Thyroid hormone metabolism during development

Dh, Polk

doi:10.1071/rd9950469

Cited by 69 publications

(86 citation statements)

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“…These include development of the hypothalamicpituitary-thyroid axis, onset of thyroid hormone production, and expression of TRs. Overall, human and ovine fetuses are similar in the timing, relative to gestational age, of the structural development of the thyroid gland and the onset of thyroid hormone activity, while rodent species show relatively delayed maturation of thyroid hormone bioavailability (Table 1; Fisher & Polk 1989, Polk 1995. From mid-gestation in human and ovine fetuses, the thyroid gland secretes T 4 and T 3 under the control of the hypothalamic-pituitary axis and the thyroid hormone axis is fully functional around the time of birth (Table 1).…”

Section: Figurementioning

confidence: 99%

“…D1 is primarily a 5 0 -monodeiodinase enzyme that catalyzes outer-ring deiodination of T 4 to T 3 and of rT 3 to T 2 . This enzyme is present in the fetal liver, kidney, and thyroid and pituitary gland, and the production of T 3 by hepatic D1 is considered to be the major endocrine source of circulating T 3 concentrations (Polk 1995). D2 is also a 5 0 -deiodinase enzyme with kinetic characteristics different from D1 that is found primarily in the brain, pituitary gland, placenta, and brown adipose tissue.…”

Section: Metabolism Of Thyroid Hormones In Uteromentioning

confidence: 99%

“…The metabolism of T 4 into more genomically potent T 3 or relatively bio-inactive reverse T 3 (rT 3 ) depends on the activity of deiodinase enzymes, which are developmentally regulated in specific tissues (Brent 2012, Table 1 Comparison of the timing of developmental stages of thyroid hormone bioavailability among human, sheep, and rat fetuses. Data adapted from Thorburn & Hopkins (1973), Bernal & Pekonen (1984, Perez-Castillo et al (1985), Ferreiro et al (1987), Polk et al (1989Polk et al ( , 1991, Thorpe-Beeston et al (1991b), Polk (1995), Brown (2004, and Chan et al (2011) et al 2002). D1 is primarily a 5 0 -monodeiodinase enzyme that catalyzes outer-ring deiodination of T 4 to T 3 and of rT 3 to T 2 .…”

Section: Metabolism Of Thyroid Hormones In Uteromentioning

confidence: 99%

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Thyroid hormones in fetal growth and prepartum maturation

Forhead

Fowden

2014

Journal of Endocrinology

359

270

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The thyroid hormones, thyroxine (T 4 ) and triiodothyronine (T 3 ), are essential for normal growth and development of the fetus. Their bioavailability in utero depends on development of the fetal hypothalamic-pituitary-thyroid gland axis and the abundance of thyroid hormone transporters and deiodinases that influence tissue levels of bioactive hormone. Fetal T 4 and T 3 concentrations are also affected by gestational age, nutritional and endocrine conditions in utero, and placental permeability to maternal thyroid hormones, which varies among species with placental morphology. Thyroid hormones are required for the general accretion of fetal mass and to trigger discrete developmental events in the fetal brain and somatic tissues from early in gestation. They also promote terminal differentiation of fetal tissues closer to term and are important in mediating the prepartum maturational effects of the glucocorticoids that ensure neonatal viability. Thyroid hormones act directly through anabolic effects on fetal metabolism and the stimulation of fetal oxygen consumption. They also act indirectly by controlling the bioavailability and effectiveness of other hormones and growth factors that influence fetal development such as the catecholamines and insulin-like growth factors (IGFs). By regulating tissue accretion and differentiation near term, fetal thyroid hormones ensure activation of physiological processes essential for survival at birth such as pulmonary gas exchange, thermogenesis, hepatic glucogenesis, and cardiac adaptations. This review examines the developmental control of fetal T 4 and T 3 bioavailability and discusses the role of these hormones in fetal growth and development with particular emphasis on maturation of somatic tissues critical for survival immediately at birth.

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Section: Figurementioning

confidence: 99%

Section: Metabolism Of Thyroid Hormones In Uteromentioning

confidence: 99%

Section: Metabolism Of Thyroid Hormones In Uteromentioning

confidence: 99%

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Thyroid hormones in fetal growth and prepartum maturation

Forhead

Fowden

2014

Journal of Endocrinology

359

270

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“…This study also examined bone development in fetuses where the prepartum rise in cortisol and T 3 was abolished by adrenalectomy. The sheep fetus is a good experimental model for the human fetus as the timing of the development of the thyroid hormone axis is similar in the two species (Polk 1995).…”

Section: Introductionmentioning

confidence: 99%

“…Developmental changes in the availability of the thyroid hormones occur before birth, and in the fetus as well as in the adult animal, the circulating and local levels of thyroid hormones are largely determined by the activities of deiodinase enzymes in specific tissues (Polk 1995). For most of gestation, thyroxine (T 4 ) is metabolized to reverse-T 3 , which is biologically inactive, by deiodinase type 3 (D3) activity in the placenta and fetal organs.…”

Section: Introductionmentioning

confidence: 99%

Effects of hypothyroidism on the structure and mechanical properties of bone in the ovine fetus

Lanham

Fowden

Roberts³

et al. 2011

Journal of Endocrinology

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Thyroid hormones are important for normal bone growth and development in postnatal life. However, little is known about the role of thyroid hormones in the control of bone development in the fetus. Using computed tomography and mechanical testing, the structure and strength of metatarsal bones were measured in sheep fetuses in which thyroid hormone levels were altered by thyroidectomy or adrenalectomy. In intact fetuses, plasma concentrations of total calcium and the degradation products of C-terminal telopeptides of type I collagen increased between 100 and 144 days of gestation (term 145G2 days), in association with various indices of bone growth and development. Thyroid hormone deficiency induced by thyroidectomy at 105-110 days of gestation caused growth retardation of the fetus and significant changes in metatarsal bone structure and strength when analyzed at both 130 and 144 days of gestation. In hypothyroid fetuses, trabecular bone was stronger with thicker, more closely spaced trabeculae, despite lower bone mineral density. Plasma osteocalcin was reduced by fetal thyroidectomy. Removal of the fetal adrenal gland at 115-120 days of gestation, and prevention of the prepartum rises in cortisol and triiodothyronine, had no effect on bodyweight, limb lengths, metatarsal bone structure or strength, or circulating markers of bone metabolism in the fetuses studied near term. This study demonstrates that hypothyroidism in utero has significant effects on the structure and strength of bone, with different consequences for cortical and trabecular bone.

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Fetal Endocrinology

and

Keller‐Wood

2007

Clinical Obstetrics

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Thyroid hormone metabolism during development

Cited by 69 publications

References 0 publications

Thyroid hormones in fetal growth and prepartum maturation

Thyroid hormones in fetal growth and prepartum maturation

Effects of hypothyroidism on the structure and mechanical properties of bone in the ovine fetus

Fetal Endocrinology

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