The hepatic biosynthesis of rat thyroxine binding globulin (TBG): Demonstration, ontogenesis, and UP-regulation in experimental hypothyroidism

Vranckx, Roger; Rouaze, Marielle; Savu, Lia; Nunez, Emmanuel A.; Beaumont, Carole; Flink, Irwin L.

doi:10.1016/0006-291x(90)91767-m

Cited by 36 publications

(22 citation statements)

References 8 publications

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“…In rats and mice, TBG is synthesised by the liver prior to the development of fur and homeothermy, and not in adulthood until senescence (36,49,50). This is a similar pattern for TBG synthesis by M.eugenii and hepatic TTR synthesis by S.crassicaudata during development.…”

Section: Discussionmentioning

confidence: 63%

Developmentally regulated thyroid hormone distributor proteins in marsupials, a reptile, and fish

Richardson¹,

Monk²,

Shepherdley³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Thyroid hormones are essential for vertebrate development. There is a characteristic rise in thyroid hormone levels in blood during critical periods of thyroid hormone-regulated development. Thyroid hormones are lipophilic compounds, which readily partition from an aqueous environment into a lipid environment. Thyroid hormone distributor proteins are required to ensure adequate distribution of thyroid hormones, throughout the aqueous environment of the blood, and to counteract the avid partitioning of thyroid hormones into the lipid environment of cell membranes. In human blood, these proteins are albumin, transthyretin and thyroxine-binding globulin. We analyzed the developmental profile of thyroid hormone distributor proteins in serum from a representative of each order of marsupials ( M. eugenii; S.crassicaudata), a reptile ( C. porosus), in two species of salmonoid fishes ( S. salar; O. tshawytsch), and throughout a calendar year for sea bream ( S. aurata). We demonstrated that during development, these animals have a thyroid hormone distributor protein present in their blood which is not present in the adult blood. At least in mammals, this additional protein has higher affinity for thyroid hormones than the thyroid hormone distributor proteins in the blood of the adult. In fish, reptile and polyprotodont marsupial, this protein was transthyretin. In a diprotodont marsupial, it was thyroxine-binding globulin. We propose an hypothesis that an augmented thyroid hormone distributor protein network contributes to the rise in total thyroid hormone levels in the blood during development.

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Section: Discussionmentioning

confidence: 63%

Developmentally regulated thyroid hormone distributor proteins in marsupials, a reptile, and fish

Richardson¹,

Monk²,

Shepherdley³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In the present case, it is clear that the TTR-bound T 4 does not delay and/or attenuate the decrease in tissue thyroid hormones, as measured at 2 and 3 weeks after removal of the thyroid gland. TBG mRNA levels, known to be up-regulated in hypothyroidism and to correlate with TBG serum levels (Vranckx et al 1990), were similarly induced by thyroidectomy in TTR-null and wildtype mice. Therefore, as we have previously shown for TTR-null mice kept in normal housing conditions (Palha et al 1994), TBG does not compensate for the absence of TTR.…”

Section: Figurementioning

confidence: 93%

Transthyretin is not necessary for thyroid hormone metabolism in conditions of increased hormone demand

Sousa¹,

Escobar²,

Oliveira³

et al. 2005

Journal of Endocrinology

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Thyroid hormones circulate in blood mainly bound to plasma proteins. Transthyretin is the major thyroxine plasma carrier in mice. Studies in transthyretin-null mice revealed that the absence of transthyretin results in euthyroid hypothyroxinemia and normal thyroid hormone tissue distribution, with the exception of the choroid plexus in the brain. Therefore, transthyretin does not influence normal thyroid hormone homeostasis under standard laboratory conditions. To investigate if transthyretin has a buffer/storage role we challenged transthyretin-null and wild-type mice with conditions of increased hormone demand: (i) exposure to cold, which elicits thermogenesis, a process that requires thyroid hormones; and (ii) thyroidectomy, which abolishes thyroid hormone synthesis and secretion and induces severe hypothyroidism. Transthyretin-null mice responded as the wild-type both to changes induced by stressful events, namely in body weight, food intake and thyroid hormone tissue content, and in the mRNA levels of genes whose expression is altered in such conditions. These results clearly exclude a role for transthyretin in thyroid hormone homeostasis even under conditions of increased hormone demand.

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“…Interestingly, 1% to 2% of total TTR circulates bound to high-density lipoproteins through interaction with apolipoprotein A-I (7), and this might account for part of the T 4 transport associated with lipoproteins (8). In adult rodents, TTR and albumin are the principal carriers, while TBG is described to be almost absent (9,10).…”

mentioning

confidence: 99%

Transthyretin as a Thyroid Hormone Carrier: Function Revisited

Palha¹

2002

Clinical Chemistry and Laboratory Medicine

110

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Thyroid hormones are essential for normal mammalian development and for normal metabolism. Thyroxine (T4) is the principal product synthesized by the thyroid follicles, and triiodothyronine (T3), the biologically active hormone, derives mainly from tissue T4 deiodination. More than 99% of the circulating hormone is bound to plasma proteins, mainly to thyroxine-binding globulin, transthyretin and albumin in man, and to transthyretin and albumin in rodents. The role of plasma proteins in the transport of hormones to target tissues has, for a long time, been controversial. The liver and the choroid plexus are the major sites of transthyretin synthesis, tissues from which transthyretin is secreted into the blood and the cerebrospinal fluid, respectively. Transthyretin has been proposed to mediate thyroid hormone transfer into the tissues, particularly into the brain across the choroid-plexus-cerebrospinal fluid barrier. Studies in a transthyretin-null mice strain have shown conclusively that transthyretin is not indespensable for thyroid hormones' entry into the brain and other tissues, nor for the maintenance of an euthyroid status. An euthyroid status is also observed in man totally deprived of thyroxine-binding globulin and in rats without albumin. Taken together, these results exclude dependence of thyroid hormone homeostasis on any major plasma carrier per se. This evidence agrees with the free hormone hypothesis which states that the biologically significant fraction, that is taken up by the tissues, is the free circulating hormone.

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The hepatic biosynthesis of rat thyroxine binding globulin (TBG): Demonstration, ontogenesis, and UP-regulation in experimental hypothyroidism

Cited by 36 publications

References 8 publications

Developmentally regulated thyroid hormone distributor proteins in marsupials, a reptile, and fish

Developmentally regulated thyroid hormone distributor proteins in marsupials, a reptile, and fish

Transthyretin is not necessary for thyroid hormone metabolism in conditions of increased hormone demand

Transthyretin as a Thyroid Hormone Carrier: Function Revisited

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