Thyroid hormone in blood

For example, alternative transcription-control elements regulate expression of the mammalian gene that encodes transthyretin (TTR), which transports thyroid hormone in blood and the cerebrospinal fluid that surrounds the brain... 

A goitre is an enlarged thyroid gland (Fig. 4). This may be as.stKiated with hypofunction. hyperfunclion or, indeed, normal concentrations of thyroid hormones in blood. With such a clinical presentation, the bitK hemistry laboratory can confirm if a patient is hypothyroid, hyperthyroid or euthyroid. 

A patient may have severe thyroid disease, such as a large goitre or thyroid cancer, yet have normal concentrations of thyroid hormones in blood. 

Deiodination of Tetra- and Triiodo-Derivatives Thyroid Hormone in Blood... 

In the human, TTR is one of three plasma proteins involved in the transport of the thyroid hormones in blood (Ingbar, 1963 Oppenheimer, 1968). The principal transport protein for thyroid hormones in human plasma is thyroxine-binding globulin, and TTR plays only a lesser role in the normal transport and metabolism of thyroid hormones in man (Woeber and Ingbar, 1968). In the rat, however, TTR appears to be the major thyroid hormone transport protein (Davis et al., 1970 Sutherland and Brandon, 1976). 

POTTER s M, FERTILE J and BERBER-JIMENEZ M D (1996) Soy protein concentrate and isolated soy protein similarly lower blood serum cholesterol hut differently affect thyroid hormones in hamsters. J Nutr. 126 (8) 2007-11. 

The concentration of thyroid hormones in a given responsive cell depends on a number of factors (Fig. 2) including 1) the production of the two major hormones in the thyroid gland and their secretion in the blood (see Ref. 6) (both the synthesis and the secretion processess are themselves regulated by TSH) 2) the transport of T4 and T3 in the blood and then their degradation in the liver and in the kidney 3) the uptake of thyroid hormones by the different target cells 4) the peripheral conversion of the prohormone, T4, to the active (T3) and the inactive ( reverse T3 or r-T3) derivatives in the responsive cells. 

Observations in experimental animals have shown that some PCBs (specifically 3,3, 4,4 -tetrachlorobiphenyl, TCB) can interfere with thyroid hormone levels. It seems that a metabolite of the TCB is similar to the thyroid hormone thyroxine and therefore competes with it for binding to a specific receptor. One of the consequences is loss of thyroxine and vitamin A from the blood. There is evidence for similar effects in humans in that higher levels of PCBs in breast milk correlated with lower levels of certain thyroid hormones in mothers and infants. 

Condhffe P, Weintraub B. Pituitary thyroid-stimulating hormone and other thyroid-stimulating substances. In Gray C, James V, eds. Hormones in blood. Vol 3. London Academic, 1979 499-574. 

Graves disease is the most common cause of hyperthyroidism, and is an autoimmune disease in which antibodies to the T.SM receptor on the surface of thyroid cells appear to mimic the action of the pituitary hormone. The normal regulatory controls on T4 synthesis and secretion are lacking. Pituitary secretion of TSH is completely inhibited by the high concentrations of thyroid hormones in the blood. 

Dohler, K-D., A. von zur Muhlen, K. Gartner, and U. Dohler. 1977. Effect of various blood sampling techniques on serum levels of pituitary and thyroid hormones in the rat. Journal of Endocrinology 74 341-342. 

TRANSPORT OF THYROID HORMONES IN THE BLOOD Iodine circulates as both organic iodine (95%) and inorganic iodide (5%). Most organic iodine is in T (90-95%), while Tj contains approximately 5%. Both T and T are transported in the blood in strong but noncovalent association with plasma proteins. 

The levels of transthyretin (binds to vitamin A and thyroid hormones in the blood) and serum albumin in the blood may be used as indicators of the degree of protein malnutrition. In the absence of hepatic disease, decreased levels of these proteins in the blood indicate insufficient availability of amino acids to the liver for synthesis of serum proteins. 

Riggs then simplified this structure into one which was accessible to experimental use, a modification of which is shown in Figure 19.1. In this model, iodide from food and water enters the body s iodide pool and is then distributed to either the thyroid gland or the kidneys for excretion in the urine. The thyroid organifies the iodine and releases the organic iodine (primarily as T4) into the blood, and hence into the body pool of organic iodine. Except for a small amount excreted in the feces, the thyroid hormone in the periphery is metabolized and the resulting iodide re-enters the iodide pool. 

The resin uptake of labeled T3 (T3U), an indirect parameter for assessing the levels of thyroid hormone in plasma, is based on an earlier technique, namely, the red blood cell uptake of added I-labeled Ts from plasma, Hamolsky et al. (H9) developing the latter technique in 1957. The principle of the test is that T3 is partitioned between the red blood eells and the plasma, depending on the occupying of specific binding sites on the plasma proteins with endogenous thyroid hormone. In other words, the uptake of T3 by the cells is inversely proportional to free TBP capacity. It was soon realized that the red blood cell is a variable in the system, which affected the final result (R3) and the cell was replaced with a fixed amount of ion-exchange resin (M13). 

J, Robbins and M.L. Johnson, Possible significance of multiple transport proteins for the thyroid hormones, in "Free Hormones in Blood", A. Albertini and R.P. Ekins, eds., Elsevier Biomedical Press, Amsterdam (1982). 

Thyroid hormones have long been known to affect lipid metabolism. Thyroxine undoubtedly controls cholesterol metabolism serum cholesterol levels are markedly increased in hypothyroidism and decreased in hyperthyroidism. There are various ways by which thyroxine could cause cholesterol to accumulate in blood direct stimulation of the pathway involved in cholesterol biosynthesis block of cholesterol use for further biosynthesis indirect stimulation of cholesterol synthesis by acceleration of pathways that provide precursors of coenzymes needed for cholesterol synthesis and indirect stimulation of cholesterol synthesis by blocking pathways that use those precursors involved in cholesterol synthesis. The exact mechanism by which thyroxine induces the accumulation of cholesterol in serum needs to be elucidated. The effect of thyroid hormones on blood cholesterol must be understood because hypothyroidism is known to enhance the development of experimental arteriosclerosis in animals. 

Isoproterenol (Iso) increased avUCP expression (+67% after I h of stimulation), as previously observed in vivo in chicken muscle, but to a greater extent (9 fold-increase Joubert et al, 2010). This discrepancy could be explained by the concomitant effect of isoproterenol on other factors regulating muscle metabolism in vivo, such as plasma thyroid hormones or blood metabolites that could not be investigated here. The use of fatty acid supplement (FA) induced a delayed increase in avUCP expression (+54% after 2 h of stimulation) and was associated with stronger activations of p38 MAPK and AMPK than with isoproterenol. 

Figure 5 SubsidenceotgoiterinaNewQuineawomanSmonths after the injection of iodized oil. This is accompanied by a feeling of well-being due to a rise in the level of the thyroid hormone in the blood. This makes the injections very popular. (Reproduced from Hetzel BS (1989) The Story of Iodine Deficiency An international Challenge in Nutrition. Oxford Oxford University Press.)...

Factors controlling calcium homeostasis are calcitonin, parathyroid hormone(PTH), and a vitamin D metabolite. Calcitonin, a polypeptide of 32 amino acid residues, mol wt - SGOO, is synthesized by the thyroid gland. Release is stimulated by small increases in blood Ca " concentration. The sites of action of calcitonin are the bones and kidneys. Calcitonin increases bone calcification, thereby inhibiting resorption. In the kidney, it inhibits Ca " reabsorption and increases Ca " excretion in urine. Calcitonin operates via a cyclic adenosine monophosphate (cAMP) mechanism. 

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