracellular cAMP levels. (The scope and diversity of hormones and other extracellular signals that activate adenylyl cyclase and increase the level of intracellular cAMP are remarkably extensive. Included in the long list of hormones that signal through this mechanism are β-adrenergic agents, glycoprotein hormones such as TSH, glucagon, adrenocorticotropic hormone (ACTH), hypothalamic hormones, and antidiuretic hormone. (LINK)) These structure parameters may therefore contribute to the diagnosis of rare or at least less obvious thyroid disorders. Additionally, they may facilitate differential diagnosis of primary and secondary disorders of thyroid homeostasis. (LINK)
The inhibitory effects of dopamine were overcome by co-incubation of the cells with dopamine plus 5 X M dibutyryl cyclic AMP (CAMP), indicating that the actions of dopamine may have been mediated by decreasing intracellular CAMP levels (LINK)
Interestingly, among the genes tested, only NIS, Adcy3, Prkar2b and Dio2 mRNA expression are known to be regulated by the second messenger cAMP, through CREB transcription factor. Thus, we next investigated basal cAMP level in mutant, Cre and control thyroids. In Cre thyroids, basal cAMP level was significantly increased, as compared to control thyroids. This is most probably the consequence of the increased TSH bioactivity observed in these mice. Based on this result, basal cAMP level should be markedly increased in mutant thyroids, since TSH bioactivity was about 7 and 4 fold-increased in these mice compared with control and Cre mice, respectively. However, in agreement with a defect in the proximal part of the TSH/cAMP signaling pathway, cAMP level in mutant mice was found only slightly increased when compared with control mice, and severely decreased when compared with Cre mice. Together, our results suggest that mutant mice present a defect in the proximal part of the TSH/TSHreceptor/cAMP signaling pathway. They also confirm that the Pax8Cre/+ mice used to induce recombination have a thyroid dysfunction which is compensated by increased TSH bioactivity. (LINK)
A transcriptional down-regulation of apo E expression by cyclic AMP has been described . We have shown that forskolin mostly does not modify apo E mRNA levels in FAO cells, but completely inhibits the cholesterol-induced apo E expression, leading to the hypothesis that cAMP is involved in this regulation. The low cAMP levels required to observe the effect of cholesterol suggest that it could induce apo E expression by a factor that is, at the same time, negatively regulated by cAMP. (LINK)