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Iodine Research

Resource Network of The Iodine Movement

                                               Iodine and the Body


Thus far, there is very little research on the effect of iodine on the adrenals.  However, it seems likely
that iodine does affect the adrenals.

Moreover, the adrenal hormones (especially hydrocortisone) affect iodide uptake in the thyroid.

Escobar, et al, examined the effects of various levels of iodine on thyroid hormone levels in different
body tissues, including the adrenals.  They found that iodine levels in the adrenals have a marked
effect on T3 as well as T4.  Increasing levels of iodine deficiency resulted in greatly reduced levels of
T3, even lower than T3 levels in the blood.

Kohn and Takiyama found that hydrocortisone affects iodide uptake in the thyroid.

Mechanisms of adaptation to iodine deficiency in rats: thyroid status is tissue specific. Its relevance
for man.
Pedraza PE, Obregon MJ, Escobar-Morreale HF, del Rey FE, de Escobar GM.
Endocrinology. 2006 May;147(5):2098-108. Epub 2006 Feb 2.

As already described for the liver, lung, brain, and BAT, the patterns of change in T3 varied greatly
among these other tissues.  The greatest difference was found between the patterns for the ovary
and adrenal.  In the ovary there is a very remarkable increase of T3... On the contrary, T3 in the
adrenal decreases steadily with decreasing I availability, almost in parallel to adrenal T4, and more
markedly than circulating T3; values in the adrenals of LID' [Low Iodine Diet + perchlorate] animals
are only 17% of those of the C [Control -- adequate iodine] group, whereas plasma T3 is still 46%.  
As already described above for the lung, the muscle and heart maintained normal T3 concentrations,
even in LID' animals.  In these animals, T3 decreased only in the cerebellum, pituitary, and kidney
and did so only to 67-73% of C values, less than the decrease in circulating T3."

"The lack of increase of T3 content of the adrenals had also not been anticipated because this
tissue has been considered dependent on serum-derived T3."

"In summary, both intra-and extrathyroidal mechanisms are involved in the response of the rat to mild
ID: the former are autoregulatory and very effective in avoiding T3 deficiency in most tissues, and
the latter occur in tissues in which D2 is important for local generation of T3.  In mild ID,
hypothyroidism, as inferred from the concentrations of T3, is avoided in all tissues studied.

Effect of hydrocortisone on the ability of thyrotropin to increase deoxyribonucleic acid synthesis and
iodide uptake in FRTL-5 rat thyroid cells: opposite regulation of adenosine 3',5'-monophosphate
signal action.
Saji M, Kohn LD.
Endocrinology. 1990 Oct;127(4):1867-76.

In FRTL-5 rat thyroid cells, hydrocortisone alters two TSH-increased cAMP-mediated activities in an
opposite manner. Thus, in a concentration-dependent fashion, hydrocortisone synergistically
enhances TSH-increased thymidine incorporation into DNA, whereas it inhibits TSH-induced iodide
uptake. The effect of hydrocortisone on TSH-increased thymidine incorporation is specific, in that it
has only a minimal ability by itself to increase thymidine incorporation into DNA and slightly inhibits
the activity of insulin or insulin-like growth factor-I. The effect of hydrocortisone on TSH-induced
iodide uptake does not result from altered iodide efflux, but, rather, from a decrease in the maximal
velocity, not the Km, of iodide influx, i.e. from a decrease in the effective number of iodide porters.
The action of a cAMP analog to increase thymidine incorporation into DNA or iodide uptake was also
increased or decreased, respectively, by hydrocortisone, whereas hydrocortisone did not diminish
the ability of TSH to increase cAMP levels in the cells. The different effect of hydrocortisone on these
two cAMP-mediated activities reflects, therefore, regulation of cAMP signal action rather than the
ability of TSH to generate a cAMP signal. Twenty-four hours after TSH, actinomycin-D superinduces
iodide uptake and abolishes the action of hydrocortisone to inhibit iodide uptake. It has been
suggested that actinomycin-D superinduces iodide uptake in FRTL-5 cells by a posttranscriptional
action, inhibition of mRNA degradation, rather than by its known transcriptional actions linked to DNA
synthesis. More recent studies of the effect of actinomycin-D, given under identical circumstances,
on TSH-stimulated malic enzyme mRNA levels directly validate this hypothesis. We, thus, suggest
that the opposite action of hydrocortisone on the two cAMP-mediated activities may reflect positive
and negative regulation of the action of cAMP at different steps in the transduction process, one
being transcriptional (DNA synthesis) and the other posttranscriptional (induction of iodide porter

The effects of hydrocortisone and RU486 (mifepristone) on iodide uptake in porcine thyroid cells in
primary culture.
Takiyama Y, Tanaka H, Takiyama Y, Makino I.
Endocrinology. 1994 Nov;135(5):1972-9.

The effects of hydrocortisone on iodide uptake and DNA synthesis were studied in porcine thyroid
cells cultured in phenol red-free medium supplemented with low concentrations (0-1%) of
charcoal-stripped fetal calf serum. Hydrocortisone dose-dependently stimulated TSH-induced iodide
uptake at physiological concentrations (1-1000 nM), and the minimum detectable dose was 33 nM
hydrocortisone. Treatment of thyroid cells with hydrocortisone for 72 h increased cAMP production
stimulated by TSH. In addition, this stimulatory effect of hydrocortisone was observed when iodide
uptake was induced with 0.25 mM 8-bromo-cAMP. These results suggest that hydrocortisone
stimulates iodide uptake, influencing cAMP production and post-cAMP pathways. The synthetic
glucocorticoid antagonist RU486 alone had no effect on iodide uptake in porcine thyroid cells;
however, along with TSH, RU486 a weak agonist activity. As a glucocorticoid antagonist, RU486
inhibited the stimulatory actions of hydrocortisone on iodide uptake in combination with TSH and also
with 8-bromo-cAMP, suggesting a specific effect of hydrocortisone mediated by a glucocorticoid
receptor. The effect of hydrocortisone on thyroid cell multiplication was also studied. Hydrocortisone
decreased [3H]thymidine incorporation into DNA slightly but not significantly when the cells were
treated with 100 ng/ml insulin-like growth factor-I and hydrocortisone. In summary, it has been
demonstrated that hydrocortisone directly stimulated the function of porcine thyroid cells at
physiological concentrations, by using a glucocorticoid receptor and by affecting cAMP pathways.
The data that RU486 inhibited iodide uptake induced by hydrocortisone and TSH propose that
monitoring of thyroid function may be necessary if RU486 is been used for a long time.