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Thyroxine conversion

Only small amounts of free T are present in plasma. Most T is bound to the specific carrier, ie, thyroxine-binding protein. T, which is very loosely bound to protein, passes rapidly from blood to cells, and accounts for 30—40% of total thyroid hormone activity (121). Most of the T may be produced by conversion of T at the site of action of the hormone by the selenoenzyme deiodinase (114). That is, T may be a prehormone requiring conversion to T to exert its metaboHc effect (123). [Pg.386]

The formation of triiodothyronine (T3) and tetra-iodothyronine (thyroxine T4) (see Figure 42—2) illustrates many of the principles of diversity discussed in this chapter. These hormones require a rare element (iodine) for bioactivity they are synthesized as part of a very large precursor molecule (thyroglobuhn) they are stored in an intracellular reservoir (colloid) and there is peripheral conversion of T4 to T3, which is a much more active hormone. [Pg.447]

The concentration of Li+ in the thyroid is three to four times that in serum [179]. It is thought that Li+ may be concentrated in the thyroid gland by a mechanism similar to the incorporation of iodide, I-, resulting in competition between Li+ and I the levels of intracellular 1 decrease when those of Li+ increase, and vice versa [182]. Li+ inhibits both the ability of the gland to accumulate 1 and the release of iodine from the gland. In vitro, Li+ has no effect on thyroid peroxidase, the enzyme that catalyzes the incorporation of I" into tyrosyl residues leading to thyroidal hormone synthesis, but does increase the activity of iodotyrosine-deio-dinase, which catalyzes the reductive deiodination of iodotyrosyls, thus maintaining the levels of intracellular I [182]. The increase in iodoty-rosine-deiodinase activity is probably a response to the Li+-induced decrease in the concentration of thyroidal I". Li+ has no effect on the conversion of thyroxine to triiodothyronine. The overall effect of this competition between Li+ and 1 is, therefore, reduced levels of thyroid hormone in the presence of Li+. [Pg.32]

Mercuric chloride, given for short time, has been reported to inhibit Na + /K + -ATPase in hog thyroid membranous preparation [149]. The blood T4 (thyroxine) levels were reduced and iodotyrosine deiodinase was inhibited, and it was suggested that mercurials might cause a coupling defect in the synthesis of iodothyronines. In mouse thyroid serum T4 level was affected by mercuric chloride, while serum T3 was not [ 150 ]. It was suggested that thyroidal secretion of T4 was inhibited by mercuric chloride, but the peripheral conversion of T4 to T3 might not be affected in the maintenance of an active hormone level. [Pg.200]

When the thyroid gland is stimulated to secrete thyroxine, a small piece of iodinated Tgb is taken from the lumen into a follicular cell, where the hormones are released from the protein. Both T3 and T4 are secreted from the vesicle directly into the bloodstream but the plasma concentration of T4 is substantially higher than that of T3. In contrast, T3 has a higher biological activity than T4 and conversion of T4 to T3 occurs at the target site. [Pg.90]

The Class III effects of amiodarone develop over several weeks. This time-course is similar to that seen in thyroid gland ablation [25]. It is well known that patients with hypothyroidism have long QT intervals which are indicative of prolonged action potentials. Amiodarone has been shown to inhibit the conversion of thyroxine (T4) to triiodothyronine (T3) both in human subjects [26] and in vitro [27]. It has been argued that the Class III effects of amiodarone are due to its effects on thyroid hormones [28]. Others, however, argue that there is no relationship between prolongation of ventricular refractory period by amiodarone and thyroid state [29]. [Pg.72]

T3 levels in the blood are low with a decreased rate of formation from thyroxine bnt increased conversion of the latter to reverse triiodothyronine (rTs). [Pg.361]

The thyroid releases predominantly thyroxine (T4). However, the active form appears to be triiodothyronine (T3) T4 is converted in part to T3, receptor affinity in target organs being 10-fold higher for T3. The effect of T3 develops more rapidly and has a shorter duration than does that of T4. Plasma elimination tip for T4 is about 7 d that for T3, however, is only 1.5 d. Conversion of T4 to T3 releases iodide 150 pg T4 contains 100 pg of iodine. [Pg.244]

Thyroid abnormalities Am o6arone inhibits peripheral conversion of thyroxine (T4) to triiodothyronine (T3), prompting increased T4levels, increased levels of inactive reverse T3 and decreased levels of T3. It is also a potential source of large amounts... [Pg.473]

Hyperthyroidism is characterized by an enhanced sympathetic activity, especially in the heart. The salutary inhibition of jS-adrenoceptors under these conditions can be achieved by all jS-blocker alike. Some of the clinically used compounds are able to reduce the conversion (de-iodination) of thyroxine (T4) to the active 3,5,3 -Triiodothyronine (T3)... [Pg.308]

PTU possesses special benefit it inhibits peripheral deiodination, thereby blocking the conversion of thyroxine to the active hormone tri-iodothyronine. PTU is rapidly absorbed from the gut, reaching peak blood levels within one hour, and is excreted in urine as the inactive glucuronide within 24 hours. In contrast methimazole which is absorbed at variable rates, is excreted slower (only 65-70% within 48 hours in urine). The short plasma half-life of... [Pg.759]

Amiodarone inhibits the peripheral and possibly in-trapituitary conversion of thyroxine (T4) to triiodothyronine (Tj) by inhibiting 5 -deiodination. The serum concentration of T4 is increased by a decrease in its clearance, and thyroid synthesis is increased by a reduced suppression of the pituitary thyrotropin T3. The concentration of T3 in the serum decreases, and reverse T3 appears in increased amounts. Despite these changes, most patients appear to be maintained in an euthyroid state. Manifestations of both hypothyroidism and hyperthyroidism have been reported. [Pg.188]

Hyperthyroidism Propranolol blocks the peripheral conversion of thyroxine to triiodothyronine. It controls palpitation, nervousness, tremor sweating etc. [Pg.150]

Excessive catecholamine action is an important aspect of the pathophysiology of hyperthyroidism, especially in relation to the heart (see Chapter 38). The 13 antagonists are beneficial in this condition. The effects presumably relate to blockade of adrenoceptors and perhaps in part to the inhibition of peripheral conversion of thyroxine to triiodothyronine. The latter action may vary from one 13 antagonist to another. Propranolol has been used extensively in patients with thyroid storm (severe hyperthyroidism) it is used cautiously in patients with this condition to control supraventricular tachycardias that often precipitate heart failure. [Pg.214]

Antithyroid drugs may also suppress lymphocytic infiltration into the thyroid and thereby directly modulate the basic disorder of autoimmune hyperthyroidism (SEDA-6, 364 SEDA-9, 344). Propylthiouracil, but not the thioimidazoles, also inhibits the conversion of thyroxine to its more active derivative triiodothyronine. This effect is significant during high-dose treatment, and propylthiouracil may therefore be preferred if a more rapid onset of action is desired, for example thyrotoxic crisis, although clear experimental proof of the advantageous effect is still lacking (3). [Pg.335]

Thyroid function tests are often altered by somatropin because of increased conversion of T4 to T3, but this is clinically insignificant at low doses (SEDA-21, 453). One child with Prader-Willi syndrome had a fall in serum thyroxine concentration during somatropin therapy and needed thyroxine replacement (33). Hypothyroidism developed in 11 of 46 growth hormone-deficient children treated with somatropin (34). Prior abnormalities in hypothalamic-pituitary function and alterations in thyroid hormone metabolism, probably both, contributed to the high incidence of hypothyroidism, which was similar to that in previous studies. [Pg.510]

Despite the fact that she was clinically euthyroid, the authors suggested that this patient had amiodarone-induced hyperthyroidism. However, amiodarone inhibits the peripheral conversion of thyroxine to triiodothyronine it can therefore increase the serum thyroxine and suppress the serum TSH, as in this case. On the other hand, the reduced uptake by the thyroid gland is consistent with type 2 amiodarone-induced hyperthyroidism. The authors did not report the serum concentrations of free thyroxine and triiodothyronine. [Pg.576]

Propranolol inhibits the conversion of thyroxine (T4) to tri-iodothyronine (T3) by peripheral tissues (180), resulting in increased formation of inactive reverse T3. There have been several reports of hyperthyroxinemia in clinically euthyroid patients taking propranolol for non-thyroid reasons in high dosages (320-480 mg/day) (181,182). The incidence was considered to be higher than could be accounted for by the development of spontaneous hyperthyroidism, but the mechanism is unknown. [Pg.586]

Heyma P, Larkins RG, Higginbotham L, Ng KW. D-pro-pranolol and DL-propranolol both decrease conversion of L-thyroxine to L-triiodothyronine. BMJ 1980 281(6232) ... [Pg.663]

An advantage of T-3/L-triiodothyronine administration over T-4/L-thyroxine was the lack of dependence upon the liver enzyme responsible for T-4/T-3 conversion. During diet restricted periods the liver naturally decreases the liver enzyme levels as a control measure to prevent metabolic rate induced starvation. Just as the liver increases production of this enzyme in response to elevated calorie intake it also reduces levels in response to decreased calorie intake. Remember that T-4 /L-thyroxine is only 20% as active as T-3/L-triiodothyronine. [Pg.111]

Synthroid is a man-made synthetically manufactured version of T-4/L-thyroxine. The average person produces about 76 MCG/d of T-4/L-thyroxine which is then converted by the liver into the more active T-3/L-triiodothyronine. This is true of the oral T-4/L-thyroxine medications as well. The average conversion rate of T-4 to T-3 is about 30-33%/ MCG. Since the conversion of T-4 to T-3 is dependent upon adequate levels of since and selenium, athletes commonly increase daily intake of these minerals during synthetic T-4/L-thyroxine use. [Pg.115]

Because thyroxine contains four iodine residues, this compound is also referred to by the abbreviation T4. Likewise, triiodothyronine contains three iodine residues, hence the abbreviation T3. There has been considerable discussion about which hormone exerts the primary physiologic effects. Plasma levels of T4 are much higher than T3 levels, but T3 may exert most of the physiologic effects on various tissues, which suggests that T4 is a precursor to T3 and that the conversion of T4 to T3 occurs in peripheral tissues.23 Regardless of which hormone ultimately affects cellular metabolism, both T4 and T3 are needed for normal thyroid function. [Pg.459]

In this chapter we will first briefly describe the major parameters controlling the level of thyroid hormone production and its concentration by the target cell (see Ref. 6), i.e., biosynthesis and output from the thyroid gland, transport in the blood, conversion of the prohormone thyroxine (T4), to the active form, 3,5,3 -triiodo-... [Pg.62]

Selenium is an essential trace element, being important in at least two critical enzymes, the antioxidant glutathione peroxidase (GPx), and type 1 iodothyronine deiodinase. GPx converts hydrogen peroxide to water, in the presence of reduced glutathione, while iodothyronine deiodinase catalyzes the conversion of thyroxine to triiodothyronine, the physiologically active hormone species. [Pg.23]

It has been reported that high doses (138 and 430 mg/kg) of omeprazole to rats interfere with the peripheral conversion of thyroxine (T4) to tri-iodothyronine (T3) resulting in the decrease of serum T3, unchanged serum T4 and no change in the morphology of the thyroid gland [119]. [Pg.253]


See other pages where Thyroxine conversion is mentioned: [Pg.326]    [Pg.477]    [Pg.42]    [Pg.71]    [Pg.144]    [Pg.100]    [Pg.1238]    [Pg.89]    [Pg.374]    [Pg.62]    [Pg.1238]    [Pg.855]    [Pg.199]    [Pg.1699]    [Pg.364]    [Pg.882]    [Pg.394]    [Pg.1498]    [Pg.408]    [Pg.410]    [Pg.46]   
See also in sourсe #XX -- [ Pg.3 , Pg.917 ]

See also in sourсe #XX -- [ Pg.5 , Pg.6 , Pg.7 , Pg.8 , Pg.9 , Pg.10 , Pg.11 , Pg.12 , Pg.13 , Pg.14 , Pg.15 , Pg.16 , Pg.17 ]




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